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  <front>
    <journal-meta>
      <journal-id journal-id-type="nlm-ta">Arq Bras Cardiol</journal-id>
      <journal-id journal-id-type="publisher-id">abc</journal-id>
      <journal-title-group>
        <journal-title>Arquivos Brasileiros de Cardiologia</journal-title>
        <abbrev-journal-title abbrev-type="publisher">Arq. Bras. Cardiol.</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="ppub">0066-782X</issn>
      <issn pub-type="epub">1678-4170</issn>
      <publisher>
        <publisher-name>Sociedade Brasileira de Cardiologia - SBC</publisher-name>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id specific-use="scielo-v3" pub-id-type="publisher-id">tNh3qfrVcdn4cDzTqmNjCtQ</article-id>
      <article-id specific-use="scielo-v2" pub-id-type="publisher-id">S0066-782X2023001201301</article-id>
      <article-id pub-id-type="other">01301</article-id>
      <article-id pub-id-type="doi">10.36660/abc.20230646</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Posicionamento</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Posicionamento do Departamento de Imagem Cardiovascular da Sociedade Brasileira de Cardiologia sobre o Uso do <italic>Strain</italic> Mioc&#225;rdico na Rotina do Cardiologista &#8211; 2023</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-1777-477X</contrib-id>
          <name>
            <surname>Almeida</surname>
            <given-names>Andr&#233; Luiz Cerqueira</given-names>
          </name>
          <xref ref-type="aff" rid="aff1">
            <sup>1</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-8809-8783</contrib-id>
          <name>
            <surname>Melo</surname>
            <given-names>Marcelo Dantas Tavares de</given-names>
          </name>
          <xref ref-type="aff" rid="aff2">
            <sup>2</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-1919-164X</contrib-id>
          <name>
            <surname>Bihan</surname>
            <given-names>David Costa de Souza Le</given-names>
          </name>
          <xref ref-type="aff" rid="aff3">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-4561-5717</contrib-id>
          <name>
            <surname>Vieira</surname>
            <given-names>Marcelo Luiz Campos</given-names>
          </name>
          <xref ref-type="aff" rid="aff3">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-8920-5173</contrib-id>
          <name>
            <surname>Pena</surname>
            <given-names>Jos&#233; Luiz Barros</given-names>
          </name>
          <xref ref-type="aff" rid="aff4">
            <sup>4</sup>
          </xref>
          <xref ref-type="aff" rid="aff5">
            <sup>5</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-2214-203X</contrib-id>
          <name>
            <surname>Del Castillo</surname>
            <given-names>Jos&#233; Maria</given-names>
          </name>
          <xref ref-type="aff" rid="aff6">
            <sup>6</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Abensur</surname>
            <given-names>Henry</given-names>
          </name>
          <xref ref-type="aff" rid="aff7">
            <sup>7</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-0031-335X</contrib-id>
          <name>
            <surname>Hortegal</surname>
            <given-names>Renato de Aguiar</given-names>
          </name>
          <xref ref-type="aff" rid="aff8">
            <sup>8</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Otto</surname>
            <given-names>Maria Estefania Bosco</given-names>
          </name>
          <xref ref-type="aff" rid="aff9">
            <sup>9</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-4154-3197</contrib-id>
          <name>
            <surname>Piveta</surname>
            <given-names>Rafael Bonafim</given-names>
          </name>
          <xref ref-type="aff" rid="aff10">
            <sup>10</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-3141-2310</contrib-id>
          <name>
            <surname>Dantas</surname>
            <given-names>Maria Rosa</given-names>
          </name>
          <xref ref-type="aff" rid="aff11">
            <sup>11</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-5153-8420</contrib-id>
          <name>
            <surname>Assef</surname>
            <given-names>Jorge Eduardo</given-names>
          </name>
          <xref ref-type="aff" rid="aff8">
            <sup>8</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-5903-987X</contrib-id>
          <name>
            <surname>Beck</surname>
            <given-names>Adenalva Lima de Souza</given-names>
          </name>
          <xref ref-type="aff" rid="aff12">
            <sup>12</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0009-0008-1958-1825</contrib-id>
          <name>
            <surname>Santo</surname>
            <given-names>Thais Harada Campos Espirito</given-names>
          </name>
          <xref ref-type="aff" rid="aff13">
            <sup>13</sup>
          </xref>
          <xref ref-type="aff" rid="aff14">
            <sup>14</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-9983-6438</contrib-id>
          <name>
            <surname>Silva</surname>
            <given-names>Tonnison de Oliveira</given-names>
          </name>
          <xref ref-type="aff" rid="aff15">
            <sup>15</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-7152-1810</contrib-id>
          <name>
            <surname>Salemi</surname>
            <given-names>Vera Maria Cury</given-names>
          </name>
          <xref ref-type="aff" rid="aff3">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-0625-1084</contrib-id>
          <name>
            <surname>Rocon</surname>
            <given-names>Camila</given-names>
          </name>
          <xref ref-type="aff" rid="aff16">
            <sup>16</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-6110-2500</contrib-id>
          <name>
            <surname>Lima</surname>
            <given-names>M&#225;rcio Silva Miguel</given-names>
          </name>
          <xref ref-type="aff" rid="aff3">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-0711-7995</contrib-id>
          <name>
            <surname>Barberato</surname>
            <given-names>Silvio Henrique</given-names>
          </name>
          <xref ref-type="aff" rid="aff17">
            <sup>17</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-4500-5270</contrib-id>
          <name>
            <surname>Rodrigues</surname>
            <given-names>Ana Clara</given-names>
          </name>
          <xref ref-type="aff" rid="aff10">
            <sup>10</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Rabschkowisky</surname>
            <given-names>Arnaldo</given-names>
          </name>
          <xref ref-type="aff" rid="aff18">
            <sup>18</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-9131-0439</contrib-id>
          <name>
            <surname>Frota</surname>
            <given-names>Daniela do Carmo Rassi</given-names>
          </name>
          <xref ref-type="aff" rid="aff19">
            <sup>19</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-0477-480X</contrib-id>
          <name>
            <surname>Gripp</surname>
            <given-names>Eliza de Almeida</given-names>
          </name>
          <xref ref-type="aff" rid="aff20">
            <sup>20</sup>
          </xref>
          <xref ref-type="aff" rid="aff21">
            <sup>21</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Barretto</surname>
            <given-names>Rodrigo Bellio de Mattos</given-names>
          </name>
          <xref ref-type="aff" rid="aff3">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-3152-298X</contrib-id>
          <name>
            <surname>Silva</surname>
            <given-names>Sandra Marques e</given-names>
          </name>
          <xref ref-type="aff" rid="aff22">
            <sup>22</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-1969-5135</contrib-id>
          <name>
            <surname>Cauduro</surname>
            <given-names>Sanderson Antonio</given-names>
          </name>
          <xref ref-type="aff" rid="aff23">
            <sup>23</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-3466-7052</contrib-id>
          <name>
            <surname>Pinheiro</surname>
            <given-names>Aur&#233;lio Carvalho</given-names>
          </name>
          <xref ref-type="aff" rid="aff24">
            <sup>24</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0009-0000-0121-2599</contrib-id>
          <name>
            <surname>Araujo</surname>
            <given-names>Salustiano Pereira de</given-names>
          </name>
          <xref ref-type="aff" rid="aff25">
            <sup>25</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-5376-1802</contrib-id>
          <name>
            <surname>Tressino</surname>
            <given-names>Cintia Galhardo</given-names>
          </name>
          <xref ref-type="aff" rid="aff8">
            <sup>8</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Silva</surname>
            <given-names>Carlos Eduardo Suaide</given-names>
          </name>
          <xref ref-type="aff" rid="aff26">
            <sup>26</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Monaco</surname>
            <given-names>Claudia Gianini</given-names>
          </name>
          <xref ref-type="aff" rid="aff10">
            <sup>10</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-8728-4357</contrib-id>
          <name>
            <surname>Paiva</surname>
            <given-names>Marcelo Goulart</given-names>
          </name>
          <xref ref-type="aff" rid="aff27">
            <sup>27</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0009-0005-7507-6338</contrib-id>
          <name>
            <surname>Fisher</surname>
            <given-names>Cl&#225;udio Henrique</given-names>
          </name>
          <xref ref-type="aff" rid="aff10">
            <sup>10</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-0794-7339</contrib-id>
          <name>
            <surname>Alves</surname>
            <given-names>Marco Stephan Lofrano</given-names>
          </name>
          <xref ref-type="aff" rid="aff28">
            <sup>28</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-2758-4793</contrib-id>
          <name>
            <surname>Grau</surname>
            <given-names>Cl&#225;udia R. Pinheiro de Castro</given-names>
          </name>
          <xref ref-type="aff" rid="aff3">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0009-0008-2038-5741</contrib-id>
          <name>
            <surname>Santos</surname>
            <given-names>Maria Veronica Camara dos</given-names>
          </name>
          <xref ref-type="aff" rid="aff29">
            <sup>29</sup>
          </xref>
          <xref ref-type="aff" rid="aff30">
            <sup>30</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-3367-5779</contrib-id>
          <name>
            <surname>Guimar&#227;es</surname>
            <given-names>Isabel Cristina Britto</given-names>
          </name>
          <xref ref-type="aff" rid="aff31">
            <sup>31</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-5531-9647</contrib-id>
          <name>
            <surname>Morhy</surname>
            <given-names>Samira Saady</given-names>
          </name>
          <xref ref-type="aff" rid="aff10">
            <sup>10</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-6600-2311</contrib-id>
          <name>
            <surname>Leal</surname>
            <given-names>Gabriela Nunes</given-names>
          </name>
          <xref ref-type="aff" rid="aff32">
            <sup>32</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-8534-5934</contrib-id>
          <name>
            <surname>Soares</surname>
            <given-names>Andressa Mussi</given-names>
          </name>
          <xref ref-type="aff" rid="aff33">
            <sup>33</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-2932-766X</contrib-id>
          <name>
            <surname>Cruz</surname>
            <given-names>Cecilia Beatriz Bittencourt Viana</given-names>
          </name>
          <xref ref-type="aff" rid="aff3">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-8760-2052</contrib-id>
          <name>
            <surname>Guimar&#227;es</surname>
            <given-names>Fabio Villa&#231;a</given-names>
            <suffix>Filho</suffix>
          </name>
          <xref ref-type="aff" rid="aff34">
            <sup>34</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-0384-348X</contrib-id>
          <name>
            <surname>Assun&#231;&#227;o</surname>
            <given-names>Bruna Morhy Borges Leal</given-names>
          </name>
          <xref ref-type="aff" rid="aff35">
            <sup>35</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-1216-8316</contrib-id>
          <name>
            <surname>Fernandes</surname>
            <given-names>Rafael Modesto</given-names>
          </name>
          <xref ref-type="aff" rid="aff36">
            <sup>36</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Saraiva</surname>
            <given-names>Roberto Magalh&#227;es</given-names>
          </name>
          <xref ref-type="aff" rid="aff37">
            <sup>37</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Tsutsui</surname>
            <given-names>Jeane Mike</given-names>
          </name>
          <xref ref-type="aff" rid="aff38">
            <sup>38</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-1632-212X</contrib-id>
          <name>
            <surname>Soares</surname>
            <given-names>F&#225;bio Luis de Jesus</given-names>
          </name>
          <xref ref-type="aff" rid="aff39">
            <sup>39</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-0448-8667</contrib-id>
          <name>
            <surname>Falc&#227;o</surname>
            <given-names>Sandra N&#237;vea dos Reis Saraiva</given-names>
          </name>
          <xref ref-type="aff" rid="aff40">
            <sup>40</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-9236-3815</contrib-id>
          <name>
            <surname>Hotta</surname>
            <given-names>Viviane Tiemi</given-names>
          </name>
          <xref ref-type="aff" rid="aff3">
            <sup>3</sup>
          </xref>
          <xref ref-type="aff" rid="aff38">
            <sup>38</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-3161-8922</contrib-id>
          <name>
            <surname>Armstrong</surname>
            <given-names>Anderson da Costa</given-names>
          </name>
          <xref ref-type="aff" rid="aff41">
            <sup>41</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-8857-3094</contrib-id>
          <name>
            <surname>Hygidio</surname>
            <given-names>Daniel de Andrade</given-names>
          </name>
          <xref ref-type="aff" rid="aff42">
            <sup>42</sup>
          </xref>
          <xref ref-type="aff" rid="aff43">
            <sup>43</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-3314-9712</contrib-id>
          <name>
            <surname>Miglioranza</surname>
            <given-names>Marcelo Haertel</given-names>
          </name>
          <xref ref-type="aff" rid="aff44">
            <sup>44</sup>
          </xref>
          <xref ref-type="aff" rid="aff45">
            <sup>45</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-9291-1308</contrib-id>
          <name>
            <surname>Camarozano</surname>
            <given-names>Ana Cristina</given-names>
          </name>
          <xref ref-type="aff" rid="aff28">
            <sup>28</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-7302-7448</contrib-id>
          <name>
            <surname>Lopes</surname>
            <given-names>Marly Maria Uellendahl</given-names>
          </name>
          <xref ref-type="aff" rid="aff46">
            <sup>46</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-3913-7181</contrib-id>
          <name>
            <surname>Cerci</surname>
            <given-names>Rodrigo Julio</given-names>
          </name>
          <xref ref-type="aff" rid="aff47">
            <sup>47</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-0298-8262</contrib-id>
          <name>
            <surname>Siqueira</surname>
            <given-names>Maria Eduarda Menezes de</given-names>
          </name>
          <xref ref-type="aff" rid="aff46">
            <sup>46</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-3418-3226</contrib-id>
          <name>
            <surname>Torre&#227;o</surname>
            <given-names>Jorge Andion</given-names>
          </name>
          <xref ref-type="aff" rid="aff48">
            <sup>48</sup>
          </xref>
          <xref ref-type="aff" rid="aff49">
            <sup>49</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-4505-3344</contrib-id>
          <name>
            <surname>Rochitte</surname>
            <given-names>Carlos Eduardo</given-names>
          </name>
          <xref ref-type="aff" rid="aff3">
            <sup>3</sup>
          </xref>
          <xref ref-type="aff" rid="aff16">
            <sup>16</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-7046-8707</contrib-id>
          <name>
            <surname>Felix</surname>
            <given-names>Alex</given-names>
          </name>
          <xref ref-type="aff" rid="aff26">
            <sup>26</sup>
          </xref>
          <xref ref-type="aff" rid="aff50">
            <sup>50</sup>
          </xref>
        </contrib>
      </contrib-group>
      <aff id="aff1">
        <label>1</label>
        <institution content-type="orgname">Santa Casa de Miseric&#243;rdia de Feira de Santana</institution>
        <addr-line>
          <named-content content-type="city">Feira de Santana</named-content>
          <named-content content-type="state">BA</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Santa Casa de Miseric&#243;rdia de Feira de Santana, Feira de Santana, BA &#8211; Brasil</institution>
      </aff>
      <aff id="aff2">
        <label>2</label>
        <institution content-type="orgname">Universidade Federal da Para&#237;ba</institution>
        <addr-line>
          <named-content content-type="city">Jo&#227;o Pessoa</named-content>
          <named-content content-type="state">PB</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Universidade Federal da Para&#237;ba,Jo&#227;o Pessoa, PB &#8211; Brasil</institution>
      </aff>
      <aff id="aff3">
        <label>3</label>
        <institution content-type="orgdiv2">Instituto do Cora&#231;&#227;o</institution>
        <institution content-type="orgdiv1">Faculdade de Medicina</institution>
        <institution content-type="orgname">Universidade de S&#227;o Paulo</institution>
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Instituto do Cora&#231;&#227;o da Faculdade de Medicina da Universidade de S&#227;o Paulo (Incor/FMUSP), S&#227;o Paulo, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff4">
        <label>4</label>
        <institution content-type="orgname">Faculdade Ci&#234;ncias M&#233;dicas de Minas Gerais</institution>
        <addr-line>
          <named-content content-type="city">Belo Horizonte</named-content>
          <named-content content-type="state">MG</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Faculdade Ci&#234;ncias M&#233;dicas de Minas Gerais, Belo Horizonte, MG &#8211; Brasil</institution>
      </aff>
      <aff id="aff5">
        <label>5</label>
        <institution content-type="orgname">Hospital Felicio Rocho</institution>
        <addr-line>
          <named-content content-type="city">Belo Horizonte</named-content>
          <named-content content-type="state">MG</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Hospital Felicio Rocho, Belo Horizonte, MG &#8211; Brasil</institution>
      </aff>
      <aff id="aff6">
        <label>6</label>
        <institution content-type="orgname">Escola de Ecografia de Pernambuco</institution>
        <addr-line>
          <named-content content-type="city">Recife</named-content>
          <named-content content-type="state">PE</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Escola de Ecografia de Pernambuco (ECOPE), Recife, PE &#8211; Brasil</institution>
      </aff>
      <aff id="aff7">
        <label>7</label>
        <institution content-type="orgname">Benefic&#234;ncia Portuguesa de S&#227;o Paulo</institution>
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Benefic&#234;ncia Portuguesa de S&#227;o Paulo, S&#227;o Paulo, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff8">
        <label>8</label>
        <institution content-type="orgname">Instituto Dante Pazzanese de Cardiologia</institution>
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Instituto Dante Pazzanese de Cardiologia, S&#227;o Paulo, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff9">
        <label>9</label>
        <institution content-type="orgname">DF Star, Rede D&#8217;Or S&#227;o Luiz</institution>
        <addr-line>
          <named-content content-type="city">Bras&#237;lia</named-content>
          <named-content content-type="state">DF</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">DF Star, Rede D&#8217;Or S&#227;o Luiz, Bras&#237;lia, DF &#8211; Brasil</institution>
      </aff>
      <aff id="aff10">
        <label>10</label>
        <institution content-type="orgname">Hospital Israelita Albert Einstein</institution>
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Hospital Israelita Albert Einstein, S&#227;o Paulo, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff11">
        <label>11</label>
        <institution content-type="orgname">Santa Casa de Feira de Santana</institution>
        <addr-line>
          <named-content content-type="city">Feira de Santana</named-content>
          <named-content content-type="state">BA</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Santa Casa de Feira de Santana, Feira de Santana, BA &#8211; Brasil</institution>
      </aff>
      <aff id="aff12">
        <label>12</label>
        <institution content-type="orgname">Instituto de Cardiologia e Transplantes do DF</institution>
        <addr-line>
          <named-content content-type="city">Bras&#237;lia</named-content>
          <named-content content-type="state">DF</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Instituto de Cardiologia e Transplantes do DF, Bras&#237;lia, DF &#8211; Brasil</institution>
      </aff>
      <aff id="aff13">
        <label>13</label>
        <institution content-type="orgname">Grupo Fleury</institution>
        <addr-line>
          <named-content content-type="city">Salvador</named-content>
          <named-content content-type="state">BA</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Diagnoson, Grupo Fleury, Salvador, BA &#8211; Brasil</institution>
      </aff>
      <aff id="aff14">
        <label>14</label>
        <institution content-type="orgname">Hospital da Bahia</institution>
        <addr-line>
          <named-content content-type="city">Salvador</named-content>
          <named-content content-type="state">BA</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Hospital da Bahia, Salvador, BA &#8211; Brasil</institution>
      </aff>
      <aff id="aff15">
        <label>15</label>
        <institution content-type="orgname">Escola Bahiana de Medicina e Sa&#250;de Publica</institution>
        <addr-line>
          <named-content content-type="city">Salvador</named-content>
          <named-content content-type="state">BA</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Escola Bahiana de Medicina e Sa&#250;de Publica, Salvador, BA &#8211; Brasil</institution>
      </aff>
      <aff id="aff16">
        <label>16</label>
        <institution content-type="orgname">Hospital do Cora&#231;&#227;o</institution>
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Hospital do Cora&#231;&#227;o (HCor), S&#227;o Paulo, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff17">
        <label>17</label>
        <institution content-type="orgname">CardioEco Centro de Diagn&#243;stico Cardiovascular e Ecocardiografia</institution>
        <addr-line>
          <named-content content-type="city">Curitiba</named-content>
          <named-content content-type="state">PR</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">CardioEco Centro de Diagn&#243;stico Cardiovascular e Ecocardiografia, Curitiba, PR &#8211; Brasil</institution>
      </aff>
      <aff id="aff18">
        <label>18</label>
        <institution content-type="orgname">UnitedHealth Group</institution>
        <addr-line>
          <named-content content-type="city">Rio de Janeiro</named-content>
          <named-content content-type="state">RJ</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">UnitedHealth Group, Rio de Janeiro, RJ &#8211; Brasil</institution>
      </aff>
      <aff id="aff19">
        <label>19</label>
        <institution content-type="orgdiv1">Faculdade de Medicina</institution>
        <institution content-type="orgname">Universidade Federal de Goi&#225;s</institution>
        <addr-line>
          <named-content content-type="city">Goi&#226;nia</named-content>
          <named-content content-type="state">GO</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Faculdade de Medicina da Universidade Federal de Goi&#225;s, Goi&#226;nia, GO &#8211; Brasil</institution>
      </aff>
      <aff id="aff20">
        <label>20</label>
        <institution content-type="orgname">Hospital Pr&#243;-Cardiaco</institution>
        <addr-line>
          <named-content content-type="city">Rio de Janeiro</named-content>
          <named-content content-type="state">RJ</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Hospital Pr&#243;-Cardiaco, Rio de Janeiro, RJ &#8211; Brasil</institution>
      </aff>
      <aff id="aff21">
        <label>21</label>
        <institution content-type="orgdiv1">Hospital Universit&#225;rio Ant&#244;nio Pedro</institution>
        <institution content-type="orgname">Universidade Federal Fluminense</institution>
        <addr-line>
          <named-content content-type="city">Rio de Janeiro</named-content>
          <named-content content-type="state">RJ</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Hospital Universit&#225;rio Ant&#244;nio Pedro da Universidade Federal Fluminense (UFF), Rio de Janeiro, RJ &#8211; Brasil</institution>
      </aff>
      <aff id="aff22">
        <label>22</label>
        <institution content-type="orgname">Secretaria de Estado de Sa&#250;de do Distrito Federal</institution>
        <addr-line>
          <named-content content-type="city">Bras&#237;lia</named-content>
          <named-content content-type="state">DF</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Secretaria de Estado de Sa&#250;de do Distrito Federal, Bras&#237;lia, DF &#8211; Brasil</institution>
      </aff>
      <aff id="aff23">
        <label>23</label>
        <institution content-type="orgname">Cl&#237;nica Cardio &amp; Sa&#250;de</institution>
        <addr-line>
          <named-content content-type="city">Curitiba</named-content>
          <named-content content-type="state">PR</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Cl&#237;nica Cardio &amp; Sa&#250;de, Curitiba, PR &#8211; Brasil</institution>
      </aff>
      <aff id="aff24">
        <label>24</label>
        <institution content-type="orgname">Heart &amp; Mind Care Servi&#231;os M&#233;dicos</institution>
        <addr-line>
          <named-content content-type="city">Manaus</named-content>
          <named-content content-type="state">AM</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Heart &amp; Mind Care Servi&#231;os M&#233;dicos (HMC), Manaus, AM &#8211; Brasil</institution>
      </aff>
      <aff id="aff25">
        <label>25</label>
        <institution content-type="orgname">Cl&#237;nica CNI</institution>
        <addr-line>
          <named-content content-type="city">Uberl&#226;ndia</named-content>
          <named-content content-type="state">MG</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Cardiologia N&#227;o Invasiva, Cl&#237;nica CNI, Uberl&#226;ndia, MG &#8211; Brasil</institution>
      </aff>
      <aff id="aff26">
        <label>26</label>
        <institution content-type="orgname">Diagn&#243;sticos da Am&#233;rica SA</institution>
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Diagn&#243;sticos da Am&#233;rica SA (DASA), S&#227;o Paulo, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff27">
        <label>27</label>
        <institution content-type="orgname">Hospital 9 de Julho</institution>
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Hospital 9 de Julho, S&#227;o Paulo, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff28">
        <label>28</label>
        <institution content-type="orgname">Universidade Federal do Paran&#225;</institution>
        <addr-line>
          <named-content content-type="city">Curitiba</named-content>
          <named-content content-type="state">PR</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Universidade Federal do Paran&#225; (UFPR), Curitiba, PR &#8211; Brasil</institution>
      </aff>
      <aff id="aff29">
        <label>29</label>
        <institution content-type="orgdiv1">Departamento de Cardiologia Pedi&#225;trica</institution>
        <institution content-type="orgname">Sociedade Brasileira de Cardiologia</institution>
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Departamento de Cardiologia Pedi&#225;trica (DCC/CP) da Sociedade Brasileira de Cardiologia (SBC), S&#227;o Paulo, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff30">
        <label>30</label>
        <institution content-type="orgname">Sociedade Brasileira de Oncologia Pedi&#225;trica</institution>
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Sociedade Brasileira de Oncologia Pedi&#225;trica, S&#227;o Paulo, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff31">
        <label>31</label>
        <institution content-type="orgname">Universidade Federal da Bahia</institution>
        <addr-line>
          <named-content content-type="city">Salvador</named-content>
          <named-content content-type="state">BA</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Universidade Federal da Bahia (UFBA), Salvador, BA &#8211; Brasil</institution>
      </aff>
      <aff id="aff32">
        <label>32</label>
        <institution content-type="orgdiv2">Instituto da Crian&#231;a e do Adolescente</institution>
        <institution content-type="orgdiv1">Hospital das Clinicas Faculdade de Medicina</institution>
        <institution content-type="orgname">Universidade de S&#227;o Paulo</institution>
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Instituto da Crian&#231;a e do Adolescente do Hospital das Clinicas Faculdade de Medicina da Universidade de S&#227;o Paulo (FMUSP), S&#227;o Paulo, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff33">
        <label>33</label>
        <institution content-type="orgname">Hospital Evang&#233;lico</institution>
        <addr-line>
          <named-content content-type="city">Cachoeiro de Itapemirim</named-content>
          <named-content content-type="state">ES</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Hospital Evang&#233;lico, Cachoeiro de Itapemirim, ES &#8211; Brasil</institution>
      </aff>
      <aff id="aff34">
        <label>34</label>
        <institution content-type="orgname">Instituto do Cora&#231;&#227;o de Mar&#237;lia</institution>
        <addr-line>
          <named-content content-type="city">Mar&#237;lia</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Instituto do Cora&#231;&#227;o de Mar&#237;lia (ICM), Mar&#237;lia, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff35">
        <label>35</label>
        <institution content-type="orgname">Instituto do C&#226;ncer do Estado de S&#227;o Paulo</institution>
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Instituto do C&#226;ncer do Estado de S&#227;o Paulo (ICESP), S&#227;o Paulo, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff36">
        <label>36</label>
        <institution content-type="orgname">Hospital Alian&#231;a Rede D&#8217;Or S&#227;o Luiz</institution>
        <addr-line>
          <named-content content-type="city">Salvador</named-content>
          <named-content content-type="state">BA</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Hospital Alian&#231;a Rede D&#8217;Or S&#227;o Luiz, Salvador, BA &#8211; Brasil</institution>
      </aff>
      <aff id="aff37">
        <label>37</label>
        <institution content-type="orgname">Funda&#231;&#227;o Oswaldo Cruz</institution>
        <addr-line>
          <named-content content-type="city">Rio de Janeiro</named-content>
          <named-content content-type="state">RJ</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Funda&#231;&#227;o Oswaldo Cruz (FIOCRUZ), Rio de Janeiro, RJ &#8211; Brasil</institution>
      </aff>
      <aff id="aff38">
        <label>38</label>
        <institution content-type="orgname">Grupo Fleury</institution>
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Grupo Fleury, S&#227;o Paulo, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff39">
        <label>39</label>
        <institution content-type="orgname">Hospital Cardio Pulmonar Rede D&#8217;or S&#227;o Luiz</institution>
        <addr-line>
          <named-content content-type="city">Salvador</named-content>
          <named-content content-type="state">BA</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Hospital Cardio Pulmonar Rede D&#8217;or S&#227;o Luiz, Salvador, BA &#8211; Brasil</institution>
      </aff>
      <aff id="aff40">
        <label>40</label>
        <institution content-type="orgname">Universidade Federal do Cear&#225;</institution>
        <addr-line>
          <named-content content-type="city">Fortaleza</named-content>
          <named-content content-type="state">CE</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Universidade Federal do Cear&#225;,Fortaleza, CE &#8211; Brasil</institution>
      </aff>
      <aff id="aff41">
        <label>41</label>
        <institution content-type="orgname">Universidade Federal do Vale do S&#227;o Francisco</institution>
        <addr-line>
          <named-content content-type="city">Petrolina</named-content>
          <named-content content-type="state">PE</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Universidade Federal do Vale do S&#227;o Francisco (UNIVASF), Petrolina, PE &#8211; Brasil</institution>
      </aff>
      <aff id="aff42">
        <label>42</label>
        <institution content-type="orgname">Hospital Nossa Senhora da Concei&#231;&#227;o</institution>
        <addr-line>
          <named-content content-type="city">Tubar&#227;o</named-content>
          <named-content content-type="state">SC</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Hospital Nossa Senhora da Concei&#231;&#227;o, Tubar&#227;o, SC &#8211; Brasil</institution>
      </aff>
      <aff id="aff43">
        <label>43</label>
        <institution content-type="orgname">Universidade do Sul de Santa Catarina</institution>
        <addr-line>
          <named-content content-type="city">Tubar&#227;o</named-content>
          <named-content content-type="state">SC</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Universidade do Sul de Santa Catarina (UNISUL), Tubar&#227;o, SC &#8211; Brasil</institution>
      </aff>
      <aff id="aff44">
        <label>44</label>
        <institution content-type="orgname">EcoHaertel - Hospital Mae de Deus</institution>
        <addr-line>
          <named-content content-type="city">Porto Alegre</named-content>
          <named-content content-type="state">RS</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">EcoHaertel - Hospital Mae de Deus, Porto Alegre, RS &#8211; Brasil</institution>
      </aff>
      <aff id="aff45">
        <label>45</label>
        <institution content-type="orgname">Universidade Federal de Ci&#234;ncias da Sa&#250;de de Porto Alegre</institution>
        <addr-line>
          <named-content content-type="city">Porto Alegre</named-content>
          <named-content content-type="state">RS</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Universidade Federal de Ci&#234;ncias da Sa&#250;de de Porto Alegre, Porto Alegre, RS &#8211; Brasil</institution>
      </aff>
      <aff id="aff46">
        <label>46</label>
        <institution content-type="orgname">Universidade Federal de S&#227;o Paulo</institution>
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Universidade Federal de S&#227;o Paulo (UNIFESP), S&#227;o Paulo, SP &#8211; Brasil</institution>
      </aff>
      <aff id="aff47">
        <label>47</label>
        <institution content-type="orgname">Quanta Diagn&#243;stico por Imagem</institution>
        <addr-line>
          <named-content content-type="city">Curitiba</named-content>
          <named-content content-type="state">PR</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Quanta Diagn&#243;stico por Imagem, Curitiba, PR &#8211; Brasil</institution>
      </aff>
      <aff id="aff48">
        <label>48</label>
        <institution content-type="orgname">Hospital Santa Izabel</institution>
        <addr-line>
          <named-content content-type="city">Salvador</named-content>
          <named-content content-type="state">BA</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Hospital Santa Izabel, Salvador, BA &#8211; Brasil</institution>
      </aff>
      <aff id="aff49">
        <label>49</label>
        <institution content-type="orgname">Santa Casa da Bahia</institution>
        <addr-line>
          <named-content content-type="city">Salvador</named-content>
          <named-content content-type="state">BA</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Santa Casa da Bahia, Salvador, BA &#8211; Brasil</institution>
      </aff>
      <aff id="aff50">
        <label>50</label>
        <institution content-type="orgname">Instituto Nacional de Cardiologia</institution>
        <addr-line>
          <named-content content-type="city">Rio de Janeiro</named-content>
          <named-content content-type="state">RJ</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Instituto Nacional de Cardiologia (INC), Rio de Janeiro, RJ &#8211; Brasil</institution>
      </aff>
      <author-notes>
        <corresp id="c01"><bold>Correspond&#234;ncia:</bold> Sociedade Brasileira de Cardiologia &#8211; Av. Marechal C&#226;mara, 360/330 &#8211; Centro &#8211; Rio de Janeiro &#8211; CEP: 20020-907. E-mail: <email>diretrizes@cardiol.br</email> </corresp>
        <fn fn-type="edited-by">
          <p><bold>Presidentes do DIC:</bold> Carlos Eduardo Rochitte (Gest&#227;o 2020/2021) e Andr&#233; Luiz Cerqueira de Almeida (Gest&#227;o 2022/2023)</p>
          <p><bold>Editores Coordenadores:</bold> Andr&#233; Luiz Cerqueira de Almeida, Marcelo Dantas Tavares de Melo, Alex dos Santos Felix e David Costa de Souza Le Bihan</p>
          <p><bold>Coeditores:</bold> Marcelo Luiz Campos Vieira e Jos&#233; Luiz Barros Pena</p>
          <p><bold>Conselho de Normatiza&#231;&#245;es e Diretrizes respons&#225;vel:</bold> Carisi Anne Polanczyk (Coordenadora), Humberto Graner Moreira, M&#225;rio de Seixas Rocha, Jose Airton de Arruda, Pedro Gabriel Melo de Barros e Silva &#8211; Gest&#227;o 2022-2024</p>
        </fn>
      </author-notes>
      <pub-date date-type="pub" publication-format="electronic">
        <day>05</day>
        <month>01</month>
        <year>2024</year>
      </pub-date>
      <pub-date date-type="collection" publication-format="electronic">
        <month>12</month>
        <year>2023</year>
      </pub-date>
      <volume>120</volume>
      <issue>12</issue>
      <elocation-id>e20230646</elocation-id>
      <permissions>
        <license license-type="open-access" xlink:href="https://creativecommons.org/licenses/by/4.0/" xml:lang="en">
          <license-p> This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. </license-p>
        </license>
      </permissions>
      <abstract abstract-type="graphical">
        <p>
          <fig id="f01">
            <label>Figura Central</label>
            <caption>
              <title>: Posicionamento do Departamento de Imagem Cardiovascular da Sociedade Brasileira de Cardiologia sobre o Uso do Strain Mioc&#225;rdico na Rotina do Cardiologista &#8211; 2023</title>
            </caption>
            <attrib>
              <italic>Proposta de inclus&#227;o do strain no algoritmo integrado de avalia&#231;&#227;o da fun&#231;&#227;o diast&#243;lica, adaptado e traduzido de Nagueh et al.</italic>
              <sup>67</sup>
              <italic>AE: &#225;trio esquerdo; Ap: dura&#231;&#227;o da onda A reversa pulmonar; Am: dura&#231;&#227;o da onda A mitral; DD: disfun&#231;&#227;o diast&#243;lica; FEVEr: fra&#231;&#227;o de eje&#231;&#227;o do ventr&#237;culo esquerdo reduzida; IT: insufici&#234;ncia tric&#250;spide; SAEr: strain do AE de reservat&#243;rio; SLGVE: strain longitudinal global do ventr&#237;culo esquerdo. Se remodelamento conc&#234;ntrico, confirmar com SLGVE. Na presen&#231;a de FEVEr, tempo de desacelera&#231;&#227;o da onda E mitral (TDE) &lt; 160 ms e onda S &lt; D pulmonar tamb&#233;m s&#227;o par&#226;metros de press&#227;o de enchimento aumentada. Esse algoritmo n&#227;o se aplica a pacientes com fibrila&#231;&#227;o atrial (FA), calcifica&#231;&#227;o do anel mitral ou valvopatia mitral maior que discreta, bloqueio de ramo esquerdo (BRE), ritmo de marca-passo, pr&#243;teses valvares ou hipertens&#227;o pulmonar (HP) prim&#225;ria grave.</italic>
            </attrib>
            <alternatives>
              <graphic xlink:href="https://minio.scielo.br/documentstore/1678-4170/tNh3qfrVcdn4cDzTqmNjCtQ/9d4c81bdc7c39f78a3352405808bca537caa4c04.tif"/>
              <graphic xlink:href="https://minio.scielo.br/documentstore/1678-4170/tNh3qfrVcdn4cDzTqmNjCtQ/7601bbe257f896e12c047cb826509d4c0f2bad2a.png" specific-use="scielo-web"/>
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            </alternatives>
          </fig>
        </p>
      </abstract>
      <counts>
        <fig-count count="84"/>
        <table-count count="36"/>
        <equation-count count="0"/>
        <ref-count count="446"/>
      </counts>
    </article-meta>
  </front>
  <body>
    <p>
      <table-wrap id="t1">
        <table frame="hsides" rules="groups">
          <colgroup width="50%">
            <col/>
            <col/>
          </colgroup>
          <thead>
            <tr>
              <th colspan="2">Posicionamento do Departamento de Imagem Cardiovascular da Sociedade Brasileira de Cardiologia sobre o Uso do Strain Mioc&#225;rdico na Rotina do Cardiologista &#8211; 2023</th>
            </tr>
            <tr>
              <th colspan="2">O relat&#243;rio abaixo lista as declara&#231;&#245;es de interesse conforme relatadas &#224; SBC pelos especialistas durante o per&#237;odo de desenvolvimento deste posicionamento, 2022/2023.</th>
            </tr>
            <tr>
              <th align="left">Especialista</th>
              <th align="left">Tipo de relacionamento com a ind&#250;stria</th>
            </tr>
          </thead>
          <tbody>
            <tr>
              <td>Adenalva Lima de Souza Beck</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Alex Felix</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Ana Clara Rodrigues</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Ana Cristina Camarozano</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Anderson da Costa Armstrong</td>
              <td>
                <list list-type="simple">
                  <list-item>
                    <p>Declara&#231;&#227;o financeira</p>
                  </list-item>
                  <list-item>
                    <p>A - Pagamento de qualquer esp&#233;cie e desde que economicamente apreci&#225;veis, feitos a (i) voc&#234;, (ii) ao seu c&#244;njuge/ companheiro ou a qualquer outro membro que resida com voc&#234;, (iii) a qualquer pessoa jur&#237;dica em que qualquer destes seja controlador, s&#243;cio, acionista ou participante, de forma direta ou indireta, recebimento por palestras, aulas, atua&#231;&#227;o como proctor de treinamentos, remunera&#231;&#245;es, honor&#225;rios pagos por participa&#231;&#245;es em conselhos consultivos, de investigadores, ou outros comit&#234;s, etc. Provenientes da ind&#250;stria farmac&#234;utica, de &#243;rteses, pr&#243;teses, equipamentos e implantes, brasileiras ou estrangeiras:</p>
                  </list-item>
                  <list-item>
                    <p>- Amiloidose: Anylam.</p>
                  </list-item>
                  <list-item>
                    <p>Outros relacionamentos</p>
                  </list-item>
                  <list-item>
                    <p>Financiamento de atividades de educa&#231;&#227;o m&#233;dica continuada, incluindo viagens, hospedagens e inscri&#231;&#245;es para congressos e cursos, provenientes da ind&#250;stria farmac&#234;utica, de &#243;rteses, pr&#243;teses, equipamentos e implantes, brasileiras ou estrangeiras:</p>
                  </list-item>
                  <list-item>
                    <p>- &#193;rea da Sa&#250;de; CARDIOVASF.</p>
                  </list-item>
                </list>
              </td>
            </tr>
            <tr>
              <td>Andr&#233; Luiz Cerqueira de Almeida</td>
              <td>
                <list list-type="simple">
                  <list-item>
                    <p>Declara&#231;&#227;o financeira</p>
                  </list-item>
                  <list-item>
                    <p>A - Pagamento de qualquer esp&#233;cie e desde que economicamente apreci&#225;veis, feitos a (i) voc&#234;, (ii) ao seu c&#244;njuge/ companheiro ou a qualquer outro membro que resida com voc&#234;, (iii) a qualquer pessoa jur&#237;dica em que qualquer destes seja controlador, s&#243;cio, acionista ou participante, de forma direta ou indireta, recebimento por palestras, aulas, atua&#231;&#227;o como proctor de treinamentos, remunera&#231;&#245;es, honor&#225;rios pagos por participa&#231;&#245;es em conselhos consultivos, de investigadores, ou outros comit&#234;s, etc. Provenientes da ind&#250;stria farmac&#234;utica, de &#243;rteses, pr&#243;teses, equipamentos e implantes, brasileiras ou estrangeiras:</p>
                  </list-item>
                  <list-item>
                    <p>- Boston Scientific: palestrante.</p>
                  </list-item>
                </list>
              </td>
            </tr>
            <tr>
              <td>Andressa Mussi Soares</td>
              <td>
                <list list-type="simple">
                  <list-item>
                    <p>Declara&#231;&#227;o financeira</p>
                  </list-item>
                  <list-item>
                    <p>A - Pagamento de qualquer esp&#233;cie e desde que economicamente apreci&#225;veis, feitos a (i) voc&#234;, (ii) ao seu c&#244;njuge/ companheiro ou a qualquer outro membro que resida com voc&#234;, (iii) a qualquer pessoa jur&#237;dica em que qualquer destes seja controlador, s&#243;cio, acionista ou participante, de forma direta ou indireta, recebimento por palestras, aulas, atua&#231;&#227;o como proctor de treinamentos, remunera&#231;&#245;es, honor&#225;rios pagos por participa&#231;&#245;es em conselhos consultivos, de investigadores, ou outros comit&#234;s, etc.</p>
                  </list-item>
                  <list-item>
                    <p>Provenientes da ind&#250;stria farmac&#234;utica, de &#243;rteses, pr&#243;teses, equipamentos e implantes, brasileiras ou estrangeiras:</p>
                  </list-item>
                  <list-item>
                    <p>- Bayer: Anticoagula&#231;&#227;o e insufici&#234;ncia card&#237;aca; Pfizer: Anticoagula&#231;&#227;o e amiloidose; Jannsen: Leucemia.</p>
                  </list-item>
                  <list-item>
                    <p>Outros relacionamentos</p>
                  </list-item>
                  <list-item>
                    <p>Financiamento de atividades de educa&#231;&#227;o m&#233;dica continuada, incluindo viagens, hospedagens e inscri&#231;&#245;es para congressos e cursos, provenientes da ind&#250;stria farmac&#234;utica, de &#243;rteses, pr&#243;teses, equipamentos e implantes, brasileiras ou estrangeiras:</p>
                  </list-item>
                  <list-item>
                    <p>- Bayer: Insufici&#234;ncia card&#237;aca.</p>
                  </list-item>
                </list>
              </td>
            </tr>
            <tr>
              <td>Arnaldo Rabischoffsky</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Aur&#233;lio Carvalho Pinheiro</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Bruna Morhy Borges Leal Assun&#231;&#227;o</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Camila Rocon</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Carlos Eduardo Suaide Silva</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Carlos Eduardo Rochitte</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Cecilia Beatriz Bittencourt Viana Cruz</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Cintia Galhardo Tressino</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Claudia Gianini Monaco</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Claudia R. Pinheiro de Castro Grau</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Cl&#225;udio Henrique Fischer</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Daniel de Andrade Hygidio</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Daniela do Carmo Rassi Frota</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>David Costa de Souza Le Bihan</td>
              <td>
                <list list-type="simple">
                  <list-item>
                    <p>Declara&#231;&#227;o financeira</p>
                  </list-item>
                  <list-item>
                    <p>A - Pagamento de qualquer esp&#233;cie e desde que economicamente apreci&#225;veis, feitos a (i) voc&#234;, (ii) ao seu c&#244;njuge/ companheiro ou a qualquer outro membro que resida com voc&#234;, (iii) a qualquer pessoa jur&#237;dica em que qualquer destes seja controlador, s&#243;cio, acionista ou participante, de forma direta ou indireta, recebimento por palestras, aulas, atua&#231;&#227;o como proctor de treinamentos, remunera&#231;&#245;es, honor&#225;rios pagos por participa&#231;&#245;es em conselhos consultivos, de investigadores, ou outros comit&#234;s, etc.</p>
                  </list-item>
                  <list-item>
                    <p>Provenientes da ind&#250;stria farmac&#234;utica, de &#243;rteses, pr&#243;teses, equipamentos e implantes, brasileiras ou estrangeiras:</p>
                  </list-item>
                  <list-item>
                    <p>- Edwards Lifescience; Abbott; GE Healthcare; Philips.</p>
                  </list-item>
                </list>
              </td>
            </tr>
            <tr>
              <td>Eliza de Almeida Gripp</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>F&#225;bio Luis de Jesus Soares</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Fabio Villa&#231;a Guimar&#227;es Filho</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Gabriela Nunes Leal</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Henry Abensur</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Isabel Cristina Britto Guimar&#227;es</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Jeane Mike Tsutsui</td>
              <td>
                <list list-type="simple">
                  <list-item>
                    <p>Outros relacionamentos</p>
                  </list-item>
                  <list-item>
                    <p>Participa&#231;&#227;o societ&#225;ria de qualquer natureza e qualquer valor economicamente apreci&#225;vel de empresas na &#225;rea de sa&#250;de, de ensino ou em empresas concorrentes ou fornecedoras da SBC:</p>
                  </list-item>
                  <list-item>
                    <p>- &#193;rea de sa&#250;de: Grupo Fleury.</p>
                  </list-item>
                </list>
              </td>
            </tr>
            <tr>
              <td>Jorge Andion Torre&#227;o</td>
              <td>
                <list list-type="simple">
                  <list-item>
                    <p>Outros relacionamentos</p>
                  </list-item>
                  <list-item>
                    <p>Participa&#231;&#227;o societ&#225;ria de qualquer natureza e qualquer valor economicamente apreci&#225;vel de empresas na &#225;rea de sa&#250;de, de ensino ou em empresas concorrentes ou fornecedoras da SBC:</p>
                  </list-item>
                  <list-item>
                    <p>- S&#243;cio de empresa de educa&#231;&#227;o na area da sa&#250;de.</p>
                  </list-item>
                </list>
              </td>
            </tr>
            <tr>
              <td>Jorge Eduardo Assef</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Jos&#233; Luiz Barros Pena</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Jose Maria Del Castillo</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Marcelo Dantas Tavares de Melo</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Marcelo Goulart Paiva</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Marcelo Haertel Miglioranza</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Marcelo Luiz Campos Vieira</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>M&#225;rcio Silva Miguel Lima</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Marco Stephan Lofrano Alves</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Maria Eduarda Menezes de Siqueira</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Maria Estef&#226;nia Bosco Otto</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Maria Rosa Dantas</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Maria Veronica Camara dos Santos</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Marly Maria Uellendahl Lopes</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Rafael Bonafim Piveta</td>
              <td>
                <list list-type="simple">
                  <list-item>
                    <p>Outros relacionamentos</p>
                  </list-item>
                  <list-item>
                    <p>Participa&#231;&#227;o societ&#225;ria de qualquer natureza e qualquer valor economicamente apreci&#225;vel de empresas na &#225;rea de sa&#250;de, de ensino ou em empresas concorrentes ou fornecedoras da SBC:</p>
                  </list-item>
                  <list-item>
                    <p>- S&#243;cio na WavesMed (plataforma digital de ensino continuado/atualiza&#231;&#245;es).</p>
                  </list-item>
                </list>
              </td>
            </tr>
            <tr>
              <td>Rafael Modesto Fernandes</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Renato de Aguiar Hortegal</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Roberto Magalh&#227;es Saraiva</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Rodrigo Bellio de Mattos Barretto</td>
              <td>
                <list list-type="simple">
                  <list-item>
                    <p>Declara&#231;&#227;o financeira</p>
                  </list-item>
                  <list-item>
                    <p>A - Pagamento de qualquer esp&#233;cie e desde que economicamente apreci&#225;veis, feitos a (i) voc&#234;, (ii) ao seu c&#244;njuge/ companheiro ou a qualquer outro membro que resida com voc&#234;, (iii) a qualquer pessoa jur&#237;dica em que qualquer destes seja controlador, s&#243;cio, acionista ou participante, de forma direta ou indireta, recebimento por palestras, aulas, atua&#231;&#227;o como proctor de treinamentos, remunera&#231;&#245;es, honor&#225;rios pagos por participa&#231;&#245;es em conselhos consultivos, de investigadores, ou outros comit&#234;s, etc. Provenientes da ind&#250;stria farmac&#234;utica, de &#243;rteses, pr&#243;teses, equipamentos e implantes, brasileiras ou estrangeiras:</p>
                  </list-item>
                  <list-item>
                    <p>- GE; Abbot; Edwards.</p>
                  </list-item>
                </list>
              </td>
            </tr>
            <tr>
              <td>Rodrigo Julio Cerci</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Salustiano Pereira de Araujo</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Samira Saady Morhy</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Sanderson Antonio Cauduro</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Sandra Marques e Silva</td>
              <td>
                <list list-type="simple">
                  <list-item>
                    <p>Outros relacionamentos</p>
                  </list-item>
                  <list-item>
                    <p>Financiamento de atividades de educa&#231;&#227;o m&#233;dica continuada, incluindo viagens, hospedagens e inscri&#231;&#245;es para congressos e cursos, provenientes da ind&#250;stria farmac&#234;utica, de &#243;rteses, pr&#243;teses, equipamentos e implantes, brasileiras ou estrangeiras:</p>
                  </list-item>
                  <list-item>
                    <p>- Pfizer: Amiloidose; Sanofi, Pint Pharma, Takeda e Chiesi: Fabry.</p>
                  </list-item>
                </list>
              </td>
            </tr>
            <tr>
              <td>Sandra N&#237;vea dos Reis Saraiva Falc&#227;o</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Silvio Henrique Barberato</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Thais Harada Campos Espirito Santo</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Tonnison de Oliveira Silva</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Vera Maria Cury Salemi</td>
              <td>Nada a ser declarado</td>
            </tr>
            <tr>
              <td>Viviane Tiemi Hotta</td>
              <td>
                <list list-type="simple">
                  <list-item>
                    <p>Declara&#231;&#227;o financeira</p>
                  </list-item>
                  <list-item>
                    <p>B - Financiamento de pesquisas sob sua responsabilidade direta/pessoal (direcionado ao departamento ou institui&#231;&#227;o) provenientes da ind&#250;stria farmac&#234;utica, de &#243;rteses, pr&#243;teses, equipamentos e implantes, brasileiras ou estrangeiras:</p>
                  </list-item>
                  <list-item>
                    <p>- Pfizer: Amiloidose.</p>
                  </list-item>
                </list>
              </td>
            </tr>
          </tbody>
        </table>
      </table-wrap>
    </p>
    <sec>
      <title>Sum&#225;rio</title>
      <p>1. Conceitos B&#225;sicos sobre o Estudo da Deforma&#231;&#227;o do Ventr&#237;culo Esquerdo 7</p>
      <p>1.1. Breve Introdu&#231;&#227;o aos Princ&#237;pios F&#237;sicos da Forma&#231;&#227;o dos Speckles na Imagem Cardiovascular 7</p>
      <p>1.2. Defini&#231;&#245;es 7</p>
      <p><bold>1.2.1.</bold><italic><bold>Strain</bold></italic><bold>e</bold><italic><bold>Strain</bold></italic><bold>Rate</bold> 7</p>
      <p><bold>1.2.2. Deforma&#231;&#227;o Longitudinal, Circunferencial e Radial</bold> 8</p>
      <p><bold>1.2.3. Tempo dos Eventos Mec&#226;nicos</bold> 8</p>
      <p><bold>1.2.4. Medidas de Pico Extra&#237;das das Curvas de Deforma&#231;&#227;o</bold> 8</p>
      <p>1.3. Fatores que Afetam a Estimativa do <italic>Strain</italic> 8</p>
      <p><bold>1.3.1 Qualidade da Imagem</bold> 8</p>
      <p><bold>1.3.2. Modalidade de Imagem Cardiovascular</bold> 9</p>
      <p><bold>1.3.3. Fabricante e Vers&#227;o do Software</bold> 9</p>
      <p><bold>1.3.4. Condi&#231;&#245;es Hemodin&#226;micas</bold> 9</p>
      <p>1.4. Strain Longitudinal Global 9</p>
      <p>2. Recomenda&#231;&#245;es Gerais para o Uso do <italic>Strain</italic>: Aplicabilidade Cl&#237;nica, Compara&#231;&#227;o com a Fra&#231;&#227;o de Eje&#231;&#227;o e Descri&#231;&#227;o Adequada no Laudo 11</p>
      <p>2.1. Valor Progn&#243;stico, Padr&#245;es Param&#233;tricos e Detec&#231;&#227;o Subcl&#237;nica de Cardiopatias da Deforma&#231;&#227;o Mioc&#225;rdica 11</p>
      <p>2.2. <italic>Strain</italic> ou Fra&#231;&#227;o de Eje&#231;&#227;o: Qual &#233; a Melhor Alternativa? 11</p>
      <p>2.3. Recomenda&#231;&#245;es Gerais de como Reportar os Resultados do <italic>Strain</italic> e os Valores de Normalidade 11</p>
      <p>2.4. Conclus&#227;o 11</p>
      <p>3. <italic>Strain</italic> na Cardio-oncologia 14</p>
      <p>4. <italic>Strain</italic> na Disfun&#231;&#227;o Diast&#243;lica 16</p>
      <p>4.1. Introdu&#231;&#227;o 16</p>
      <p>4.2. <italic>Strain</italic> do Ventr&#237;culo Esquerdo 16</p>
      <p>4.3. <italic>Strain</italic> do &#193;trio Esquerdo 16</p>
      <p>4.4. Conclus&#227;o 16</p>
      <p>5. <italic>Strain</italic> nas Cardiomiopatias 17</p>
      <p>5.1. Introdu&#231;&#227;o 17</p>
      <p>5.2. Cardiomiopatia Dilatada 17</p>
      <p>5.3. Cardiomiopatia Arritmog&#234;nica 17</p>
      <p>5.4. Cardiomiopatia Hipertr&#243;fica 18</p>
      <p>5.5. Endomiocardiofibrose 18</p>
      <p>5.6. Mioc&#225;rdio N&#227;o Compactado 18</p>
      <p>6. <italic>Strain</italic> nas Valvopatias 19</p>
      <p>7. <italic>Strain</italic> nas Cardiopatias Isqu&#234;micas 20</p>
      <p>7.1. Introdu&#231;&#227;o 20</p>
      <p>7.2. <italic>Strain</italic> na S&#237;ndrome Coronariana Aguda 20</p>
      <p>7.3. <italic>Strain</italic> na S&#237;ndrome Coronariana Cr&#244;nica 20</p>
      <p>7.4. <italic>Strain</italic> do Ventr&#237;culo Direito na Cardiopatia Isqu&#234;mica 21</p>
      <p>8. <italic>Strain</italic> nas Doen&#231;as Sist&#234;micas (Amiloidose e Doen&#231;a de Fabry) 22</p>
      <p>8.1. <italic>Strain</italic> na Amiloidose Card&#237;aca 22</p>
      <p><bold>8.1.1. Papel da An&#225;lise da Deforma&#231;&#227;o Mioc&#225;rdica no Diagn&#243;stico da Amiloidose Card&#237;aca</bold> 22</p>
      <p>8.2. Doen&#231;a de Fabry 25</p>
      <p>9. <italic>Strain</italic> na Hipertens&#227;o Arterial Sist&#234;mica 26</p>
      <p>9.1. Introdu&#231;&#227;o 26</p>
      <p>9.2. Hipertens&#227;o Arterial Sist&#234;mica sem Crit&#233;rios para Hipertrofia Ventricular Esquerda 26</p>
      <p>9.3. Hipertens&#227;o Arterial Sist&#234;mica com Crit&#233;rios para Hipertrofia Ventricular Esquerda 27</p>
      <p>9.4. Tratamento Cl&#237;nico 27</p>
      <p>9.5. Conclus&#227;o 27</p>
      <p>10. <italic>Strain</italic> em Atletas 27</p>
      <p>11. <italic>Strain</italic> na Ecocardiografia com Estresse 29</p>
      <p>12. <italic>Strain</italic> nas Cardiopatias Cong&#234;nitas 29</p>
      <p>13. <italic>Strain</italic> do Ventr&#237;culo Direito 30</p>
      <p>13.1. Introdu&#231;&#227;o 30</p>
      <p>13.2. Caracter&#237;sticas Anat&#244;micas e Funcionais do Ventr&#237;culo Direito 30</p>
      <p>13.3. Ventr&#237;culo Direito e Par&#226;metros Ecocardiogr&#225;ficos na Avalia&#231;&#227;o da Fun&#231;&#227;o Sist&#243;lica 30</p>
      <p>13.4. Aquisi&#231;&#227;o e Limita&#231;&#245;es 31</p>
      <p>13.5. Indica&#231;&#245;es/Valores de Normalidade 32</p>
      <p>14. <italic>Strain</italic> do &#193;trio Esquerdo e do &#193;trio Direito 33</p>
      <p>14.1. T&#233;cnica de Obten&#231;&#227;o e An&#225;lise do <italic>strain</italic> do &#193;trio Esquerdo 33</p>
      <p>14.2. Valores de Normalidade 33</p>
      <p>14.3. Aplicabilidade Cl&#237;nica do <italic>Strain</italic> do &#193;trio Esquerdo 33</p>
      <p><bold>14.3.1. Insufici&#234;ncia Card&#237;aca e Avalia&#231;&#227;o de Fun&#231;&#227;o Diast&#243;lica</bold> 33</p>
      <p><bold>14.3.2. Fibrila&#231;&#227;o Atrial</bold> 34</p>
      <p><bold>14.3.3. Valvopatias</bold> 34</p>
      <p><bold>14.3.4. Doen&#231;a Arterial Coronariana</bold> 34</p>
      <p>14.4. <italic>Strain</italic> Atrial Direito 34</p>
      <p>15. Avalia&#231;&#227;o da Tor&#231;&#227;o do Ventr&#237;culo Esquerdo 34</p>
      <p>15.1. Introdu&#231;&#227;o 34</p>
      <p>15.2. Defini&#231;&#245;es e Nomenclaturas 35</p>
      <p>15.3. Passo a Passo da Avalia&#231;&#227;o da Tor&#231;&#227;o Ventricular pelo Ecocardiograma com Speckle Tracking 35</p>
      <p>15.4. Aplica&#231;&#245;es Cl&#237;nicas 35</p>
      <p>16. <italic>Strain</italic> na An&#225;lise da Dissincronia Ventricular 36</p>
      <p>16.1. Introdu&#231;&#227;o 36</p>
      <p>16.2. Avalia&#231;&#227;o da Dissincronia na Sele&#231;&#227;o dos Pacientes para a Terapia de Ressincroniza&#231;&#227;o Card&#237;aca 37</p>
      <p>16.3. Avalia&#231;&#227;o de Viabilidade Mioc&#225;rdica 37</p>
      <p>16.4. Orienta&#231;&#227;o do Local de Implante dos Eletrodos 38</p>
      <p>16.5. Avalia&#231;&#227;o Progn&#243;stica ap&#243;s a Terapia de Ressincroniza&#231;&#227;o Card&#237;aca 38</p>
      <p>16.6. Ajuste nos Par&#226;metros de Ressincroniza&#231;&#227;o 38</p>
      <p>17. Myocardial Work (Trabalho Mioc&#225;rdico) 38</p>
      <p>17.1. Introdu&#231;&#227;o 38</p>
      <p>17.2. Aquisi&#231;&#227;o do Trabalho Mioc&#225;rdico 38</p>
      <p>17.3. Valores de Normalidade 39</p>
      <p>17.4. Potencial Uso Cl&#237;nico 42</p>
      <p>18. <italic>Strain</italic> no 3D: O Que Pode Acrescentar ao Exame 43</p>
      <p>18.1. Introdu&#231;&#227;o 43</p>
      <p>18.2. <italic>Strain</italic> Ventricular Esquerdo 43</p>
      <p>18.3. <italic>Strain</italic> Ventricular Direito 43</p>
      <p><bold>18.3.1. Aquisi&#231;&#227;o e An&#225;lise do Full-volume 3D</bold> 44</p>
      <p>18.4. <italic>Strain</italic> Atrial Esquerdo 44</p>
      <p>19. O papel da Resson&#226;ncia e Tomografia Card&#237;acas na Avalia&#231;&#227;o do <italic>Strain</italic> 44</p>
      <p>19.1. Introdu&#231;&#227;o 44</p>
      <p>19.2. M&#233;todos de Aquisi&#231;&#227;o do <italic>Strain</italic> pela Resson&#226;ncia Magn&#233;tica Card&#237;aca 44</p>
      <p>19.3. <italic>Strain</italic> do Ventr&#237;culo Direito pela Resson&#226;ncia Magn&#233;tica Card&#237;aca 44</p>
      <p>19.4. <italic>Strain</italic> do Ventr&#237;culo Esquerdo pela Resson&#226;ncia Magn&#233;tica Card&#237;aca 44</p>
      <p>19.5. <italic>Strain</italic> do &#193;trio Esquerdo pela Resson&#226;ncia Magn&#233;tica Card&#237;aca 46</p>
      <p>19.6. <italic>Strain</italic> pela Tomografia Card&#237;aca 46</p>
      <p>Refer&#234;ncias 46</p>
    </sec>
    <sec>
      <title>1. Conceitos B&#225;sicos sobre o Estudo da Deforma&#231;&#227;o do Ventr&#237;culo Esquerdo</title>
      <sec>
        <title>1.1. Breve Introdu&#231;&#227;o aos Princ&#237;pios F&#237;sicos da Forma&#231;&#227;o dos Speckles na Imagem Cardiovascular</title>
        <p>A palavra &#8220;<italic>speckle</italic>&#8221; refere-se &#224; apar&#234;ncia granular da imagem gerada por um sistema de imagem de coer&#234;ncia &#243;ptica, tal como o <italic>laser</italic>, tomografia de coer&#234;ncia &#243;ptica ou ultrassonografia.<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B2">2</xref></sup></p>
        <p>Na ecocardiografia, um pulso de ultrassom emitido propaga-se em linha reta, interagindo com as diferentes interfaces ac&#250;sticas da cavidade tor&#225;cica at&#233; atingir o cora&#231;&#227;o. Entre os diversos fen&#244;menos ac&#250;sticos que ocorrem nesse percurso, parte do feixe de ultrassom emitido sofre reflex&#227;o pelas diferentes estruturas card&#237;acas, gerando um eco que &#233; parcialmente captado de volta pelo transdutor e utilizado pelo <italic>software</italic> como entrada (<italic>input</italic>) para a elabora&#231;&#227;o das imagens de ecocardiografia. Nesse caso, o comprimento de onda do feixe ultrassonogr&#225;fico &#233; habitualmente menor do que o tamanho das estruturas refletoras.</p>
        <p>Entretanto, quando o comprimento de onda &#233; maior do que a microestrutura com a qual interage, h&#225; uma dispers&#227;o do feixe de ultrassom, que se irradia para todas as dire&#231;&#245;es (dispers&#227;o difusiva ou &#8220;<italic>diffusive scattering&#8221;</italic>). Esse fen&#244;meno &#233; o resultado do padr&#227;o de interfer&#234;ncia de todas as frentes de onda que sofreram dispers&#227;o a partir dos diferentes dispersores (diferen&#231;as locais de densidade e compressibilidade dos tecidos).</p>
        <p>Parte da dispers&#227;o difusiva &#233; capturada pelo transdutor, formando a imagem de aspecto granular que denominamos <italic>speckle</italic>.</p>
        <p>A presen&#231;a de <italic>speckles</italic> torna a imagem do modo B menos n&#237;tida para o operador humano, por&#233;m ela n&#227;o deve ser vista como um ru&#237;do, pois traz consigo informa&#231;&#245;es &#250;nicas de forma a atuar como uma &#8220;impress&#227;o digital&#8221; do meio estudado pelo ultrassom.<sup><xref ref-type="bibr" rid="B1">1</xref></sup></p>
      </sec>
      <sec>
        <title>1.2. Defini&#231;&#245;es</title>
        <sec>
          <title>1.2.1. <italic>Strain</italic> e <italic>Strain Rate</italic></title>
          <p><italic>Strain</italic> corresponde &#224; quantidade deforma&#231;&#227;o de um objeto em rela&#231;&#227;o &#224; sua forma original.<sup><xref ref-type="bibr" rid="B3">3</xref></sup> Na cardiologia, esse conceito &#233; representado como o percentual (%) de encurtamento/alongamento do cora&#231;&#227;o em rela&#231;&#227;o &#224; sua medida inicial. Esse conceito pode ser aplicado para um segmento mioc&#225;rdico (<italic>strain</italic> regional) ou para a totalidade de uma das c&#226;maras do cora&#231;&#227;o como o ventr&#237;culo esquerdo (VE) (<italic>strain</italic> global).</p>
          <p>O <italic>strain rate</italic> indica a taxa de deforma&#231;&#227;o mioc&#225;rdica (%) a cada segundo(s<sup>-<xref ref-type="bibr" rid="B1">1</xref></sup>) ou, em outras palavras, a velocidade com que a deforma&#231;&#227;o ocorre.<sup><xref ref-type="bibr" rid="B3">3</xref>-<xref ref-type="bibr" rid="B4">4</xref></sup></p>
        </sec>
        <sec>
          <title>1.2.2. Deforma&#231;&#227;o Longitudinal, Circunferencial e Radial</title>
          <p>A aplica&#231;&#227;o do conceito de deforma&#231;&#227;o nos permite pormenorizar o estudo do encurtamento/alongamento do mioc&#225;rdio do VE a partir de sua orienta&#231;&#227;o em diferentes eixos.</p>
          <p>De fato, devido &#224; disposi&#231;&#227;o helicoidal das fibras musculares card&#237;acas, o encurtamento sist&#243;lico do VE &#233; determinado pela a&#231;&#227;o de fibras no sentido longitudinal e de fibras no sentindo circunferencial,<sup><xref ref-type="bibr" rid="B5">5</xref></sup> o que determina os dois vetores-for&#231;a ativos da deforma&#231;&#227;o (<xref ref-type="fig" rid="f02">Figura 1.1</xref> A).</p>
          <p>
            <fig id="f02">
              <label>Figura 1.1</label>
              <caption>
                <title>&#8211; A deforma&#231;&#227;o mioc&#225;rdica pormenorizada em diferentes eixos. A) A deforma&#231;&#227;o b&#225;sica pode ser aferida nos sentidos longitudinal, circunferencial e radial.4 A partir da intera&#231;&#227;o de dois desses vetores-for&#231;a, h&#225; o surgimento de um terceiro vetor resultante. B) Shear-strain radial-circunferencial. C) Shear-strain longitudinal-circunferencial (que equivale a tor&#231;&#227;o ventricular/torsion). D) Shear-strain radial-circunferencial.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf01.tif"/></fig>
          </p>
          <p>A aplica&#231;&#227;o dessas for&#231;as no sentido longitudinal e circunferencial sobre um material de baixa compressibilidade (tecido mioc&#225;rdico) resulta em um espessamento do mioc&#225;rdio no sentindo radial (componente passivo da deforma&#231;&#227;o).<sup><xref ref-type="bibr" rid="B6">6</xref></sup> Em &#250;ltima an&#225;lise, este responde pela diminui&#231;&#227;o radial da cavidade ventricular.<sup><xref ref-type="bibr" rid="B4">4</xref></sup></p>
          <p>&#201; preciso ter em conta que o processo de deforma&#231;&#227;o &#233; bem mais complexo do que podemos aferir, pois, para cada processo de intera&#231;&#227;o entre os vetores-for&#231;a, surge um novo vetor resultante do cisalhamento entre as diferentes deforma&#231;&#245;es, o <italic>shear-strain</italic> (<xref ref-type="fig" rid="f02">Figura 1.1</xref> B, C e D).</p>
          <p>O encurtamento sist&#243;lico da fibra no sentido longitudinal e circunferencial produz valores negativos de <italic>strain</italic>. J&#225; o espessamento sist&#243;lico radial atribui um valor positivo ao <italic>strain</italic>. Muitos autores optam por expressar apenas o valor absoluto (valor em m&#243;dulo), e adotaremos essa abordagem aqui.</p>
        </sec>
        <sec>
          <title>1.2.3. Tempo dos Eventos Mec&#226;nicos</title>
          <p>Descrevemos, a seguir, algumas defini&#231;&#245;es fundamentais para a pr&#225;tica cl&#237;nica:<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B7">7</xref></sup></p>
          <list list-type="simple">
            <list-item>
              <p><bold>&#8226; Final da s&#237;stole (<italic>end-systole</italic>):</bold> definido como o ponto temporal de fechamento da valva a&#243;rtica. Potenciais substitutos: nadir do <italic>strain</italic> global ou da curva de volume. &#201; recomendado que os <italic>softwares</italic> informem qual crit&#233;rio foi adotado para definir o final da s&#237;stole.</p>
            </list-item>
            <list-item>
              <p><bold>&#8226; Final da di&#225;stole (<italic>end-diastole</italic>)</bold>: definido como o ponto temporal no qual ocorre o pico do complexo QRS. A marca&#231;&#227;o de eventos (<italic>event timing</italic>) deve ser feita preferencialmente utilizando o Doppler e tendo como refer&#234;ncia o eletrocardiograma (ECG).</p>
            </list-item>
          </list>
        </sec>
        <sec>
          <title>1.2.4. Medidas de Pico Extra&#237;das das Curvas de Deforma&#231;&#227;o (<xref ref-type="fig" rid="f03">Figura 1.2</xref>)</title>
          <list list-type="simple">
            <list-item>
              <p><bold><italic>&#8226; Strain</italic> do final da s&#237;stole <italic>(end-systolic strain)</italic>:</bold> o ponto da curva de deforma&#231;&#227;o no final da s&#237;stole, conforme previamente definido (fechamento da valva a&#243;rtica). Esse &#233; o par&#226;metro padr&#227;o para descrever a deforma&#231;&#227;o mioc&#225;rdica.</p>
            </list-item>
            <list-item>
              <p><bold><italic>&#8226; Strain</italic> de pico sist&#243;lico <italic>(peak systolic strain)</italic>:</bold> o ponto onde ocorre o pico da curva durante toda a s&#237;stole.</p>
            </list-item>
            <list-item>
              <p><bold><italic>&#8226; Strain</italic> de pico sist&#243;lico positivo <italic>(positive peak systolic strain)</italic>:</bold> valor mais positivo registrado em casos em que a curva de um determinado segmento apresente esse comportamento em algum momento da s&#237;stole.</p>
            </list-item>
            <list-item>
              <p><bold><italic>&#8226; Strain de pico (peak strain)</italic>:</bold> o ponto onde ocorre o pico da curva de deforma&#231;&#227;o, considerando todo o ciclo card&#237;aco. Habitualmente, esse ponto &#233; alcan&#231;ado at&#233; o fechamento da valva a&#243;rtica. Quando ocorre ap&#243;s, &#233; descrito como <italic>strain</italic> p&#243;s-sist&#243;lico (<italic>post systolic strain)</italic><sup><xref ref-type="bibr" rid="B8">8</xref></sup> ou encurtamento p&#243;s-sist&#243;lico (EPS, <italic>post-systolic shortening</italic>). O <italic>strain</italic> p&#243;s-sist&#243;lico reflete a deforma&#231;&#227;o de segmentos que se contraem ap&#243;s o fechamento da valva a&#243;rtica e n&#227;o contribuem para a eje&#231;&#227;o ventricular.</p>
            </list-item>
          </list>
          <p>
            <fig id="f03">
              <label>Figura 1.2</label>
              <caption>
                <title>&#8211; Medidas de pico extra&#237;das das curvas de deforma&#231;&#227;o. A) O strain pico sist&#243;lico, o strain pico e strain do final da s&#237;stole (ES) coincidem no momento do fechamento da valva a&#243;rtica (AVC). B) O strain de pico sist&#243;lico e o strain de pico coincidem, por&#233;m ambos acontecem imediatamente antes do fechamento da valva a&#243;rtica (pequena barra vermelha), produzindo uma discreta dissocia&#231;&#227;o entre aqueles e o strain do final da s&#237;stole (ES). C) O strain de pico sist&#243;lico e o strain do final da s&#237;stole (ES) coincidem (ambos apresentando valores absolutos reduzidos), por&#233;m o strain de pico ocorre ap&#243;s o fechamento da valva a&#243;rtica (fen&#244;meno de encurtamento p&#243;s-sist&#243;lico).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf02.tif"/></fig>
          </p>
        </sec>
      </sec>
    </sec>
    <sec>
      <title>1.3. Fatores que Afetam a Estimativa do <italic>Strain</italic></title>
      <sec>
        <title>1.3.1 Qualidade da Imagem</title>
        <p>A qualidade da imagem &#233; um fator cr&#237;tico que afeta a <italic>performance</italic> de qualquer <italic>software</italic> que estime a deforma&#231;&#227;o mioc&#225;rdica. V&#225;rios autores reportaram a sensibilidade da estimativa do <italic>strain</italic> e <italic>strain rate</italic> proporcionais &#224; qualidade da imagem e do algoritmo de <italic>tracking.</italic><sup><xref ref-type="bibr" rid="B9">9</xref>-<xref ref-type="bibr" rid="B11">11</xref></sup></p>
      </sec>
      <sec>
        <title>1.3.2. Modalidade de Imagem Cardiovascular</title>
        <p>Diferentes modalidades de imagem cardiovascular fornecem valores diferentes de <italic>strain</italic>. Tee et al.<sup><xref ref-type="bibr" rid="B12">12</xref></sup> reportaram tais diferen&#231;as aferidas entre a ecocardiografia transtor&#225;cica, a tomografia computadorizada e a resson&#226;ncia magn&#233;tica card&#237;aca (RMC).</p>
      </sec>
      <sec>
        <title>1.3.3. Fabricante e Vers&#227;o do <italic>Software</italic></title>
        <p>Estudos organizados pela European Association of Cardiovascular Imaging (EACVI) e American Society of Echocardiography (ASE) testaram a variabilidade de medidas do <italic>strain</italic> longitudinal global (SLG) obtidas entre diferentes fabricantes de aparelhos e <italic>softwares,</italic> com evid&#234;ncia de diverg&#234;ncias significativas.<sup><xref ref-type="bibr" rid="B13">13</xref>-<xref ref-type="bibr" rid="B14">14</xref></sup> Contudo, h&#225; de se considerar que tais diferen&#231;as ainda s&#227;o menores que a variabilidade da fra&#231;&#227;o de eje&#231;&#227;o (FE) reportadas na literatura.<sup><xref ref-type="bibr" rid="B9">9</xref>-<xref ref-type="bibr" rid="B10">10</xref>,<xref ref-type="bibr" rid="B15">15</xref></sup></p>
        <p>Al&#233;m da variabilidade interfabricante, deve-se estar atento &#224; variabilidade <italic>intersoftwares</italic> do mesmo fabricante. Mudan&#231;as significativas no SLG foram previamente reportadas.<sup><xref ref-type="bibr" rid="B11">11</xref>,<xref ref-type="bibr" rid="B15">15</xref></sup></p>
        <p>Dessa forma, estudos ecocardiogr&#225;ficos seriados deveriam, idealmente, ser realizados com o mesmo aparelho/<italic>software</italic> e sob condi&#231;&#245;es hemodin&#226;micas semelhantes, sobretudo em situa&#231;&#245;es cuja varia&#231;&#227;o do SLG pode levar a implica&#231;&#245;es terap&#234;uticas profundas, como no contexto de avalia&#231;&#227;o de cardiotoxicidade induzida por quimioter&#225;picos, por exemplo.<sup><xref ref-type="bibr" rid="B4">4</xref></sup></p>
      </sec>
      <sec>
        <title>1.3.4. Condi&#231;&#245;es Hemodin&#226;micas</title>
        <p>A deforma&#231;&#227;o do VE varia consideravelmente de acordo com as condi&#231;&#245;es de pr&#233;-carga e p&#243;s-carga &#224;s quais o ventr&#237;culo est&#225; submetido.</p>
      </sec>
    </sec>
    <sec>
      <title>1.4. <italic>Strain</italic> Longitudinal Global</title>
      <p>&#201; o par&#226;metro de deforma&#231;&#227;o card&#237;aca com evid&#234;ncias cient&#237;ficas mais robustas e o &#250;nico com uso de maior relev&#226;ncia na pr&#225;tica cl&#237;nica.<sup><xref ref-type="bibr" rid="B9">9</xref></sup> Ele reflete a deforma&#231;&#227;o longitudinal relativa (%) do mioc&#225;rdio do VE, que ocorre desde o per&#237;odo de contra&#231;&#227;o isovolum&#233;trica at&#233; o final do per&#237;odo de eje&#231;&#227;o.<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B5">5</xref>,<xref ref-type="bibr" rid="B15">15</xref></sup></p>
      <p>Matematicamente, a contra&#231;&#227;o em cada instante &#233; computada pelo algoritmo como:<inline-formula><mml:math><mml:mrow><mml:mi>S</mml:mi><mml:mi>L</mml:mi><mml:mi>G</mml:mi></mml:mrow><mml:mo>(</mml:mo><mml:mrow><mml:mi>t</mml:mi></mml:mrow><mml:mo>)</mml:mo><mml:mo>=</mml:mo><mml:mn>100</mml:mn><mml:mo>[</mml:mo><mml:mrow><mml:mtext> </mml:mtext><mml:mi>L</mml:mi></mml:mrow><mml:mo>(</mml:mo><mml:mrow><mml:mi>t</mml:mi></mml:mrow><mml:mo>)</mml:mo><mml:mo>&#8722;</mml:mo><mml:mtext> L(ED)/L(ED)] </mml:mtext></mml:math></inline-formula>, em que L(t) &#233; o comprimento longitudinal no tempo t, e L(ED) &#233; o comprimento no fim da di&#225;stole.<sup><xref ref-type="bibr" rid="B1">1</xref></sup></p>
      <p>H&#225; diverg&#234;ncias significativas entre <italic>softwares</italic> quanto ao comprimento L(ED) utilizado: linha inteira da regi&#227;o de interesse (ROI) vs. m&#233;dia de determinado n&#250;mero de pontos do ROI x m&#233;dia dos valores em cada segmento do mesmo quadro.</p>
      <p>O valor de normalidade do SLG &#233; de, aproximadamente, 20%.<sup><xref ref-type="bibr" rid="B9">9</xref></sup> H&#225; evid&#234;ncias de varia&#231;&#245;es dos valores de normalidade de acordo com sexo e idade.<sup><xref ref-type="bibr" rid="B7">7</xref></sup></p>
      <p>Para a an&#225;lise do SLG do VE (SLGVE) por <italic>speckle tracking</italic>, &#233; necess&#225;ria uma s&#233;rie de cuidados relacionados &#224; aquisi&#231;&#227;o das imagens:</p>
      <list list-type="simple">
        <list-item>
          <p>1) O paciente deve estar sob monitoriza&#231;&#227;o eletrocardiogr&#225;fica.</p>
        </list-item>
        <list-item>
          <p>2) Se poss&#237;vel, deve-se tentar apneia expirat&#243;ria, evitando os movimentos de transla&#231;&#227;o do cora&#231;&#227;o com as incurs&#245;es respirat&#243;rias.</p>
        </list-item>
        <list-item>
          <p>3) Deve-se buscar um ponto de equil&#237;brio entre aspectos de resolu&#231;&#227;o espacial e temporal do m&#233;todo ecocardiogr&#225;fico, ponderando os ajustes do aparelho em rela&#231;&#227;o ao foco, &#224; profundidade e &#224; largura, de modo que otimizem a c&#226;mara card&#237;aca de interesse, <italic>versus</italic> o <italic>frame rate</italic> (FR). Este &#250;ltimo deve ser mantido entre 40 e 80 quadros por segundo (em pacientes com frequ&#234;ncia card&#237;aca normal). &#201; importante ratificar que, quanto maior a frequ&#234;ncia card&#237;aca, valores mais altos de FR ser&#227;o necess&#225;rios.</p>
        </list-item>
        <list-item>
          <p>4) Evitar &#8220;imagens truncadas&#8221; do VE (<italic>foreshortening</italic>).</p>
        </list-item>
        <list-item>
          <p>5) Clipes das janelas ac&#250;sticas apicais de 3, 4 e 2 c&#226;maras devem ser adquiridos, preferencialmente com o m&#237;nimo de tr&#234;s batimentos, excluindo-se extrass&#237;stoles.</p>
        </list-item>
      </list>
      <p>A <xref ref-type="table" rid="t2">Tabela 1.1</xref> e a <xref ref-type="fig" rid="f04">Figura 1.3</xref> trazem um resumo dos passos a serem seguidos para realizar a medida do SLG.</p>
      <p>
        <table-wrap id="t2">
          <label>Tabela 1.1</label>
          <caption>
            <title>&#8211; Passo a passo para medida do strain longitudinal global para a maioria dos fabricantes<bold>4</bold></title>
          </caption>
          <table frame="hsides" rules="groups">
            <colgroup width="100%">
              <col/>
            </colgroup>
            <tbody>
              <tr>
                <td align="left">
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;Realizar monitoriza&#231;&#227;o eletrocardiogr&#225;fica card&#237;aca com boa qualidade.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;Obter janelas ac&#250;sticas de 3, 4 e 2 c&#226;maras com frame rate entre 40 e 80 quadros por segundo.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;Marcar fechamento da valva a&#243;rtica (AVC).</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;Marcar defini&#231;&#245;es topogr&#225;ficas para delimitar a ROI nas janelas de 3, 4 e 2 c&#226;maras.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;Aceitar ou descartar os segmentos mioc&#225;rdicos rastreados em cada janela e fazer ajustes, se necess&#225;rio.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;Avaliar as curvas e interpretar resultados obtidos no mapa polar.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;Registrar adequadamente as condi&#231;&#245;es hemodin&#226;micas sob as quais o SLG foi aferido.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
            </tbody>
          </table>
        </table-wrap>
      </p>
      <p>
        <fig id="f04">
          <label>Figura 1.3</label>
          <caption>
            <title>&#8211; Passo a passo para obten&#231;&#227;o do strain longitudinal global. Inicialmente, adquirem-se imagens em 3, 4 e 2 c&#226;maras, com eletrocardiograma de boa qualidade e com frame rate adequado (entre 40 e 80 quadros por segundo) (Imagem A, ovoide azul). Marca-se o fechamento da valva a&#243;rtica (AVC) a partir do tra&#231;ado de Doppler puls&#225;til ou cont&#237;nuo (Imagem B). Em seguida, faz-se a marca&#231;&#227;o de tr&#234;s pontos (dois na base e um no &#225;pice), nas tr&#234;s imagens adquiridas, observando se o software faz um de rastreio adequado das imagens 2D (Imagens C e D). Finalmente, obtemos as curvas (Imagem E), o bull&#8217;s eye (Imagem F) e o valor obtido do strain longitudinal global. Adaptado de Tressino et al.4</title>
          </caption>
          <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf03.tif"/></fig>
      </p>
    </sec>
    <sec>
      <title>2. Recomenda&#231;&#245;es Gerais para o Uso do <italic>Strain</italic>: Aplicabilidade Cl&#237;nica, Compara&#231;&#227;o com a Fra&#231;&#227;o de Eje&#231;&#227;o e Descri&#231;&#227;o Adequada no Laudo</title>
      <sec>
        <title>2.1. Valor Progn&#243;stico, Padr&#245;es Param&#233;tricos e Detec&#231;&#227;o Subcl&#237;nica de Cardiopatias da Deforma&#231;&#227;o Mioc&#225;rdica</title>
        <p>A an&#225;lise de deforma&#231;&#227;o mioc&#225;rdica (<italic>strain</italic>) &#233; uma ferramenta robusta e vers&#225;til que oferece informa&#231;&#245;es adicionais e com menor variabilidade em rela&#231;&#227;o aos par&#226;metros habituais sobre progn&#243;stico, padr&#245;es param&#233;tricos peculiares das cardiomiopatias (CMPs) e detec&#231;&#227;o de les&#227;o subcl&#237;nica.</p>
        <p>Estudos recentes demostraram o valor incremental do SLGVE sobre a fra&#231;&#227;o de eje&#231;&#227;o do ventr&#237;culo esquerdo (FEVE).<sup><xref ref-type="bibr" rid="B10">10</xref></sup> &#201; importante real&#231;ar que a an&#225;lise do <italic>strain</italic> apresenta uma variabilidade inter e intraobservador de 4,9 a 8,6%, bem menor que a FEVE, provavelmente por sofrer menos influ&#234;ncia da pr&#233;- e p&#243;s-carga ventricular.<sup><xref ref-type="bibr" rid="B13">13</xref>,<xref ref-type="bibr" rid="B16">16</xref></sup> Al&#233;m disso, o SLGVE vem se tornando uma ferramenta superior &#224; FEVE naqueles pacientes com insufici&#234;ncia card&#237;aca com fra&#231;&#227;o de eje&#231;&#227;o reduzida (ICFEr) e preservada (ICFEp).<sup><xref ref-type="bibr" rid="B17">17</xref>,<xref ref-type="bibr" rid="B18">18</xref></sup> Al&#233;m da an&#225;lise do VE, a piora do <italic>strain</italic> do ventr&#237;culo direito (VD) fornece valor aditivo progn&#243;stico naqueles pacientes com ICFEp.<sup><xref ref-type="bibr" rid="B19">19</xref></sup></p>
        <p>As CMPs compartilham achados morfol&#243;gicos semelhantes na maioria das vezes, sendo um grande desafio diagn&#243;stico na pr&#225;tica cl&#237;nica di&#225;ria. &#201; comum haver a presen&#231;a de aumento da massa e da espessura ventricular, associada &#224; disfun&#231;&#227;o diast&#243;lica (DD) e com FEVE preservada nos est&#225;gios mais iniciais. A an&#225;lise param&#233;trica do SLGVE pelo mapa polar possibilita que o exame de ecocardiograma desmascare alguns diagn&#243;sticos que n&#227;o eram percebidos pelos par&#226;metros habituais, sendo descrito como uma &#8220;impress&#227;o digital&#8221; de algumas delas. O exemplo cl&#225;ssico &#233; o padr&#227;o de poupar a ponta <italic>(apical sparing)</italic> da amiloidose, que ser&#225; descrito com mais detalhes em cap&#237;tulo espec&#237;fico.<sup><xref ref-type="bibr" rid="B20">20</xref></sup> Essa caracteriza&#231;&#227;o fenot&#237;pica vem despertando muito entusiasmo por favorecer uma facilidade diagn&#243;stica nas patologias raras. Por outro lado, &#233; importante ressaltar que, se n&#227;o combinarmos o <italic>strain</italic> com dados da hist&#243;ria cl&#237;nica, aspectos morfol&#243;gicos e hemodin&#226;micos, favoreceremos o excesso e o erro diagn&#243;stico. Veja esses exemplos de <italic>&#8220;apical sparing&#8221;</italic> (<xref ref-type="fig" rid="f05">Figura 2.1</xref>).</p>
        <p>
          <fig id="f05">
            <label>Figura 2.1</label>
            <caption>
              <title>&#8211; Padr&#245;es de SLG com aspecto de poupar a ponta em diferentes cardiopatias. 1: Cardiotoxicidade por antrac&#237;clico; 2: Mioc&#225;rdio n&#227;o compactado; 3: Hipotireoidismo; 4: Amiloidose por transtirretina.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf04.tif"/></fig>
        </p>
        <p>A utiliza&#231;&#227;o do <italic>strain</italic> como ferramenta diagn&#243;stica e progn&#243;stica se consolidou atrav&#233;s de sua aplica&#231;&#227;o na cardio-oncologia, quando h&#225; a oportunidade de ajustar a conduta terap&#234;utica, baseada na varia&#231;&#227;o se seu valor, em rela&#231;&#227;o ao valor do exame basal durante a quimioterapia. Quando h&#225; uma redu&#231;&#227;o relativa maior que 15%, considera-se cardiotoxicidade com les&#227;o mioc&#225;rdica subcl&#237;nica.<sup><xref ref-type="bibr" rid="B21">21</xref></sup> Em 2019, um posicionamento das diversas sociedades elaborou crit&#233;rios para o uso adequado das diversas modalidades de imagens para avalia&#231;&#227;o das estruturas card&#237;acas nas doen&#231;as n&#227;o valvares. Nesse documento, das 81 indica&#231;&#245;es descritas, apenas quatro consideraram o uso do <italic>strain</italic> adequado, sendo tr&#234;s na cardio-oncologia e uma para avalia&#231;&#227;o da CMP hipertr&#243;fica.<sup><xref ref-type="bibr" rid="B22">22</xref></sup> Apesar da falta de estudos bem desenhados que validem essa ferramenta nas demais situa&#231;&#245;es descritas por esse posicionamento, o <italic>strain</italic> &#233; largamente utilizado nos grandes centros de cardio-oncologia. Recentemente, a atualiza&#231;&#227;o da Diretriz Brasileira de Cardio-Oncologia refor&#231;ou a sua utiliza&#231;&#227;o.<sup><xref ref-type="bibr" rid="B23">23</xref></sup></p>
      </sec>
      <sec>
        <title>2.2. <italic>Strain</italic> ou Fra&#231;&#227;o de Eje&#231;&#227;o: Qual &#233; a Melhor Alternativa?</title>
        <p>A FEVE &#233; um dos principais par&#226;metros ecocardiogr&#225;ficos utilizados para a avalia&#231;&#227;o da fun&#231;&#227;o ventricular na pr&#225;tica di&#225;ria, sendo um dado de f&#225;cil interpreta&#231;&#227;o pelos cl&#237;nicos, al&#233;m de ser amplamente dispon&#237;vel e obtida em equipamentos b&#225;sicos de ultrassom. H&#225; extensa valida&#231;&#227;o do uso desse par&#226;metro para o manejo de pacientes portadores de cardiopatias, sendo utilizado em grandes estudos de interven&#231;&#227;o terap&#234;utica como crit&#233;rio de inclus&#227;o de pacientes e, muitas vezes, servindo como par&#226;metro para a avalia&#231;&#227;o e o acompanhamento de resultados.<sup><xref ref-type="bibr" rid="B24">24</xref></sup> O valor progn&#243;stico da FEVE &#233; bastante estabelecido na insufici&#234;ncia card&#237;aca (IC) cr&#244;nica<sup><xref ref-type="bibr" rid="B25">25</xref></sup> e, por isso, na atual recomenda&#231;&#227;o da Sociedade Europeia de Cardiologia, as ICs s&#227;o classificadas com base no valor da FEVE em: <bold>1</bold>) IC com FE preservada (ICFEp: FE &#8805; 50%); <bold>2</bold>) IC com FE em meio termo (ICFEmr: <inline-formula><mml:math><mml:mrow><mml:mi>F</mml:mi><mml:mi>E</mml:mi></mml:mrow><mml:mo>=</mml:mo><mml:mn>40</mml:mn><mml:mo>&#8722;</mml:mo><mml:mn>49</mml:mn><mml:mi>%</mml:mi></mml:math></inline-formula>); e <bold>3</bold>) ICs com FE de eje&#231;&#227;o reduzida (ICFEr: FE &lt; 40%).<sup><xref ref-type="bibr" rid="B26">26</xref></sup></p>
        <p>A FEVE tem importante papel como par&#226;metro quantitativo para a defini&#231;&#227;o de estrat&#233;gias espec&#237;ficas em IC, por exemplo, servindo de crit&#233;rio para a indica&#231;&#227;o de terapia de ressincroniza&#231;&#227;o card&#237;aca em pacientes com IC refrat&#225;ria (FEVE &#8804; 35%) ou mesmo na detec&#231;&#227;o de cardiotoxicidade em pacientes com c&#226;ncer em uso de antrac&#237;clicos (queda evolutiva de FEVE &#8805; 10% em rela&#231;&#227;o ao basal com valor menor que o limite inferior da normalidade).<sup><xref ref-type="bibr" rid="B27">27</xref></sup> No entanto, deve-se ressaltar que h&#225; limita&#231;&#227;o da acur&#225;cia da FEVE estimada pelo Simpson biplanar pela grande variabilidade interobservador dessa medida, que pode chegar at&#233; 13%.<sup><xref ref-type="bibr" rid="B28">28</xref></sup> A ecocardiografia tridimensional (ECO3D), diferente do m&#233;todo Simpson biplanar, n&#227;o se baseia em assun&#231;&#245;es geom&#233;tricas e, por isso, mede diretamente os volumes das cavidades e a FEVE, com resultados bastante compar&#225;veis aos obtidos pela RMC. Pelo uso de algoritmos autom&#225;ticos e pela menor suscetibilidade a varia&#231;&#245;es nas janelas de aquisi&#231;&#227;o (orienta&#231;&#227;o dos cortes apicais), a ECO3D possui menor variabilidade intra e interobservador que o m&#233;todo biplanar (0.4 &#177; 4.5%),<sup><xref ref-type="bibr" rid="B29">29</xref></sup> sendo uma boa alternativa para o acompanhamento e a vigil&#226;ncia de pacientes com disfun&#231;&#227;o ventricular ou sob risco de dano mioc&#225;rdico.</p>
        <p>As t&#233;cnicas de avalia&#231;&#227;o da deforma&#231;&#227;o mioc&#225;rdica, como o <italic>strain</italic>, permitem a avalia&#231;&#227;o dos tr&#234;s componentes de contra&#231;&#227;o das fibras mioc&#225;rdicas: longitudinal, radial e circunferencial. A FEVE &#233; determinada sobretudo pelos componentes radial e circunferencial da contra&#231;&#227;o mioc&#225;rdica, que resultam no espessamento das paredes do mioc&#225;rdio e na redu&#231;&#227;o da cavidade ventricular na s&#237;stole. &#201; importante notar, por&#233;m, que a FEVE n&#227;o &#233; um determinante &#250;nico da <italic>performance</italic> ventricular (fun&#231;&#227;o &#8220;ejetiva&#8221;), sendo esta tamb&#233;m dependente de um volume diast&#243;lico final (VDF) do VE adequado para gerar um volume sist&#243;lico normal. Isso explica por que, em pacientes com CMPs com express&#227;o fenot&#237;pica de hipertrofia parietal conc&#234;ntrica, como nas infiltrativas ou hipertr&#243;ficas, podemos ter FEVE normal e baixo d&#233;bito card&#237;aco. Esses pacientes se apresentam clinicamente como ICFEp e, &#224; despeito de FEVE normal, t&#234;m geralmente pior progn&#243;stico que pacientes com FEVE normal e d&#233;bito card&#237;aco preservado, com altera&#231;&#245;es da fun&#231;&#227;o contr&#225;til detect&#225;veis apenas pelo SLG.<sup><xref ref-type="bibr" rid="B30">30</xref></sup></p>
        <p>De fato, a deforma&#231;&#227;o longitudinal &#233; o componente da contratilidade mioc&#225;rdica que se altera mais precocemente em grande parte das CMPs, podendo sinalizar um processo em est&#225;gio inicial e subcl&#237;nico (ainda sem redu&#231;&#227;o da FEVE), fase de doen&#231;a em que a institui&#231;&#227;o de medidas terap&#234;uticas ou cardioprotetoras pode apresentar melhores resultados. O SLG pode se encontrar alterado at&#233; mesmo em doen&#231;as gen&#233;ticas n&#227;o fenotipicamente expressas, tal como em portadores de Ataxia de Friedreich com massa e FEVE normais, podendo, inclusive, predizer a queda da FEVE e o progn&#243;stico nesses pacientes.<sup><xref ref-type="bibr" rid="B31">31</xref></sup></p>
        <p>Estudos demonstram o valor progn&#243;stico adicional do SLG em pacientes com IC, com valor incremental ao efeito progn&#243;stico da FEVE, sobretudo em pacientes com FE &gt; 35%.<sup><xref ref-type="bibr" rid="B32">32</xref></sup> Dessa forma, Potter et al. sugeriram uma nova classifica&#231;&#227;o de fun&#231;&#227;o ventricular, incorporando &#224; pr&#225;tica cl&#237;nica o uso valores de SLGVE de forma complementar &#224; quantifica&#231;&#227;o da FEVE, auxiliando na decis&#227;o cl&#237;nica e na avalia&#231;&#227;o progn&#243;stica dos pacientes, sobretudo nos com FEVE &gt; 53% (ICFEp).<sup><xref ref-type="bibr" rid="B10">10</xref></sup></p>
      </sec>
      <sec>
        <title>2.3. Recomenda&#231;&#245;es Gerais de como Reportar os Resultados do <italic>Strain</italic> e os Valores de Normalidade</title>
        <p>Com o objetivo de simplificar a descri&#231;&#227;o do <italic>strain</italic> no laudo de ecocardiograma, &#233; recomendada a utiliza&#231;&#227;o do tipo de <italic>strain</italic> analisado (o qual define os movimentos de contra&#231;&#227;o ou alongamento) e sua avalia&#231;&#227;o num&#233;rica em valores absolutos, principalmente em estudos comparativos sequenciais, com o objetivo de n&#227;o levar a interpreta&#231;&#245;es equivocadas de piora do <italic>strain</italic>. Outras informa&#231;&#245;es cruciais que devem ser descritas s&#227;o os sinais vitais do paciente (press&#227;o arterial e frequ&#234;ncia card&#237;aca), devido a altera&#231;&#245;es de pr&#233;- e p&#243;s-carga que influenciam o valor global do <italic>strain</italic>, a marca do equipamento de ultrassom utilizado, bem como a vers&#227;o do <italic>software</italic> de an&#225;lise, em decorr&#234;ncia da variabilidade da normalidade entre os fabricantes.<sup><xref ref-type="bibr" rid="B33">33</xref>,<xref ref-type="bibr" rid="B34">34</xref></sup> A <xref ref-type="table" rid="t3">Tabela 2.1</xref> abaixo descreve as informa&#231;&#245;es essenciais que devem constar no laudo para descri&#231;&#227;o completa do <italic>strain.</italic><sup><xref ref-type="bibr" rid="B9">9</xref></sup></p>
        <p>
          <table-wrap id="t3">
            <label>Tabela 2.1</label>
            <caption>
              <title>&#8211; Elementos essenciais para a descri&#231;&#227;o do <italic>strain</italic> no laudo de ecocardiograma</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="50%">
                <col/>
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left">Informa&#231;&#245;es relevantes do <italic>strain</italic> no laudo</th>
                  <th align="left">Descri&#231;&#227;o</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>Sinais Vitais</td>
                  <td>Press&#227;o arterial e frequ&#234;ncia card&#237;aca<sup>16</sup></td>
                </tr>
                <tr>
                  <td>Tipo de <italic>strain</italic></td>
                  <td>Longitudinal, circunferencial e radial</td>
                </tr>
                <tr>
                  <td>Valor absoluto do <italic>strain</italic></td>
                  <td>Na descri&#231;&#227;o da fun&#231;&#227;o da c&#226;mara analisada</td>
                </tr>
                <tr>
                  <td>C&#226;mara card&#237;aca analisada</td>
                  <td>VE, VD ou AE</td>
                </tr>
                <tr>
                  <td>Padr&#227;o de mapa polar (<xref ref-type="fig" rid="f06">Figura 2.2</xref>)</td>
                  <td>Se h&#225; algum padr&#227;o t&#237;pico, como em amiloidose ou cardiomiopatia hipertr&#243;fica<sup>40</sup></td>
                </tr>
                <tr>
                  <td>Varia&#231;&#227;o percentual em exames sequenciais</td>
                  <td>Utiliza&#231;&#227;o comprovada em cardio-oncologia. &#8710;%= <italic>strain</italic> exame basal, atual/basal<sup>21</sup></td>
                </tr>
                <tr>
                  <td>Equipamento e vers&#227;o do <italic>software</italic> utilizado</td>
                  <td>H&#225; variabilidade do valor normal do <italic>strain</italic> segundo a marca e a vers&#227;o do equipamento<sup>37</sup></td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>&#8710;%: varia&#231;&#227;o (delta) percentual; AE: &#225;trio esquerdo; VD: ventr&#237;culo direito; VE: ventr&#237;culo esquerdo.</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
        <p>
          <fig id="f06">
            <label>Figura 2.2</label>
            <caption>
              <title>&#8211; Padr&#227;o de strain avaliado no mapa polar: A: Padr&#227;o t&#237;pico de amiloidose (poupa o &#225;pex); B: Padr&#227;o t&#237;pico de cardiomiopatia hipertr&#243;fica com predom&#237;nio apical (strain reduzido predominante no &#225;pex, em que a hipertrofia foi evidenciada como mais acentuada no estudo bidimensional).</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf05.tif"/></fig>
        </p>
        <p>Os valores normais de refer&#234;ncia para o <italic>strain</italic> analisado<sup><xref ref-type="bibr" rid="B9">9</xref>,<xref ref-type="bibr" rid="B35">35</xref>-<xref ref-type="bibr" rid="B39">39</xref></sup> devem ser inclu&#237;dos no laudo. A <xref ref-type="table" rid="t4">Tabela 2.2</xref> descreve valores m&#233;dios da normalidade de forma simplificada dos diversos tipos de <italic>strain</italic>, bem como o grau de evid&#234;ncia para sua utiliza&#231;&#227;o na pr&#225;tica cl&#237;nica. Diferentemente da FEVE, o valor de normalidade do <italic>strain</italic> ainda n&#227;o foi assimilado de maneira consistente pelo cardiologista cl&#237;nico e, portanto, devem constar no laudo como refer&#234;ncia.</p>
        <p>
          <table-wrap id="t4">
            <label>Tabela 2.2</label>
            <caption>
              <title>&#8211; Valores de normalidade gerais para as diferentes modalidades de strain e c&#226;maras card&#237;acas. Grau de comprova&#231;&#227;o da aplica&#231;&#227;o cl&#237;nica</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="33%">
                <col/>
                <col/>
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left">C&#226;mara/Tipo de <italic>strain</italic></th>
                  <th>Valor de normalidade (valor absoluto)</th>
                  <th>Aplica&#231;&#227;o na pr&#225;tica cl&#237;nica</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>
                          <bold>VE</bold>
                        </p>
                      </list-item>
                      <list-item>
                        <p>Longitudinal (negativo)</p>
                      </list-item>
                      <list-item>
                        <p>Radial (positivo)</p>
                      </list-item>
                      <list-item>
                        <p>Circunferencial (negativo)</p>
                      </list-item>
                    </list>
                  </td>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>18%<sup>35,39</sup>20%<sup>35</sup></p>
                      </list-item>
                      <list-item>
                        <p>40%<sup>35</sup></p>
                      </list-item>
                      <list-item>
                        <p>20%</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>++++</p>
                      </list-item>
                      <list-item>
                        <p>+</p>
                      </list-item>
                      <list-item>
                        <p>+</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>
                          <bold>VD</bold>
                        </p>
                      </list-item>
                      <list-item>
                        <p>Longitudinal parede livre (negativo)</p>
                      </list-item>
                    </list>
                  </td>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>20%<sup>35,36</sup></p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>+++</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p><bold>AE</bold> (varia com a idade, &#233; positivo)</p>
                      </list-item>
                      <list-item>
                        <p>Reservat&#243;rio (mais utilizada)</p>
                      </list-item>
                      <list-item>
                        <p>Conduto Bomba</p>
                      </list-item>
                    </list>
                  </td>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>39%<sup>38,39</sup></p>
                      </list-item>
                      <list-item>
                        <p>23%<sup>38</sup></p>
                      </list-item>
                      <list-item>
                        <p>17%<sup>38,41</sup></p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>+++</p>
                      </list-item>
                      <list-item>
                        <p>+</p>
                      </list-item>
                      <list-item>
                        <p>+</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>AE: &#225;trio esquerdo; VD: ventr&#237;culo direito; VE: ventr&#237;culo esquerdo. ++++ Muito utilizado; +++ Utilizado; ++ Utiliza&#231;&#227;o limitada na pr&#225;tica cl&#237;nica; + Utiliza&#231;&#227;o limitada na pr&#225;tica cl&#237;nica, e n&#227;o acessado em softwares embutidos nos equipamentos de ecocardio.</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
      </sec>
      <sec>
        <title>2.4. Conclus&#227;o</title>
        <p>A evid&#234;ncia atual &#233; robusta para a incorpora&#231;&#227;o do <italic>strain</italic> na pr&#225;tica cl&#237;nica di&#225;ria. Por&#233;m, ainda temos desafios para nossa realidade nacional, como a falta de democratiza&#231;&#227;o de acesso nos servi&#231;os de ecocardiograma com aparelhos com <italic>softwares</italic> para sua an&#225;lise e falta de dados sobre a popula&#231;&#227;o brasileira. Utilizamos valores extrapolados de popula&#231;&#227;o com perfil sociodemogr&#225;fico bem distinto de nossa realidade, com aplica&#231;&#227;o adaptada para a popula&#231;&#227;o brasileira. O Departamento de Imagem Cardiovascular est&#225; promovendo um trabalho multic&#234;ntrico (j&#225; em andamento), quando est&#227;o sendo analisados dados ecocardiogr&#225;ficos de brasileiros h&#237;gidos, para que possamos ter um retrospecto dos valores de normalidade em nossa popula&#231;&#227;o. O <italic>strain</italic> vem para se somar aos valores habituais do ecocardiograma, trazendo mais robustez progn&#243;stica, possibilitando diagn&#243;stico de CMPs, particularmente nas que se apresentam com aumento da espessura mioc&#225;rdica, e, por &#250;ltimo, diagn&#243;stico de les&#227;o mioc&#225;rdica subcl&#237;nica.</p>
      </sec>
    </sec>
    <sec>
      <title>3. <italic>Strain</italic> na Cardio-oncologia</title>
      <p>A disfun&#231;&#227;o card&#237;aca relacionada ao tratamento contra o c&#226;ncer representa uma importante causa de morbidade e mortalidade nos pacientes oncol&#243;gicos.<sup><xref ref-type="bibr" rid="B42">42</xref>,<xref ref-type="bibr" rid="B43">43</xref></sup> Essa complica&#231;&#227;o pode interromper o tratamento e comprometer a cura ou o adequado controle do c&#226;ncer.<sup><xref ref-type="bibr" rid="B44">44</xref>,<xref ref-type="bibr" rid="B45">45</xref></sup>Al&#233;m disso, a IC relacionada &#224; cardiotoxicidade por quimioter&#225;picos frequentemente tem pior progn&#243;stico que muitas neoplasias, com mortalidade de at&#233; 60% em 2 anos.<sup><xref ref-type="bibr" rid="B42">42</xref></sup></p>
      <p>A identifica&#231;&#227;o precoce da cardiotoxicidade com a institui&#231;&#227;o de medidas cardioprotetoras tem potencial impacto progn&#243;stico nesse cen&#225;rio.<sup><xref ref-type="bibr" rid="B46">46</xref>,<xref ref-type="bibr" rid="B47">47</xref></sup> Contudo, os m&#233;todos usualmente utilizados para esse diagn&#243;stico, como a FEVE pela t&#233;cnica bidimensional, t&#234;m baixa sensibilidade.<sup><xref ref-type="bibr" rid="B48">48</xref>,<xref ref-type="bibr" rid="B49">49</xref></sup> Assim, a utiliza&#231;&#227;o de marcadores mais precoces para a identifica&#231;&#227;o dessa complica&#231;&#227;o, como a an&#225;lise do <italic>strain</italic>, tem grande destaque nesse contexto.</p>
      <p>Os m&#233;todos de diagn&#243;stico por imagem t&#234;m papel fundamental nesse cen&#225;rio, e o ecocardiograma tem sido a ferramenta mais utilizada em fun&#231;&#227;o de sua correspond&#234;ncia anat&#244;mica, car&#225;ter n&#227;o invasivo, f&#225;cil acesso, baixo custo e isen&#231;&#227;o de radia&#231;&#227;o ionizante.<sup><xref ref-type="bibr" rid="B27">27</xref></sup> A FEVE &#233; o par&#226;metro mais utilizado para o diagn&#243;stico de cardiotoxicidade. Utilizando a t&#233;cnica bidimensional, ela deve ser calculada pelo m&#233;todo de Simpson biplanar.<sup><xref ref-type="bibr" rid="B21">21</xref></sup> A ECO3D, quando dispon&#237;vel, &#233; a t&#233;cnica de escolha para monitorar a FEVE em pacientes com c&#226;ncer. Suas principais vantagens incluem maior acur&#225;cia no reconhecimento de FEVE abaixo do limite inferior da normalidade e maior reprodutibilidade que a t&#233;cnica bidimensional, com acur&#225;cia semelhante &#224; resson&#226;ncia card&#237;aca. Entretanto, sua baixa disponibilidade, seu alto custo e a experi&#234;ncia do operador representam barreiras da t&#233;cnica tridimensional.<sup><xref ref-type="bibr" rid="B27">27</xref>,<xref ref-type="bibr" rid="B50">50</xref></sup></p>
      <p>A disfun&#231;&#227;o ventricular relacionada ao tratamento contra o c&#226;ncer &#233; definida por queda absoluta da FEVE em mais de 10 pontos percentuais, para um valor inferior a 50%, na presen&#231;a ou n&#227;o de sintomas de IC. Recomenda-se que esse estudo ecocardiogr&#225;fico seja repetido dentro de 2 a 3 semanas para se avaliar os efeitos da pr&#233; e p&#243;s-carga sobre a FEVE.</p>
      <p>Apesar de ser um importante e j&#225; estabelecido fator progn&#243;stico, a FEVE tem baixa sensibilidade para o diagn&#243;stico de cardiotoxicidade, sendo dependente de alguns fatores como pr&#233;-carga card&#237;aca, qualidade da imagem e experi&#234;ncia do examinador. Al&#233;m disso, ela pode subestimar o real dano card&#237;aco, uma vez que mecanismos hemodin&#226;micos compensat&#243;rios permitem o adequado desempenho sist&#243;lico do VE, mesmo na presen&#231;a de disfun&#231;&#227;o dos mi&#243;citos.<sup><xref ref-type="bibr" rid="B48">48</xref></sup> Assim, a redu&#231;&#227;o da FEVE ocorre frequentemente em um momento muito tardio, quando, mesmo com a interven&#231;&#227;o terap&#234;utica, a maioria dos pacientes n&#227;o tem recupera&#231;&#227;o funcional.<sup><xref ref-type="bibr" rid="B46">46</xref>,<xref ref-type="bibr" rid="B48">48</xref>,<xref ref-type="bibr" rid="B49">49</xref></sup></p>
      <p>Quando a detec&#231;&#227;o da cardiotoxicidade &#233; precoce, com institui&#231;&#227;o de tratamento cardioprotetor, os pacientes t&#234;m maior potencial para a recupera&#231;&#227;o da fun&#231;&#227;o ventricular.<sup><xref ref-type="bibr" rid="B46">46</xref>,<xref ref-type="bibr" rid="B51">51</xref></sup> Nesse cen&#225;rio, o estudo da deforma&#231;&#227;o mioc&#225;rdica ou <italic>strain</italic> tem grande destaque. O <italic>strain</italic> calculado pela t&#233;cnica de <italic>speckle tracking</italic> bidimensional (ST2D) tem surgido como um marcador sens&#237;vel e reprodut&#237;vel de an&#225;lise da fun&#231;&#227;o sist&#243;lica e da contratilidade do VE, validado em modelos <italic>in vitro</italic> e <italic>in vivo.</italic><sup><xref ref-type="bibr" rid="B52">52</xref>,<xref ref-type="bibr" rid="B53">53</xref></sup> Tem sido crescente o n&#250;mero de publica&#231;&#245;es que demonstram a utilidade do estudo da deforma&#231;&#227;o mioc&#225;rdica pelo ST2D na detec&#231;&#227;o precoce e subcl&#237;nica da cardiotoxicidade induzida por quimioter&#225;picos, especialmente atrav&#233;s da queda relativa do SLG.<sup><xref ref-type="bibr" rid="B23">23</xref>,<xref ref-type="bibr" rid="B54">54</xref>-<xref ref-type="bibr" rid="B57">57</xref></sup></p>
      <p>&#201; recomendada a an&#225;lise do SLG nos pacientes que ir&#227;o se submeter a tratamento quimioter&#225;pico potencialmente cardiot&#243;xico. O diagn&#243;stico subcl&#237;nico de cardiotoxicidade &#233; sugerido quando h&#225; uma queda do SLG maior ou igual a 12% em rela&#231;&#227;o ao seu valor basal.<sup><xref ref-type="bibr" rid="B21">21</xref>,<xref ref-type="bibr" rid="B27">27</xref></sup>Na aus&#234;ncia de um estudo ecocardiogr&#225;fico basal (pr&#233;-quimioterapia) para compara&#231;&#227;o, &#233; sugerido, com base na opini&#227;o de especialistas, um valor absoluto de <italic>strain</italic> inferior a 17% como marcador de cardiotoxicidade subcl&#237;nica, desde que n&#227;o haja outros dados cl&#237;nicos de sobreposi&#231;&#227;o de outra doen&#231;a mioc&#225;rdica de base. Uma queda do SLG inferior a 8% do valor basal &#233; considerada n&#227;o significativa. A <xref ref-type="fig" rid="f07">Figura 3.1</xref> apresenta um exemplo de cardiotoxicidade subcl&#237;nica sugerida pela queda relativa do SLG.</p>
      <p>
        <fig id="f07">
          <label>Figura 3.1</label>
          <caption>
            <title>&#8211; Exemplo de cardiotoxicidade subcl&#237;nica em paciente com c&#226;ncer de mama. An&#225;lise da FEVE pelo m&#233;todo de Simpson e do SLG com imagem do bull&#8217;s eye. Em A e B, avalia&#231;&#227;o pr&#233;-quimioterapia; em B e C, avalia&#231;&#227;o ap&#243;s dose cumulativa de 240 mg/m2 de doxorrubicina. N&#227;o houve queda expressiva da FEVE, entretanto, foi observada queda relativa de 22% no SLG. FEVE: fra&#231;&#227;o de eje&#231;&#227;o do ventr&#237;culo esquerdo; SLG: strain longitudinal global.</title>
          </caption>
          <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf06.tif"/></fig>
      </p>
      <p>A <xref ref-type="fig" rid="f08">Figura 3.2</xref> apresenta o algoritmo do seguimento ecocardiogr&#225;fico no paciente oncol&#243;gico, baseado na FEVE e no SLG. As <xref ref-type="fig" rid="f09">Figuras 3.3</xref> e <xref ref-type="fig" rid="f10">3.4</xref> apresentam o monitoramento ecocardiogr&#225;fico em pacientes sob tratamento com antrac&#237;clicos e trastuzumabe, respectivamente.</p>
      <p>
        <fig id="f08">
          <label>Figura 3.2</label>
          <caption>
            <title>&#8211; Algoritmo de avalia&#231;&#227;o do paciente oncol&#243;gico durante o tratamento quimioter&#225;pico, baseado na FEVE e SLG. CV: cardiovascular; ECA: enzima conversora da angiotensina; FEVE: fra&#231;&#227;o de eje&#231;&#227;o do ventr&#237;culo esquerdo; QT: quimioterapia; SLG: strain longitudinal global.</title>
          </caption>
          <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf07.tif"/></fig>
      </p>
      <p>
        <fig id="f09">
          <label>Figura 3.3</label>
          <caption>
            <title>&#8211; Monitoramento ecocardiogr&#225;fico durante o tratamento com antraciclinas. FEVE: fra&#231;&#227;o de eje&#231;&#227;o do ventr&#237;culo esquerdo; SLG: strain global longitudinal.</title>
          </caption>
          <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf08.tif"/></fig>
      </p>
      <p>
        <fig id="f10">
          <label>Figura 3.4</label>
          <caption>
            <title>&#8211; Monitoramento ecocardiogr&#225;fico durante o tratamento com trastuzumabe. FEVE: fra&#231;&#227;o de eje&#231;&#227;o do ventr&#237;culo esquerdo; SLG: strain global longitudinal.</title>
          </caption>
          <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf09.tif"/></fig>
      </p>
      <p>O ensaio cl&#237;nico randomizado SUCCOUR foi o primeiro estudo prospectivo e multic&#234;ntrico com maior poder cient&#237;fico que demonstrou o impacto progn&#243;stico da cardioprote&#231;&#227;o guiada pelo SLG em compara&#231;&#227;o &#224; cardioprote&#231;&#227;o guiada pela queda da FEVE pela ECO3D. Esse estudo revelou que, em pacientes recebendo quimioterapia com antrac&#237;clicos e com risco elevado de cardiotoxicidade, a cardioprote&#231;&#227;o (incluindo inibidor da enzima conversora de angiotensina [ECA] e betabloqueador) guiada por uma queda relativa do SLG maior ou igual a 12% do valor basal resultou em menor grau de queda da FEVE e menor incid&#234;ncia de disfun&#231;&#227;o card&#237;aca relacionada ao tratamento contra o c&#226;ncer em 1 ano de seguimento.<sup><xref ref-type="bibr" rid="B58">58</xref></sup></p>
      <p>O <italic>strain</italic> calculado pelo <italic>speckle tracking</italic> tridimensional (ST3D) tem demonstrado vantagens t&#233;cnicas em rela&#231;&#227;o ao ST2D com acur&#225;cia, reprodutibilidade e aplicabilidade j&#225; demonstradas em diferentes cen&#225;rios.<sup><xref ref-type="bibr" rid="B59">59</xref>-<xref ref-type="bibr" rid="B62">62</xref></sup> Recentemente, pequenos estudos demonstraram o impacto do ST3D no reconhecimento precoce de altera&#231;&#245;es mec&#226;nicas relacionadas &#224; quimioterapia.<sup><xref ref-type="bibr" rid="B63">63</xref>-<xref ref-type="bibr" rid="B66">66</xref></sup> Entretanto, s&#227;o necess&#225;rios estudos maiores e principalmente com maior tempo de seguimento para avaliar o valor progn&#243;stico dessa t&#233;cnica.</p>
      <p>Entre as limita&#231;&#245;es da an&#225;lise do SLG, destacamos a variabilidade das medidas em equipamentos de diferentes fabricantes, de modo que as medi&#231;&#245;es devem ser sempre feitas nos mesmos aparelhos. Assim como a FEVE, o SLG sofre influ&#234;ncia pelos efeitos da pr&#233;- e p&#243;s-carga, geometria ventricular, altera&#231;&#245;es teciduais (infarto, miocardite, por exemplo) e dist&#250;rbios de condu&#231;&#227;o. Por &#250;ltimo, determinadas informa&#231;&#245;es cl&#237;nicas e oncol&#243;gicas s&#227;o fundamentais e devem ser reportadas no laudo para uma acurada interpreta&#231;&#227;o ecocardiogr&#225;fica, conforme apresentado na <xref ref-type="table" rid="t5">Tabela 3.1</xref>.</p>
      <p>
        <table-wrap id="t5">
          <label>Tabela 3.1</label>
          <caption>
            <title>&#8211; Informa&#231;&#245;es cl&#237;nicas e oncol&#243;gicas relevantes no laudo ecocardiogr&#225;fico</title>
          </caption>
          <table frame="hsides" rules="groups">
            <colgroup width="100%">
              <col/>
            </colgroup>
            <tbody>
              <tr>
                <td align="left">Tempo entre a infus&#227;o do quimioter&#225;pico e a realiza&#231;&#227;o do eco (pr&#233; ou p&#243;s)</td>
              </tr>
              <tr>
                <td>Frequ&#234;ncia card&#237;aca Press&#227;o arterial Estado vol&#234;mico (descri&#231;&#227;o do di&#226;metro e varia&#231;&#227;o da veia cava inferior)</td>
              </tr>
              <tr>
                <td>Compara&#231;&#227;o com estudo basal, em especial FEVE e SLG &#8211; em caso de queda relativa, descrever o percentual desta redu&#231;&#227;o</td>
              </tr>
              <tr>
                <td>Aparelho/<italic>software</italic> utilizado para a an&#225;lise do SLG</td>
              </tr>
            </tbody>
          </table>
          <table-wrap-foot>
            <attrib>FEVE: fra&#231;&#227;o de eje&#231;&#227;o do ventr&#237;culo esquerdo; SLG: strain longitudinal global.</attrib>
          </table-wrap-foot>
        </table-wrap>
      </p>
    </sec>
    <sec>
      <title>4. <italic>Strain</italic> na Disfun&#231;&#227;o Diast&#243;lica</title>
      <sec>
        <title>4.1. Introdu&#231;&#227;o</title>
        <p>A DD &#233; considerada um marcador precoce de dano mioc&#225;rdico e, mesmo quando assintom&#225;tica, pode determinar maiores taxas de mortalidade. Com a progress&#227;o da DD, ocorre aumento das press&#245;es de enchimento do VE e ICFEp,<sup><xref ref-type="bibr" rid="B67">67</xref>,<xref ref-type="bibr" rid="B68">68</xref></sup> sendo que esta &#250;ltima responde por mais de 50% das interna&#231;&#245;es por IC e apresenta taxas de mortalidade equipar&#225;veis &#224;s da ICFEr.<sup><xref ref-type="bibr" rid="B69">69</xref></sup> Ao contr&#225;rio da ICFEp, a DD pr&#233;-cl&#237;nica &#233; potencialmente revers&#237;vel. Entretanto, a sua fisiopatologia &#233; complexa e, apesar do uso integrado de v&#225;rios par&#226;metros, o algoritmo atualmente recomendado &#233; pouco sens&#237;vel para detectar est&#225;gios subcl&#237;nicos de DD.<sup><xref ref-type="bibr" rid="B70">70</xref>,<xref ref-type="bibr" rid="B71">71</xref></sup></p>
        <p>Casos indeterminados ainda s&#227;o frequentes porque esses par&#226;metros nem sempre se alteram simultaneamente ou de forma linear.<sup><xref ref-type="bibr" rid="B70">70</xref></sup> Fatores n&#227;o diast&#243;licos tamb&#233;m podem contribuir para a ICFEp levando a express&#245;es fenot&#237;picas variadas, a depender do mecanismo fisiopatol&#243;gico predominante.<sup><xref ref-type="bibr" rid="B72">72</xref></sup> Ferramentas que avaliam as mec&#226;nicas ventricular e atrial esquerdas pela medida do <italic>strain</italic> podem suplantar esses desafios diagn&#243;sticos.<sup><xref ref-type="bibr" rid="B73">73</xref>,<xref ref-type="bibr" rid="B74">74</xref></sup> O papel da mec&#226;nica ventricular direita nesse contexto ainda est&#225; sob investiga&#231;&#227;o.<sup><xref ref-type="bibr" rid="B75">75</xref></sup></p>
      </sec>
      <sec>
        <title>4.2. <italic>Strain</italic> do Ventr&#237;culo Esquerdo</title>
        <p>Diversos estudos t&#234;m demonstrado que par&#226;metros de deforma&#231;&#227;o mioc&#225;rdica avaliados por meio do <italic>speckle tracking</italic>, especialmente o SLGVE, t&#234;m melhor correla&#231;&#227;o com o relaxamento do VE e maior acur&#225;cia em predizer press&#245;es de enchimento e intoler&#226;ncia ao exerc&#237;cio quando comparados a &#237;ndices derivados do Doppler tecidual.<sup><xref ref-type="bibr" rid="B76">76</xref>-<xref ref-type="bibr" rid="B78">78</xref></sup> A queda do SLGVE auxilia na detec&#231;&#227;o da DD em est&#225;gios mais iniciais e tamb&#233;m prediz eventos cardiovasculares (CV) na ICFEp.<sup><xref ref-type="bibr" rid="B17">17</xref>,<xref ref-type="bibr" rid="B79">79</xref>-<xref ref-type="bibr" rid="B82">82</xref></sup> Diante dessas evid&#234;ncias, o SLGVE reduzido (&lt; 16%) j&#225; foi inclu&#237;do como crit&#233;rio diagn&#243;stico no novo algoritmo proposto pelas recentes diretrizes de ICFEp.<sup><xref ref-type="bibr" rid="B83">83</xref></sup></p>
      </sec>
      <sec>
        <title>4.3. <italic>Strain</italic> do &#193;trio Esquerdo</title>
        <p>O <italic>strain</italic> atrial esquerdo (SAE) permite uma an&#225;lise mais detalhada da fun&#231;&#227;o do &#225;trio esquerdo (AE) e dos seus diversos componentes (reservat&#243;rio, conduto e de bomba).<sup><xref ref-type="bibr" rid="B70">70</xref></sup> Altera&#231;&#245;es no SAE expressam o acoplamento ventr&#237;culo-atrial e s&#227;o resultantes da exposi&#231;&#227;o cr&#244;nica &#224; eleva&#231;&#227;o das press&#245;es do VE, redu&#231;&#245;es da complac&#234;ncia e do relaxamento do AE,<sup><xref ref-type="bibr" rid="B41">41</xref>,<xref ref-type="bibr" rid="B84">84</xref>,<xref ref-type="bibr" rid="B85">85</xref></sup> podendo preceder o seu remodelamento morfol&#243;gico.<sup><xref ref-type="bibr" rid="B86">86</xref>-<xref ref-type="bibr" rid="B88">88</xref></sup> Embora tenha sido descrita redu&#231;&#227;o de todos componentes do SAE,<sup><xref ref-type="bibr" rid="B86">86</xref>,<xref ref-type="bibr" rid="B89">89</xref>,<xref ref-type="bibr" rid="B90">90</xref></sup> o SAE de reservat&#243;rio (SAEr) tem se mostrado o par&#226;metro mais robusto e se altera de forma linear com a progress&#227;o da DD.<sup><xref ref-type="bibr" rid="B91">91</xref>-<xref ref-type="bibr" rid="B93">93</xref></sup> Morris et al., entre outros, demonstraram que o SAEr reduzido (&lt; 23%) aumentou a detec&#231;&#227;o de DD, al&#233;m de se correlacionar com press&#245;es de enchimento e desfechos cl&#237;nicos.<sup><xref ref-type="bibr" rid="B93">93</xref>-<xref ref-type="bibr" rid="B99">99</xref></sup></p>
        <p>Diante do n&#250;mero crescente de evid&#234;ncias, o SLGVE e o SAEr poderiam ser integrados ao algoritmo de DD vigente, conforme proposto na <xref ref-type="fig" rid="f01">Figura Central</xref>. Essa estrat&#233;gia pode ajudar a reclassificar os casos indeterminados e aumentar a acur&#225;cia para identificar est&#225;gios mais precoces de DD, especialmente em indiv&#237;duos com fatores de risco cardiovascular ou dispneia inexplicada.<sup><xref ref-type="bibr" rid="B97">97</xref></sup></p>
        <p>Consensos com padroniza&#231;&#227;o da metodologia do <italic>strain</italic> foram publicados para minimizar a variabilidade entre os fabricantes, o que ainda &#233; uma limita&#231;&#227;o.<sup><xref ref-type="bibr" rid="B7">7</xref>,<xref ref-type="bibr" rid="B92">92</xref>,<xref ref-type="bibr" rid="B100">100</xref>,<xref ref-type="bibr" rid="B101">101</xref></sup> Esperam-se novos estudos prospectivos e multic&#234;ntricos para avaliar se a modifica&#231;&#227;o desses &#237;ndices, com o tratamento, muda o progn&#243;stico da DD e ICFEp.</p>
      </sec>
      <sec>
        <title>4.4. Conclus&#227;o</title>
        <p>O SLGVE e o SAEr s&#227;o marcadores de doen&#231;a subcl&#237;nica que podem ser incorporados &#224;s recomenda&#231;&#245;es vigentes para refinar o diagn&#243;stico, o estadiamento e progn&#243;stico da DD. Considerando-se a natureza complexa dessa avalia&#231;&#227;o, seria salutar a implementa&#231;&#227;o e valida&#231;&#227;o de algoritmos desenvolvidos por meio de intelig&#234;ncia artificial.</p>
      </sec>
    </sec>
    <sec>
      <title>5. <italic>Strain</italic> nas Cardiomiopatias</title>
      <sec>
        <title>5.1. Introdu&#231;&#227;o</title>
        <p>Seguindo um termo geral, as CMPs s&#227;o afec&#231;&#245;es do m&#250;sculo card&#237;aco. Em uma conota&#231;&#227;o mais pura e prim&#225;ria, elas n&#227;o guardam uma associa&#231;&#227;o com importantes causas sabidamente agressivas ao mioc&#225;rdio, como a doen&#231;a arterial coronariana (DAC), hipertens&#227;o arterial, valvopatias e cardiopatias cong&#234;nitas. Podem ser divididas nos principais grandes grupos: dilatada, hipertr&#243;fica, restritiva, CMP arritmog&#234;nica e &#8220;miscel&#226;neas n&#227;o classificadas&#8221;.<sup><xref ref-type="bibr" rid="B102">102</xref></sup></p>
      </sec>
      <sec>
        <title>5.2. Cardiomiopatia Dilatada</title>
        <p>Por defini&#231;&#227;o, a CMP dilatada se caracteriza como uma doen&#231;a que acomete o tecido mioc&#225;rdico e que leva &#224; progressiva redu&#231;&#227;o da fun&#231;&#227;o sist&#243;lica e dilata&#231;&#227;o da cavidade do VE. Clinicamente, os indiv&#237;duos podem apresentar sinais e sintomas de IC, com necessidade de tratamento, hospitaliza&#231;&#245;es, e por fim, transplante card&#237;aco.<sup><xref ref-type="bibr" rid="B102">102</xref>-<xref ref-type="bibr" rid="B107">107</xref></sup></p>
        <p>O ecocardiograma faz parte do arsenal diagn&#243;stico de primeira-linha, com um papel extremamente importante no diagn&#243;stico e progn&#243;stico. Seus principais objetivos s&#227;o a avalia&#231;&#227;o da dimens&#227;o volum&#233;trica das c&#226;maras card&#237;acas e a avalia&#231;&#227;o do desempenho sist&#243;lico do VE, classicamente realizada pela estimativa da FE, e que deve ser executada preferencialmente atrav&#233;s do m&#233;todo de Simpson.</p>
        <p>O <italic>strain</italic> &#233; uma ferramenta ecocardiogr&#225;fica adicional para agregar informa&#231;&#227;o a essa avalia&#231;&#227;o e tamb&#233;m possibilita detectar anormalidades sutis, subcl&#237;nicas e em est&#225;gios iniciais de doen&#231;as.</p>
        <p>Abduch et al<italic>.</italic> demonstraram excelente correla&#231;&#227;o entre par&#226;metros volum&#233;tricos obtidos pela ECO3D e o <italic>strain</italic> em pacientes com CMP dilatada.<sup><xref ref-type="bibr" rid="B108">108</xref></sup> Com a evolu&#231;&#227;o da CMP dilatada para fases mais acentuadas de comprometimento sist&#243;lico do VE, haver&#225; redu&#231;&#227;o mais importante do <italic>strain</italic> e do <italic>strain rate</italic> nas tr&#234;s principais orienta&#231;&#245;es (longitudinal, radial e circunferencial) (<xref ref-type="fig" rid="f11">Figura 5.1</xref>).<sup><xref ref-type="bibr" rid="B109">109</xref></sup> A tor&#231;&#227;o do VE tamb&#233;m acompanha essa tend&#234;ncia de diminui&#231;&#227;o com a progress&#227;o da doen&#231;a. Adicionalmente, em fases muito avan&#231;adas, tamb&#233;m pode haver invers&#227;o das rota&#231;&#245;es: segmentos basais com rota&#231;&#227;o anti-hor&#225;ria e os apicais em sentido hor&#225;rio.<sup><xref ref-type="bibr" rid="B110">110</xref>-<xref ref-type="bibr" rid="B112">112</xref></sup></p>
        <p>
          <fig id="f11">
            <label>Figura 5.1</label>
            <caption>
              <title>&#8211; A) exemplo de strain longitudinal global (SLG) normal do ventr&#237;culo esquerdo. Observam-se as deflex&#245;es negativas das curvas, que se apresentam relativamente homog&#234;neas nas tr&#234;s incid&#234;ncias. Abaixo e &#224; direita, a representa&#231;&#227;o param&#233;trica em bull&#8217;s eye, com todos os campos em vermelho mais intenso, significando uma boa deforma&#231;&#227;o global. B) exemplo de strain em um indiv&#237;duo portador de cardiomiopatia dilatada de etiologia chag&#225;sica. &#201; poss&#237;vel observar a redu&#231;&#227;o de amplitude das curvas, que aqui se apresentam tamb&#233;m muito heterog&#234;neas. As curvas de strain septal e na parede inferior t&#234;m deflex&#227;o positiva, ou seja, indicando distens&#227;o ou discinesia, o que est&#225; bem demonstrado mapa de bull&#180;s eye em azul (setas amarelas), al&#233;m do vermelho menos intenso, representando baixos valores de strain (SLG = -5,6%).</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf10.tif"/></fig>
        </p>
        <p>O SLG &#233; um preditor independente de mortalidade por todas as causas em pacientes com ICFEr, especialmente em pacientes do sexo masculino sem FA.<sup><xref ref-type="bibr" rid="B113">113</xref></sup> J&#225; nos pacientes com FEVE recuperada, um SLG anormal prev&#234; a probabilidade de diminui&#231;&#227;o da FEVE durante o acompanhamento, enquanto um SLG normal prev&#234; a probabilidade de FEVE est&#225;vel durante a recupera&#231;&#227;o.<sup><xref ref-type="bibr" rid="B114">114</xref></sup></p>
      </sec>
      <sec>
        <title>5.3. Cardiomiopatia Arritmog&#234;nica</title>
        <p>A CMP arritmog&#234;nica &#233; uma entidade histologicamente caracterizada por infiltra&#231;&#227;o fibrogordurosa no tecido mioc&#225;rdico. Essa infiltra&#231;&#227;o ocorre preferencialmente nas vias de entrada, sa&#237;da e &#225;pice do VD, o chamado &#8220;tri&#226;ngulo da displasia&#8221;, entretanto o VE tamb&#233;m pode ser acometido de forma concomitante ou at&#233; mesmo exclusiva.<sup><xref ref-type="bibr" rid="B115">115</xref>-<xref ref-type="bibr" rid="B117">117</xref></sup></p>
        <p>Macroscopicamente, a parede ventricular tende a se afilar, com forma&#231;&#227;o de microaneurismas, e a tend&#234;ncia &#233; progredir para comprometimento sist&#243;lico e dilata&#231;&#227;o da cavidade. O m&#233;todo diagn&#243;stico padr&#227;o-ouro &#233; a RMC, contudo o ecocardiograma &#233; o exame inicial, e o <italic>strain</italic> da parede livre do VD pode auxiliar na determina&#231;&#227;o do comprometimento sist&#243;lico dessa cavidade.</p>
        <p>Prakasa et al. foram os primeiros a analisar o <italic>strain</italic> na CMP arritmog&#234;nica com acometimento do VD, em 2007. Eles mostraram uma diferen&#231;a consistente entre os valores do <italic>strain</italic> nos indiv&#237;duos doentes (10 &#177; 6%) em compara&#231;&#227;o com os normais (28 &#177; 11%, P = 0,001).<sup><xref ref-type="bibr" rid="B118">118</xref></sup></p>
        <p>O <italic>strain</italic> longitudinal da parede livre do VD (SL-PLVD) est&#225; associado &#224; taxa de progress&#227;o estrutural em pacientes com CMP arritmog&#234;nica. Ele pode ser um marcador &#250;til para determinar quais pacientes requerem acompanhamento e tratamento mais pr&#243;ximos. Pacientes com <italic>strain</italic> de VD menor que 20% tiveram um risco maior de progress&#227;o estrutural (<italic>odds ratio</italic>: 18,4; IC95% 2,7&#8211;125,8; P = 0,003).<sup><xref ref-type="bibr" rid="B119">119</xref></sup></p>
        <p>Pacientes com CMP arritmog&#234;nica apresentam redu&#231;&#227;o do <italic>strain</italic> atrial direito (AD) em todas as fases da di&#225;stole, mesmo quando o volume do AD &#233; normal. O <italic>strain</italic> do AD, obtido nas fases reservat&#243;rio e bomba, est&#225; associado a um risco aumentado de eventos CV.<sup><xref ref-type="bibr" rid="B120">120</xref></sup></p>
      </sec>
      <sec>
        <title>5.4. Cardiomiopatia Hipertr&#243;fica</title>
        <p>A CMP hipertr&#243;fica (CMPH) &#233; uma doen&#231;a autoss&#244;mica dominante, sendo a doen&#231;a card&#237;aca de etiologia gen&#233;tica mais comum. Caracteriza-se pelo aumento da espessura mioc&#225;rdica ventricular de diferentes morfologias (podendo ser conc&#234;ntrica, apical, septal, hipertrofia da parede livre do VE e do VD) e est&#225; relacionada ao aumento da morbimortalidade dos pacientes acometidos.<sup><xref ref-type="bibr" rid="B121">121</xref>-<xref ref-type="bibr" rid="B123">123</xref></sup></p>
        <p>O ecocardiograma &#233; o m&#233;todo de imagem mais utilizado para o diagn&#243;stico morfol&#243;gico e hemodin&#226;mico na CMPH. Cerca de 25% desses pacientes apresentam gradiente em via de sa&#237;da do VE maior de 30 mmHg no repouso, que pode ser quantificado pelo Doppler cont&#237;nuo.<sup><xref ref-type="bibr" rid="B124">124</xref></sup> O gradiente din&#226;mico tamb&#233;m pode estar presente nesses pacientes e pode ser mais bem avaliado pela realiza&#231;&#227;o das manobras de Valsalva durante o ecocardiograma, pelo ecocardiograma com estresse f&#237;sico ou farmacol&#243;gico com dobutamina.<sup><xref ref-type="bibr" rid="B125">125</xref></sup> N&#237;veis elevados de gradiente intraventricular na CMPH podem ser um dos determinantes para a queda da deformidade mioc&#225;rdica e dos mecanismos de tor&#231;&#227;o, assim como do <italic>strain</italic> no AE.<sup><xref ref-type="bibr" rid="B126">126</xref></sup></p>
        <p>A t&#233;cnica do <italic>strain</italic> mioc&#225;rdico auxilia na an&#225;lise da mec&#226;nica card&#237;aca regional e global na CMPH, sendo medida atrav&#233;s do <italic>speckle tracking</italic>, e &#233; capaz de detectar precocemente altera&#231;&#245;es da fun&#231;&#227;o sist&#243;lica, fibrose e at&#233; maior risco de o paciente desenvolver arritmia, mesmo nos casos de pacientes com fun&#231;&#227;o sist&#243;lica normal.<sup><xref ref-type="bibr" rid="B126">126</xref>-<xref ref-type="bibr" rid="B130">130</xref></sup> O padr&#227;o do mapa polar auxilia na diferencia&#231;&#227;o das fenoc&#243;pias que cursam com aumento da espessura, visto que a deforma&#231;&#227;o mioc&#225;rdica longitudinal apresenta-se reduzida no local da hipertrofia<sup><xref ref-type="bibr" rid="B20">20</xref>,<xref ref-type="bibr" rid="B131">131</xref>,<xref ref-type="bibr" rid="B132">132</xref></sup> (<xref ref-type="fig" rid="f12">Figura 5.2</xref>).</p>
        <p>
          <fig id="f12">
            <label>Figura 5.2</label>
            <caption>
              <title>&#8211; A. Imagem bidimensional demonstrando hipertrofia septal assim&#233;trica n&#227;o obstrutiva, com septo interventricular medindo 23 mm e parede posterior de 11 mm. B. Strain longitudinal global normal do ventr&#237;culo esquerdo (20%), com representa&#231;&#227;o param&#233;trica em bull&#8217;s eye, demonstrando segmentos com boa deforma&#231;&#227;o mioc&#225;rdica em vermelho mais intenso e menores valores de deforma&#231;&#227;o nos segmentos septais, representados na cor rosa (8%). C. Incid&#234;ncia de 4 c&#226;maras, com pior deforma&#231;&#227;o mioc&#225;rdica nos segmentos m&#233;dio e basal &#237;nfero-septal. D. Observa-se a redu&#231;&#227;o de amplitude das curvas que representam os segmentos septais, tamb&#233;m demonstrado mapa de bull&#180;s eye em rosa, representando valores menores de strain (8%).</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf11.tif"/></fig>
        </p>
        <p>Hiemstra et al. identificaram que o volume atrial esquerdo indexado e o SLGVE s&#227;o fatores progn&#243;sticos independentes de desfechos adversos como morte s&#250;bita e transplante card&#237;aco em pacientes com CMPH.<sup><xref ref-type="bibr" rid="B133">133</xref></sup> Embora o SLG do VD (SLGVD) possa estar alterado no paciente com CMPH por ser uma doen&#231;a estrutural card&#237;aca, seu significado progn&#243;stico &#233; desconhecido.<sup><xref ref-type="bibr" rid="B133">133</xref>,<xref ref-type="bibr" rid="B134">134</xref></sup></p>
      </sec>
      <sec>
        <title>5.5. Endomiocardiofibrose</title>
        <p>A endomiocardiofibrose (EMF) &#233; a CMP restritiva mais comum em nosso meio, na &#193;frica equatorial e na &#205;ndia, afetando cerca de 10 milh&#245;es de pessoas no mundo. Ela &#233; caracterizada pela deposi&#231;&#227;o de tecido fibroso no endomioc&#225;rdio do &#225;pice e da via de entrada de um ou ambos os ventr&#237;culos. A etiologia permanece desconhecida at&#233; hoje, podendo estar relacionada a hipereosinofilia, infesta&#231;&#245;es parasit&#225;rias e desnutri&#231;&#227;o proteica, especialmente em popula&#231;&#245;es de padr&#227;o socioecon&#244;mico comprometido.</p>
        <p>O ecocardiograma mostra ventr&#237;culos de tamanho normal ou reduzidos, com morfologia ventricular em &#8220;cogumelo&#8221; ou em &#8220;V&#8221; pela deposi&#231;&#227;o da fibrose, podendo estar associado &#224; trombose endoc&#225;rdica apical, hipermotilidade da regi&#227;o basal ventricular (sinal de Merlon), &#225;trios de volume geralmente muito aumentados, fun&#231;&#227;o ventricular sist&#243;lica comumente preservada e DD.<sup><xref ref-type="bibr" rid="B135">135</xref>-<xref ref-type="bibr" rid="B137">137</xref></sup></p>
        <p>Poucos artigos avaliaram a EMF utilizando a ECO3D com <italic>speckle tracking.</italic> Esses estudos mostram redu&#231;&#227;o do SLG, especialmente com comprometimento mais importante da regi&#227;o apical.<sup><xref ref-type="bibr" rid="B137">137</xref>,<xref ref-type="bibr" rid="B138">138</xref></sup></p>
      </sec>
      <sec>
        <title>5.6. Mioc&#225;rdio N&#227;o Compactado</title>
        <p>O mioc&#225;rdio n&#227;o compactado (MNC) &#233; caracterizado pela presen&#231;a de trab&#233;culas proeminentes e espa&#231;os intertrabeculares profundos na cavidade do VE devido &#224; compacta&#231;&#227;o incompleta do mioc&#225;rdio na vida embrion&#225;ria. Isso pode levar a quadro cl&#237;nico de IC, arritmias e eventos tromboemb&#243;licos. Existem duas formas, a espor&#225;dica e a familiar, sendo que a &#250;ltima est&#225; relacionada a muta&#231;&#245;es de prote&#237;nas do sarc&#244;mero. Os &#237;ndices de deforma&#231;&#227;o mioc&#225;rdica permitem uma an&#225;lise regional adequada da fun&#231;&#227;o ventricular em pacientes com MNC e auxiliam na diferencia&#231;&#227;o de outras CMPs.</p>
        <p>Um estudo indiano comparou a deforma&#231;&#227;o mioc&#225;rdica de 12 pacientes com MNC, 18 pacientes com CMPH e 18 indiv&#237;duos saud&#225;veis. Ambos os grupos de pacientes apresentaram redu&#231;&#227;o do <italic>strain</italic> longitudinal, entretanto, os pacientes com MNC apresentaram maior redu&#231;&#227;o do <italic>strain</italic> longitudinal na regi&#227;o apical quando comparados com o grupo de CMPH (12,18 &#177; 6,25 vs. 18,37 &#177; 3,67; p &lt; 0,05), sugerindo um comprometimento maior dessa regi&#227;o na n&#227;o compacta&#231;&#227;o mioc&#225;rdica. Al&#233;m disso, um gradiente &#225;pico-basal no <italic>strain</italic> longitudinal foi observado nos pacientes com MNC, mas n&#227;o nos com CMPH.<sup><xref ref-type="bibr" rid="B139">139</xref></sup> Ambos os grupos apresentam DD quando comparados com o grupo-controle. Outro estudo mostrou que o <italic>strain</italic> longitudinal &#233; maior no grupo de MNC em rela&#231;&#227;o &#224; CMP dilatada idiop&#225;tica e que o gradiente base-&#225;pice do <italic>strain</italic> &#233; um &#237;ndice &#250;til para diferenciar essas doen&#231;as com sensibilidade de 88,4% e especificidade de 66,7%.<sup><xref ref-type="bibr" rid="B140">140</xref></sup></p>
        <p>No cora&#231;&#227;o normal, a base do VE gira no sentido hor&#225;rio durante a s&#237;stole, enquanto o &#225;pice gira no sentido anti-hor&#225;rio, sendo que a tor&#231;&#227;o &#233; a diferen&#231;a entre a rota&#231;&#227;o apical menos a basal. Um estudo pr&#233;vio mostra que 50% dos pacientes com MNC apresentam rota&#231;&#227;o em corpo r&#237;gido (RCR), com rota&#231;&#227;o hor&#225;ria do &#225;pice e da base; entretanto, estudos anteriores mostraram preval&#234;ncia de 53,3% e 83%.<sup><xref ref-type="bibr" rid="B141">141</xref>,<xref ref-type="bibr" rid="B142">142</xref></sup> Um estudo com 28 crian&#231;as com MNC mostrou que 39% dos pacientes apresentavam RCR, al&#233;m de apresentarem menor <italic>strain</italic> longitudinal, mas n&#227;o FEVE, em rela&#231;&#227;o ao grupo sem RCR, podendo ter valor progn&#243;stico.<sup><xref ref-type="bibr" rid="B143">143</xref></sup> Al&#233;m disso, os autores sugerem que o RCR est&#225; possivelmente relacionado principalmente &#224; disfun&#231;&#227;o da camada apical subepic&#225;rdica compactada, sem rela&#231;&#227;o com a distribui&#231;&#227;o de trab&#233;culas. Outro estudo em 101 crian&#231;as com MNC mostrou que o grupo que apresentou desfecho adverso tinha redu&#231;&#227;o do <italic>strain</italic> longitudinal, radial e circunferencial, sugerindo ser uma doen&#231;a que afeta globalmente o cora&#231;&#227;o e n&#227;o apenas a regi&#227;o n&#227;o compactada.<sup><xref ref-type="bibr" rid="B144">144</xref></sup></p>
      </sec>
    </sec>
    <sec>
      <title>6. <italic>Strain</italic> nas Valvopatias</title>
      <p>O ecodopplercardiograma transtor&#225;cico &#233; o m&#233;todo de primeira linha para o diagn&#243;stico e a classifica&#231;&#227;o da gravidade das valvopatias, por meio de uma an&#225;lise combinada das altera&#231;&#245;es da anatomia e da fun&#231;&#227;o valvar.<sup><xref ref-type="bibr" rid="B145">145</xref></sup> Esse m&#233;todo diagn&#243;stico participa ativamente na defini&#231;&#227;o do momento correto e do tipo de interven&#231;&#227;o que deve ser realizada para o tratamento das valvopatias.</p>
      <p>Classicamente, a indica&#231;&#227;o de tratamento &#233; baseada na presen&#231;a de sintomas ou de fatores complicadores.<sup><xref ref-type="bibr" rid="B145">145</xref></sup> Entre os fatores complicadores, a disfun&#231;&#227;o ventricular esquerda &#233; considerada o fator mais importante.<sup><xref ref-type="bibr" rid="B145">145</xref></sup></p>
      <p>A avalia&#231;&#227;o da fun&#231;&#227;o ventricular esquerda &#233; habitualmente realizada pela ecocardiografia, por meio da medida da FEVE.<sup><xref ref-type="bibr" rid="B146">146</xref></sup> Entretanto, v&#225;rias evid&#234;ncias cient&#237;ficas t&#234;m demonstrado que a medida do <italic>strain</italic> ventricular esquerdo pode identificar a presen&#231;a de disfun&#231;&#227;o ventricular antes da queda da FE.</p>
      <p>A insufici&#234;ncia mitral (IM), talvez seja a valvopatia que melhor representa esse paradoxo, uma vez que, nessa doen&#231;a, o estado de alta pr&#233;-carga e baixa p&#243;s-carga faz com que a FE n&#227;o represente adequadamente a fun&#231;&#227;o sist&#243;lica do VE. Por essa raz&#227;o, as diretrizes cl&#237;nicas s&#227;o bastante conservadoras na defini&#231;&#227;o de disfun&#231;&#227;o ventricular esquerda nessa condi&#231;&#227;o.<sup><xref ref-type="bibr" rid="B145">145</xref>,<xref ref-type="bibr" rid="B147">147</xref>-<xref ref-type="bibr" rid="B149">149</xref></sup> Entretanto, alguns estudos indicam que, mesmo utilizando esses par&#226;metros, o desfecho cl&#237;nico ap&#243;s corre&#231;&#227;o cir&#250;rgica da IM pode n&#227;o ser satisfat&#243;rio, especialmente no que se refere &#224; queda da FE e &#224; presen&#231;a de IC.<sup><xref ref-type="bibr" rid="B150">150</xref>-<xref ref-type="bibr" rid="B151">151</xref></sup> Dessa forma, estudos t&#234;m demonstrado que mesmo em pacientes com FE acima de 60% e com di&#226;metro sist&#243;lico final do VE menor que 40 mm, a presen&#231;a de SLG reduzido (&#8804; 19%) se associou &#224; queda da FE abaixo de 50% no p&#243;s-operat&#243;rio.<sup><xref ref-type="bibr" rid="B152">152</xref>-<xref ref-type="bibr" rid="B154">154</xref></sup> Um SLG reduzido, abaixo de 18,1%, tamb&#233;m se associou &#224; maior mortalidade e a mais eventos CV em pacientes com IM seguidos prospectivamente e submetidos &#224; cirurgia corretiva.<sup><xref ref-type="bibr" rid="B155">155</xref></sup></p>
      <p>Na insufici&#234;ncia a&#243;rtica (IAo), demonstrou-se que a gravidade da valvopatia se correlaciona com a queda do <italic>strain</italic> ventricular esquerdo.<sup><xref ref-type="bibr" rid="B156">156</xref></sup> Al&#233;m disso, em pacientes com IAo importante e cr&#244;nica, assintom&#225;ticos e com FE preservada, um SLG abaixo de 19% se associou &#224; maior mortalidade ao longo do tempo, que era corrigida com a realiza&#231;&#227;o de troca valvar.<sup><xref ref-type="bibr" rid="B157">157</xref></sup> O mesmo grupo mostrou que uma medida menor que 19% do SLG ap&#243;s a cirurgia, bem como uma queda de mais de 5 pontos percentuais no SLG, implicava em maior mortalidade.<sup><xref ref-type="bibr" rid="B158">158</xref></sup></p>
      <p>Na estenose a&#243;rtica (EA) importante, a presen&#231;a de FE menor que 50% e/ou de sintomas t&#234;m sido os pilares para indica&#231;&#227;o de tratamento.<sup><xref ref-type="bibr" rid="B145">145</xref>,<xref ref-type="bibr" rid="B147">147</xref>-<xref ref-type="bibr" rid="B149">149</xref></sup> Entretanto, uma estrat&#233;gia baseada em aguardar que a FEVE caia para &lt; 50% para indicar a interven&#231;&#227;o cir&#250;rgica a&#243;rtica pode levar a desfechos cl&#237;nicos insatisfat&#243;rios.<sup><xref ref-type="bibr" rid="B159">159</xref></sup> Assim, o emprego de um par&#226;metro robusto de detec&#231;&#227;o de disfun&#231;&#227;o mioc&#225;rdica subcl&#237;nica, como o SLG, parece ser uma ferramenta de grande valor na estratifica&#231;&#227;o do risco (<xref ref-type="fig" rid="f13">Figura 6.1</xref>). Enquanto a FEVE n&#227;o difere entre os graus de EA, o SLG diminui linearmente conforme a doen&#231;a progride,<sup><xref ref-type="bibr" rid="B160">160</xref></sup> acarretando maior risco de desfechos cl&#237;nicos adversos, mesmo em assintom&#225;ticos.<sup><xref ref-type="bibr" rid="B161">161</xref></sup></p>
      <p>
        <fig id="f13">
          <label>Figura 6.1</label>
          <caption>
            <title>&#8211; Dois pacientes com estenose a&#243;rtica grave cl&#225;ssica, de alto fluxo, com fra&#231;&#227;o de eje&#231;&#227;o (FE) do ventr&#237;culo esquerdo normal, mas valores bastante distintos de strain longitudinal global (SLG). (A) Gradiente transvalvar a&#243;rtico m&#233;dio = 61 mmHg, com FE e SLG normais. (B) Gradiente transvalvar a&#243;rtico m&#233;dio = 88 mmHg, com FE normal e SLG diminu&#237;do.</title>
          </caption>
          <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf12.tif"/></fig>
      </p>
      <p>Diversos estudos examinaram o valor progn&#243;stico do SLG para predizer a mortalidade e eventos CV em indiv&#237;duos assintom&#225;ticos com EA e FEVE preservada, visando selecionar quais devem ser encaminhados precocemente para a interven&#231;&#227;o valvar.<sup><xref ref-type="bibr" rid="B162">162</xref>-<xref ref-type="bibr" rid="B164">164</xref></sup> Os resultados desses estudos foram condensados em uma metan&#225;lise que definiu SLG &lt; 14,7% como o valor de corte associado com maior risco de morte (sensibilidade de 60% e especificidade de 70%; &#225;rea sob a curva [ASC] = 0,68).<sup><xref ref-type="bibr" rid="B165">165</xref></sup> Foi encontrado SLG &lt; 14,7% em aproximadamente um ter&#231;o da popula&#231;&#227;o de indiv&#237;duos com EA moderada a grave e FEVE preservada, acarretando risco de morte 2,6 vezes maior. &#201; importante ressaltar que a rela&#231;&#227;o entre SLG e mortalidade foi significativa, tanto naqueles com FEVE entre 50-59% quanto naqueles com FEVE &#8805; 60%. Em contraste, o achado de SLG &gt; 18% se associou com excelente evolu&#231;&#227;o cl&#237;nica (97&#177;1% de sobrevida em 2 anos). Portanto, o SLG diminu&#237;do, a despeito da FEVE preservada, configura-se como um poderoso preditor progn&#243;stico a ser considerado na tomada de decis&#227;o cl&#237;nica para indicar interven&#231;&#227;o na EA grave assintom&#225;tica, em conjunto com outros dados cl&#237;nicos e ecocardiogr&#225;ficos.</p>
    </sec>
    <sec>
      <title>7. <italic>Strain</italic> nas Cardiopatias Isqu&#234;micas</title>
      <sec>
        <title>7.1. Introdu&#231;&#227;o</title>
        <p>A ecocardiografia &#233; uma excelente ferramenta a ser utilizada nas unidades de emerg&#234;ncia para o diagn&#243;stico de s&#237;ndrome coronariana aguda e suas complica&#231;&#245;es. Ela oferece informa&#231;&#245;es sobre o progn&#243;stico desses pacientes a curto e a longo prazo, e o seu papel est&#225; bem definido na estratifica&#231;&#227;o de risco da DAC est&#225;vel e na avalia&#231;&#227;o de viabilidade mioc&#225;rdica.</p>
        <p>Entre as t&#233;cnicas existentes, a ecocardiografia bidimensional com <italic>strain</italic> pelo <italic>speckle tracking</italic> (2DST) ratifica e acrescenta informa&#231;&#245;es, sem estender em demasiado o tempo de exame. Ela avalia com boa acur&#225;cia a isquemia subendoc&#225;rdica atrav&#233;s do <italic>strain</italic> longitudinal em eventos agudos e cr&#244;nicos.</p>
        <p>Ao longo do texto, ser&#227;o revisadas as indica&#231;&#245;es sobre o uso do <italic>strain</italic> longitudinal, circunferencial e radial nas cardiopatias isqu&#234;micas, assim como outros dados fornecidos ao se calcular o <italic>strain</italic>, como a dispers&#227;o mec&#226;nica. Na <xref ref-type="table" rid="t6">Tabela 7.1</xref> est&#227;o as principais indica&#231;&#245;es do <italic>strain</italic> na cardiopatia isqu&#234;mica</p>
        <p>
          <table-wrap id="t6">
            <label>Tabela 7.1</label>
            <caption>
              <title>&#8211; Principais aplica&#231;&#245;es do <italic>strain</italic> na cardiopatia isqu&#234;mica</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="100%">
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left">Indica&#231;&#245;es do <italic>strain</italic> na cardiopatia isqu&#234;mica</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>Avalia&#231;&#227;o da altera&#231;&#227;o segmentar e global</td>
                </tr>
                <tr>
                  <td>Diferencia&#231;&#227;o de infartos subendoc&#225;rdicos dos transmurais (acometimento longitudinal, radial e circunferencial)</td>
                </tr>
                <tr>
                  <td>Discriminar a art&#233;ria culpada de acordo com o acometimento pelo <italic>bull&#8217;s eye</italic></td>
                </tr>
                <tr>
                  <td>Avalia&#231;&#227;o da melhora do <italic>strain</italic> global e segmentar ap&#243;s a revasculariza&#231;&#227;o mioc&#225;rdica</td>
                </tr>
                <tr>
                  <td>Melhora a detec&#231;&#227;o de doen&#231;a arterial coronariana</td>
                </tr>
                <tr>
                  <td>Preditor desfechos e de remodelamento ap&#243;s infarto agudo do mioc&#225;rdio</td>
                </tr>
                <tr>
                  <td>Preditor de desfechos como hospitaliza&#231;&#245;es por insufici&#234;ncia card&#237;aca e mortalidade por todas as causas</td>
                </tr>
                <tr>
                  <td>Identifica pacientes com risco de arritmias</td>
                </tr>
              </tbody>
            </table>
          </table-wrap>
        </p>
      </sec>
      <sec>
        <title>7.2. <italic>Strain</italic> na S&#237;ndrome Coronariana Aguda</title>
        <p>O <italic>strain</italic> bidimensional &#233; um marcador com boa sensibilidade para detectar isquemia mioc&#225;rdica, considerado mais reprodut&#237;vel que a FEVE e com acur&#225;cia confirmada pela RMC.<sup><xref ref-type="bibr" rid="B52">52</xref>,<xref ref-type="bibr" rid="B166">166</xref></sup> A fibra subendoc&#225;rdica &#233; mais sens&#237;vel &#224; isquemia no seu est&#225;gio inicial, e o componente longitudinal predomina nesse tipo de isquemia.<sup><xref ref-type="bibr" rid="B167">167</xref></sup> O SLG apresenta-se reduzido no infarto agudo do mioc&#225;rdio (IAM) e correlaciona-se com a extens&#227;o do infarto, FE, eventos adversos e resposta &#224;s estrat&#233;gias de reperfus&#227;o.<sup><xref ref-type="bibr" rid="B168">168</xref>-<xref ref-type="bibr" rid="B172">172</xref></sup></p>
        <p>Pacientes com infartos de pequena extens&#227;o, apresentam o SLG e radial reduzidos, enquanto o circunferencial e o <italic>twist</italic> se mant&#234;m preservados. No entanto, o <italic>strain</italic> circunferencial estar&#225; comprometido tamb&#233;m no infarto transmural.<sup><xref ref-type="bibr" rid="B173">173</xref></sup></p>
        <p>A identifica&#231;&#227;o da extens&#227;o do infarto transmural apresenta uma implica&#231;&#227;o progn&#243;stica importante, pois est&#225; associada a progn&#243;stico reservado e a um maior n&#250;mero de eventos adversos. Os infartos subendoc&#225;rdicos e n&#227;o transmurais s&#227;o associados com recupera&#231;&#227;o ap&#243;s revasculariza&#231;&#227;o (<xref ref-type="fig" rid="f14">Figura 7.1</xref>).<sup><xref ref-type="bibr" rid="B174">174</xref></sup></p>
        <p>
          <fig id="f14">
            <label>Figura 7.1</label>
            <caption>
              <title>&#8211; Strain 2D visualizado atrav&#233;s do bull&#8217;s eye demonstra altera&#231;&#227;o de deformidade na regi&#227;o apical do ventr&#237;culo esquerdo, com valores dos segmentos envolvidos reduzidos, compat&#237;vel com les&#227;o de art&#233;ria descendente anterior.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf13.tif"/></fig>
        </p>
        <p>Um valor do <italic>strain</italic> longitudinal de 15% correlaciona-se com altera&#231;&#245;es segmentares (sensibilidade de 76% e especificidade de 95%).<sup><xref ref-type="bibr" rid="B168">168</xref></sup>O <italic>strain</italic> radial com o ponto de corte de 16,5% diferencia infartos transmurais dos n&#227;o transmurais (sensibilidade de 70% e especificidade de 71,2%). O valor do <italic>strain</italic> circunferencial &lt; 11% diferencia infarto transmural de n&#227;o transmural (sensibilidade de 70% e especificidade de 71,2%).<sup><xref ref-type="bibr" rid="B175">175</xref></sup>Al&#233;m disso, o <italic>strain</italic> longitudinal regional de 4,5% distingue infarto transmural de n&#227;o transmural (sensibilidade de 81,2% e especificidade de 81,6%).<sup><xref ref-type="bibr" rid="B176">176</xref>,<xref ref-type="bibr" rid="B177">177</xref></sup></p>
        <p>Um outro dado importante em rela&#231;&#227;o ao SLG &#233; o seu valor diagn&#243;stico na doen&#231;a coronariana aguda (DCA) sem supra de ST para discriminar a art&#233;ria culpada. Uma coorte com 58 pacientes, dos quais 33 tinham DAC significativa (les&#227;o acima de 50%) definida pela cineangiocoronariografia e submetidos &#224; an&#225;lise do <italic>strain</italic> antes do procedimento, demonstrou um ponto de corte de 19,7% (sensibilidade de 81% e especificidade de 88%, com ASC = 0,92) para detec&#231;&#227;o de DAC. O emprego de um ponto de corte de 21% foi capaz de excluir estenose coronariana significativa em 100% dos pacientes. O <italic>strain</italic> longitudinal territorial foi calculado como a m&#233;dia dos <italic>strain</italic> de pico sist&#243;lico dos segmentos que pertencem ao territ&#243;rio daquele vaso estudado. Nesse trabalho, se o ponto de corte de 21% fosse aplicado, 16 pacientes seriam poupados da cineangiocoronariografia.<sup><xref ref-type="bibr" rid="B178">178</xref>,<xref ref-type="bibr" rid="B179">179</xref></sup></p>
        <p>O <italic>strain</italic> pode ser uma ferramenta para auxiliar na detec&#231;&#227;o de oclus&#227;o coronariana aguda em pacientes sem supra de ST, que podem se beneficiar de terapia de reperfus&#227;o precoce. Um estudo avaliou 150 pacientes, que realizaram o exame ecocardiogr&#225;fico antes de serem encaminhados &#224; cineangiocoronariografia. Desse total, 33 apresentaram oclus&#227;o coronariana aguda. Observou-se que um <italic>strain</italic> menor que 14% identificou a oclus&#227;o coronariana aguda (sensibilidade de 85% e especificidade de 70%), mas estudos mais robustos necessitam ser realizados para valida&#231;&#227;o da t&#233;cnica.<sup><xref ref-type="bibr" rid="B180">180</xref></sup></p>
        <p>O <italic>strain</italic> emergiu como uma nova t&#233;cnica para detectar altera&#231;&#245;es subcl&#237;nicas segmentares e globais, com <italic>performance</italic> acima de testes enzim&#225;ticos, ECG e escores de risco, al&#233;m do seu papel na avalia&#231;&#227;o progn&#243;stica desses pacientes com DCA. Trata-se de um exame r&#225;pido dispon&#237;vel &#224; beira do leito e que pode ser realizado antes da cineangiocoronariografia, especialmente por ecocardiografistas treinados. Essa t&#233;cnica est&#225; indicada, conforme os estudos citados, na DCA sem supra de ST para a avalia&#231;&#227;o das altera&#231;&#245;es segmentares e da fun&#231;&#227;o ventricular global, para diferenciar infartos pequenos dos infartos transmurais, discriminar a prov&#225;vel art&#233;ria culpada e para a avalia&#231;&#227;o p&#243;s-revasculariza&#231;&#227;o percut&#226;nea. Tamb&#233;m &#233; poss&#237;vel utiliz&#225;-la para a avalia&#231;&#227;o da viabilidade mioc&#225;rdica ap&#243;s epis&#243;dios de IAM.<sup><xref ref-type="bibr" rid="B181">181</xref>,<xref ref-type="bibr" rid="B182">182</xref></sup></p>
      </sec>
      <sec>
        <title>7.3. <italic>Strain</italic> na S&#237;ndrome Coronariana Cr&#244;nica</title>
        <p>A &#225;rea mais suscet&#237;vel a isquemia est&#225; localizada na regi&#227;o subendoc&#225;rdica e, nessa localidade, as fibras est&#227;o orientadas no sentido longitudinal, portanto a avalia&#231;&#227;o da deforma&#231;&#227;o longitudinal utilizando o 2DST seria um excelente marcador para a presen&#231;a isquemia em compara&#231;&#227;o &#224; avalia&#231;&#227;o somente pela ecocardiografia convencional.<sup><xref ref-type="bibr" rid="B183">183</xref></sup></p>
        <p>A intera&#231;&#227;o do mioc&#225;rdio normal e anormal gera padr&#245;es regionais t&#237;picos de deforma&#231;&#227;o mioc&#225;rdica, indicando que a contra&#231;&#227;o mioc&#225;rdica e a deforma&#231;&#227;o mioc&#225;rdica n&#227;o s&#227;o par&#226;metros intercambi&#225;veis.<sup><xref ref-type="bibr" rid="B16">16</xref>,<xref ref-type="bibr" rid="B184">184</xref></sup></p>
        <p>O SLG pode ser muito mais sens&#237;vel do que a FEVE na capacidade de detectar altera&#231;&#245;es precoces na isquemia mioc&#225;rdica, pois avalia a fun&#231;&#227;o longitudinal do VE, por&#233;m ele n&#227;o tem especificidade superior quando comparado &#224;s altera&#231;&#245;es da mobilidade de parede.<sup><xref ref-type="bibr" rid="B185">185</xref>,<xref ref-type="bibr" rid="B186">186</xref></sup></p>
        <p>A variabilidade das medidas regionais do <italic>strain</italic> pelo <italic>speckle tracking</italic> &#233; relativamente alta, o que torna essas avalia&#231;&#245;es menos adequadas para o uso de rotina. No entanto, as medidas do SLG mostraram-se reprodut&#237;veis e robustas, provavelmente devido &#224; avalia&#231;&#227;o amplamente automatizada desse m&#233;todo.<sup><xref ref-type="bibr" rid="B187">187</xref></sup> A outra altera&#231;&#227;o &#233; a heterogeneidade regional de ativa&#231;&#227;o mioc&#225;rdica, que altera a sequ&#234;ncia temporal de encurtamento e alongamento do mioc&#225;rdio.</p>
        <p>Na isquemia, n&#227;o somente a amplitude do encurtamento &#233; reduzida, como tamb&#233;m o in&#237;cio e a dura&#231;&#227;o da contra&#231;&#227;o das fibras s&#227;o alterados, o que gera um encurtamento ou espessamento caracter&#237;stico do mioc&#225;rdio ap&#243;s o fechamento da v&#225;lvula a&#243;rtica.<sup><xref ref-type="bibr" rid="B187">187</xref></sup> Essa altera&#231;&#227;o, chamada de encurtamento p&#243;s-sist&#243;lico (EPS), &#233; caracter&#237;stica do desenvolvimento de isquemia, apesar de poder ocorrer tamb&#233;m na disfun&#231;&#227;o regional de qualquer causa (cicatriz, dissincronia etc.).<sup><xref ref-type="bibr" rid="B187">187</xref>,<xref ref-type="bibr" rid="B188">188</xref></sup> Esse EPS pode ser entendido como um sinal de atraso do relaxamento para que a regi&#227;o isqu&#234;mica possa encurtar, enquanto a press&#227;o do VE reduz e o tecido circundante relaxa.<sup><xref ref-type="bibr" rid="B16">16</xref></sup> Um menor EPS com fun&#231;&#227;o sist&#243;lica normal &#233; um achado frequente em 30% a 40% dos segmentos mioc&#225;rdicos de cora&#231;&#245;es saud&#225;veis e pode ser encontrado principalmente no &#225;pice e na base das paredes inferior, septal e antero-septal.<sup><xref ref-type="bibr" rid="B16">16</xref>,<xref ref-type="bibr" rid="B189">189</xref></sup> Um dado importante no contexto da CMP isqu&#234;mica &#233; a avalia&#231;&#227;o temporal do padr&#227;o das curvas do SLG, pois, muitas vezes, os segmentos isqu&#234;micos podem ter valores do pico sist&#243;lico preservados, por&#233;m apresentam atraso temporal em rela&#231;&#227;o aos outros segmentos n&#227;o isqu&#234;micos.</p>
        <p>&#201; importante ressaltar que as medidas do <italic>strain</italic> longitudinal regional n&#227;o necessariamente refletem a impress&#227;o visual das altera&#231;&#245;es da contra&#231;&#227;o, que &#233; determinada pelo espessamento radial e pelo movimento endoc&#225;rdico para o interior da cavidade.<sup><xref ref-type="bibr" rid="B16">16</xref></sup></p>
        <p>O SLG contribui para a detec&#231;&#227;o de DAC em pacientes com angina est&#225;vel (estenose maior ou igual a 70%), com valores reduzidos na presen&#231;a de DAC (17,1 &#177; 2,5% vs. 18,8 &#177; 2.6%; p &lt; 0,001), especialmente quando associado ao teste ergom&#233;trico, e, al&#233;m disso, identifica a prov&#225;vel art&#233;ria culpada.<sup><xref ref-type="bibr" rid="B183">183</xref></sup> O emprego do <italic>strain</italic> longitudinal e, especialmente, do <italic>strain rate</italic> melhorou a sensibilidade e a acur&#225;cia na detec&#231;&#227;o das altera&#231;&#245;es segmentares no per&#237;odo tardio do p&#243;s-infarto do mioc&#225;rdio.<sup><xref ref-type="bibr" rid="B189">189</xref></sup></p>
        <p>Na estratifica&#231;&#227;o dos pacientes p&#243;s-IAM, um valor SLG menor que 15% antes da alta hospitalar foi um preditor independente de dilata&#231;&#227;o do VE em um seguimento de 3 a 6 meses, al&#233;m de servir como um marcador do tamanho da &#225;rea do infarto.<sup><xref ref-type="bibr" rid="B190">190</xref></sup>Nesse mesmo contexto de p&#243;s-IAM, um valor do SLG menor do que 14% foi um preditor independente de morte cardiovascular e interna&#231;&#245;es por IC.<sup><xref ref-type="bibr" rid="B191">191</xref></sup> Nos pacientes com doen&#231;a cr&#244;nica est&#225;vel, um valor do SLG menor que 11,5% tamb&#233;m demonstrou ser um preditor de morte por todas as causas e de desfechos combinados (morte por todas as causas e interna&#231;&#227;o por IC).<sup><xref ref-type="bibr" rid="B192">192</xref></sup></p>
        <p>A heterogeneidade regional da contra&#231;&#227;o mioc&#225;rdica tamb&#233;m pode ser avaliada pela dispers&#227;o mec&#226;nica, que &#233; definida como o desvio padr&#227;o de tempo para atingir o pico tens&#227;o negativa entre todos os segmentos do VE. Esse &#237;ndice tem um valor preditivo para taquiarritmia ventricular em pacientes p&#243;s-infarto. Foi demostrado que valores maiores de dispers&#227;o foram encontrados em pacientes que apresentaram arritmias no p&#243;s-IAM (85 +/- 29 ms vs. 56 +/-13 ms, p &lt; 0,001).<sup><xref ref-type="bibr" rid="B193">193</xref></sup></p>
      </sec>
      <sec>
        <title>7.4. <italic>Strain</italic> do Ventr&#237;culo Direito na Cardiopatia Isqu&#234;mica</title>
        <p>A fun&#231;&#227;o do VD &#233; comprometida em aproximadamente um ter&#231;o dos infartos de parede inferior e seu envolvimento tem sido descrito como um preditor importante de mortalidade hospitalar e de complica&#231;&#245;es maiores. A avalia&#231;&#227;o da fun&#231;&#227;o do VD &#233; desafiadora devido &#224; sua complexidade estrutural. O valor do <italic>strain</italic> da parede livre do VD demostrou ser um preditor de oclus&#227;o proximal da art&#233;ria coron&#225;ria direita em pacientes com IAM de parede inferior (<italic>strain</italic> da parede livre do VD &lt; 14,5%, ASC = 0,81; p &lt; 0,001).<sup><xref ref-type="bibr" rid="B194">194</xref></sup></p>
        <p>Na doen&#231;a isqu&#234;mica cr&#244;nica est&#225;vel, o <italic>strain</italic> da parede livre do VD apresenta-se alterado em pacientes com estenose da coron&#225;ria direita (les&#227;o maior que 50%) e pode ser usado para detectar disfun&#231;&#227;o subcl&#237;nica nesse contexto.<sup><xref ref-type="bibr" rid="B195">195</xref></sup></p>
      </sec>
    </sec>
    <sec>
      <title>8. <italic>Strain</italic> nas Doen&#231;as Sist&#234;micas (Amiloidose e Doen&#231;a de Fabry)</title>
      <sec>
        <title>8.1. <italic>Strain</italic> na Amiloidose Card&#237;aca</title>
        <p>A amiloidose &#233; uma doen&#231;a sist&#234;mica causada pela deposi&#231;&#227;o extracelular de fibrilas amiloides insol&#250;veis nos tecidos. O acometimento card&#237;aco &#233; um importante fator progn&#243;stico e causa grande impacto na qualidade de vida dos pacientes, ocorrendo mais comumente nas formas causadas por cadeias leves (AL) e na amiloidose por transtirretina (ATTR).<sup><xref ref-type="bibr" rid="B196">196</xref></sup></p>
        <p>A ecocardiografia &#233; um m&#233;todo de primeira linha para o diagn&#243;stico e a avalia&#231;&#227;o progn&#243;stica da amiloidose card&#237;aca (AC) e de outras doen&#231;as card&#237;acas infiltrativas. A maioria dos achados cl&#225;ssicos e sinais mais espec&#237;ficos da AC ao ecocardiograma ocorre somente em est&#225;gios muito avan&#231;ados da doen&#231;a.<sup><xref ref-type="bibr" rid="B30">30</xref></sup> Situa&#231;&#245;es cl&#237;nicas como a IC com FE preservada e a presen&#231;a de hipertrofia ventricular podem servir como sinais de alerta para a suspei&#231;&#227;o diagn&#243;stica de AC.<sup><xref ref-type="bibr" rid="B197">197</xref></sup></p>
        <sec>
          <title>8.1.1. Papel da An&#225;lise da Deforma&#231;&#227;o Mioc&#225;rdica no Diagn&#243;stico da Amiloidose Card&#237;aca</title>
          <p>O SLGVE encontra-se consistentemente alterado em pacientes com AC e est&#225; diretamente relacionado ao grau de infiltra&#231;&#227;o amiloide, quantificado na resson&#226;ncia magn&#233;tica (RM) pelo grau de realce tardio por gadol&#237;neo (LGE) e pelo volume extracelular (VEC) calculado em imagens de sequ&#234;ncia T1.<sup><xref ref-type="bibr" rid="B30">30</xref></sup> Um padr&#227;o de altera&#231;&#227;o regional dos valores de <italic>strain</italic> longitudinal (SL), com preserva&#231;&#227;o relativa dos valores de deforma&#231;&#227;o longitudinal dos segmentos apicais (RELAPS) foi descrita na literatura, definindo um gradiente basal-apical caracter&#237;stico, conhecido como <italic>apical sparing</italic> ou <italic>cherry on top</italic> (<xref ref-type="fig" rid="f15">Figura 8.1</xref>).</p>
          <p>
            <fig id="f15">
              <label>Figura 8.1</label>
              <caption>
                <title>&#8211; Strain 2D longitudinal do ventr&#237;culo esquerdo em paciente com amiloidose card&#237;aca ATTR, demonstrando padr&#227;o de preserva&#231;&#227;o relativa apical ou apical sparing, com maior acometimento da deforma&#231;&#227;o segmentar em segmentos m&#233;dios e basais, com maior deforma&#231;&#227;o nos segmentos apicais.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf14.tif"/></fig>
          </p>
          <p>Na publica&#231;&#227;o original de Phelan et al., o RELAPS foi calculado a partir da seguinte equa&#231;&#227;o: m&#233;dia do SL apical/(m&#233;dia do SL dos segmentos m&#233;dios + m&#233;dia do SL dos segmentos basais), com valores &gt; 1,0 apresentando boa acur&#225;cia para o diagn&#243;stico de AC, com boa diferencia&#231;&#227;o de hipertrofias ventriculares causadas por EA e pela CMPH (ASC: 0,94).<sup><xref ref-type="bibr" rid="B20">20</xref></sup></p>
          <p>Esse padr&#227;o regional do SL, com gradiente basal-apical, &#233; encontrado indistintamente nos tipos de amiloidose AL e ATTR. &#201; importante enfatizar que o padr&#227;o cl&#225;ssico de <italic>apical sparing</italic>, embora descrito como caracter&#237;stico para AC, pode estar ausente, conforme exemplificado no estudo de Ternacle et al., em que 52% dos pacientes com diagn&#243;stico de AC tinham RELAPS &#8220;n&#227;o diagn&#243;stico&#8221; (&lt; 1,0).<sup><xref ref-type="bibr" rid="B198">198</xref></sup> Isso pode ser explicado, em alguns casos, pelo baixo grau de infiltra&#231;&#227;o amiloide do mioc&#225;rdio, em est&#225;gios bastante precoces da doen&#231;a. Valores de SL regional septal apical/septal basal &gt; 2,1 (SAB), quanto associados a tempo de desacelera&#231;&#227;o do influxo mitral &lt; 200 ms, tamb&#233;m demonstraram boa acur&#225;cia para a diferencia&#231;&#227;o de AC de outras doen&#231;as com fen&#243;tipo de hipertrofia parietal do VE, como doen&#231;a de Fabry, ataxia de Friedreich, e hipertrofia do VE relacionada &#224; hipertens&#227;o arterial sist&#234;mica (HAS).<sup><xref ref-type="bibr" rid="B199">199</xref></sup></p>
          <p>A rela&#231;&#227;o da FE do VE/SLG &gt; 4,1 tamb&#233;m foi demonstrada como um bom par&#226;metro para diferenciar AC de CMPH, com <italic>performance</italic> superior ao RELAPS ou SAB, independentemente do tipo de AC.<sup><xref ref-type="bibr" rid="B200">200</xref></sup></p>
          <p>A deforma&#231;&#227;o mioc&#225;rdica do VD est&#225; geralmente reduzida em pacientes com AC, e seu achado pode ajudar a diferenciar de outras causas de hipertrofias parietais (<xref ref-type="fig" rid="f16">Figura 8.2</xref>), tendo sido descrito tamb&#233;m um padr&#227;o de preserva&#231;&#227;o relativa apical, similar ao que &#233; descrito no VE.<sup><xref ref-type="bibr" rid="B201">201</xref></sup> Bellavia et al. demonstraram que altera&#231;&#245;es do VD podem ocorrer precocemente em pacientes com AC do tipo AL, mesmo em casos em que as espessuras parietais do VE ainda s&#227;o normais.<sup><xref ref-type="bibr" rid="B202">202</xref></sup></p>
          <p>
            <fig id="f16">
              <label>Figura 8.2</label>
              <caption>
                <title>&#8211; Strain 2D longitudinal do ventr&#237;culo direito em paciente com amiloidose card&#237;aca ATTR, demonstrando redu&#231;&#227;o do valor absoluto global (SLGVD = 9,9%) e redu&#231;&#227;o absoluta do strain m&#233;dio de parede livre (11,4%), com maior acometimento da deforma&#231;&#227;o segmentar em segmentos m&#233;dios e basais, com maior deforma&#231;&#227;o nos segmentos apicais.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf15.tif"/></fig>
          </p>
          <p>Na AC, assim como observado em outras CMPs infiltrativas, pode haver acometimento significativo de outros componentes da deforma&#231;&#227;o mioc&#225;rdica, como o <italic>strain</italic> circunferencial,<sup><xref ref-type="bibr" rid="B203">203</xref></sup> <italic>strain</italic> radial,<sup><xref ref-type="bibr" rid="B204">204</xref></sup> <italic>twist</italic> e tor&#231;&#227;o (<xref ref-type="fig" rid="f17">Figura 8.3</xref>). Em pacientes com amiloidose sist&#234;mica em est&#225;gios iniciais de doen&#231;a, sem evid&#234;ncia de AC, o <italic>twist</italic> e <italic>untwist</italic> podem estar aumentados de forma compensat&#243;ria,<sup><xref ref-type="bibr" rid="B205">205</xref></sup> sendo a deteriora&#231;&#227;o desses par&#226;metros progressiva com o evoluir da doen&#231;a,<sup><xref ref-type="bibr" rid="B206">206</xref></sup> podendo levar, em casos avan&#231;ados, &#224; rota&#231;&#227;o da base e &#225;pice card&#237;acos na mesma dire&#231;&#227;o, criando um padr&#227;o chamado de <italic>rigid body rotation</italic>, com perda completa de importante contribui&#231;&#227;o da tor&#231;&#227;o card&#237;aca &#224; mec&#226;nica ventricular.</p>
          <p>
            <fig id="f17">
              <label>Figura 8.3</label>
              <caption>
                <title>&#8211; Amiloidose ATTR. Strain 2D radial do ventr&#237;culo esquerdo (VE) na por&#231;&#227;o basal, demonstrando importante redu&#231;&#227;o dos valores absolutos em todos os segmentos (A). H&#225; tamb&#233;m altera&#231;&#227;o do strain circunferencial, resultando em significativa redu&#231;&#227;o do twist (4o) e tor&#231;&#227;o do VE (B).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf16.tif"/></fig>
          </p>
          <p>O <italic>strain</italic> do AE tamb&#233;m se encontra frequentemente alterado de forma significativa nos pacientes com AC, em parte como resultado da pr&#243;pria DD do VE, mas tamb&#233;m de forma importante pelo efeito da infiltra&#231;&#227;o direta da parede atrial por fibrilas amiloides (<xref ref-type="fig" rid="f18">Figura 8.4</xref>). Em um estudo recente de Aimo et al., apenas o SL atrial de pico (LA-PALS) apresentou uma associa&#231;&#227;o independente com o diagn&#243;stico de AC, al&#233;m das vari&#225;veis ecocardiogr&#225;ficas cl&#225;ssicas e dos biomarcadores card&#237;acos.<sup><xref ref-type="bibr" rid="B207">207</xref></sup> Foi tamb&#233;m reconhecido que a miopatia infiltrativa atrial avan&#231;ada poderia causar grave disfun&#231;&#227;o e perda da efici&#234;ncia mec&#226;nica da cavidade, levando a uma situa&#231;&#227;o de &#8220;dissocia&#231;&#227;o eletromec&#226;nica&#8221; atrial (DEMA).<sup><xref ref-type="bibr" rid="B208">208</xref></sup> Em uma grande coorte de pacientes, Bandera et al. demonstraram a presen&#231;a de DEMA (determinados pela an&#225;lise do SL) em 22,1% dos pacientes em ritmo sinusal, que era fator determinante de mau progn&#243;stico, quando comparado com a evolu&#231;&#227;o de pacientes em ritmo sinusal e fun&#231;&#227;o mec&#226;nica atrial preservada.<sup><xref ref-type="bibr" rid="B209">209</xref></sup> Em uma s&#233;rie de 156 pacientes com AC da Mayo Clinic, trombos intracard&#237;acos foram detectados pelo ecocardiograma transesof&#225;gico em 27%,<sup><xref ref-type="bibr" rid="B210">210</xref></sup> dados reproduzidos por outros estudos, com ocorr&#234;ncia de trombos inclusive em pacientes em ritmo sinusal<sup><xref ref-type="bibr" rid="B211">211</xref>,<xref ref-type="bibr" rid="B212">212</xref></sup>(<xref ref-type="fig" rid="f19">Figura 8.5</xref>).</p>
          <p>
            <fig id="f18">
              <label>Figura 8.4</label>
              <caption>
                <title>&#8211; Amiloidose AL. Strain bidimensional do &#225;trio esquerdo (AE), com an&#225;lise das janelas apical 4 c&#226;maras e apical 2 c&#226;maras demonstrando importante redu&#231;&#227;o do valor do strain de AE biplanar (strain reservat&#243;rio = 4%).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf17.tif"/></fig>
          </p>
          <p>
            <fig id="f19">
              <label>Figura 8.5</label>
              <caption>
                <title>&#8211; Amiloidose ATTR. Na janela apical ao bidimensional (A), podemos observar a presen&#231;a de grande massa m&#243;vel no interior do &#225;trio direito em paciente com ritmo sinusal. Ao ecocardiograma transesof&#225;gico tridimensional (B), em imagem renderizada, observa-se a grande massa aderida ao ap&#234;ndice atrial direito, correspondendo a trombo. IAS: septo interatrial; SVC: veia cava superior; TV: valva tric&#250;spide.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf18.tif"/></fig>
          </p>
          <p>O <italic>strain</italic> 3D pode ser &#250;til em demonstrar altera&#231;&#227;o de todos os componentes da deforma&#231;&#227;o mioc&#225;rdica em pacientes com AC. Vitarelli et al. demonstraram que a rota&#231;&#227;o basal de pico do VE, SL basal do VD e SL basal do VE foram capazes de distinguir com grande acur&#225;cia pacientes com AC de pacientes portadores de outras hipertrofias ventriculares.<sup><xref ref-type="bibr" rid="B213">213</xref></sup> Em estudo de Baccouche et al.<sup><xref ref-type="bibr" rid="B214">214</xref></sup> usando SL derivado da ECO3D, foi poss&#237;vel demonstrar o mesmo padr&#227;o de <italic>apical sparing</italic>, com gradiente basal-apical caracter&#237;stico.</p>
          <p>O trabalho mioc&#225;rdico (TM), do ingl&#234;s <italic>myocardial work</italic> (MW), tamb&#233;m foi avaliado em pacientes com AC. Clemmensen et al. demonstraram que pacientes com AC tiveram menor &#237;ndice de TM do VE (<italic>left ventricular myocardial work index</italic>, LVMWI) que o grupo-controle, com altera&#231;&#245;es mais pronunciadas nos segmentos basais e, quando submetidos a ecocardiograma de estresse, o aumento de LVMWI do repouso ao pico do exerc&#237;cio foi de 1.974 mmHg% em pacientes do grupo-controle (IC95% 1.699&#8211;2.250 mmHg%; p &lt; 0,0001) comparado com apenas 496 mmHg% em pacientes com AC (IC95% 156&#8211;835 mmHg%; p &lt; 0,01).<sup><xref ref-type="bibr" rid="B215">215</xref></sup></p>
          <p>O uso de <italic>strain</italic> para a avalia&#231;&#227;o evolutiva e para monitorar a resposta de pacientes em uso de tratamentos espec&#237;ficos para AC &#233; bastante promissor. Giblin et al. avaliaram retrospectivamente 45 pacientes com AC ATTR em seguimento de 1 ano, comparando os valores de SL e MW entre os grupos de pacientes tratados e n&#227;o tratados com Tafamidis.<sup><xref ref-type="bibr" rid="B216">216</xref></sup> No grupo de pacientes n&#227;o tratados, foi encontrada uma maior deteriora&#231;&#227;o de SLG (p = 0,02), LVMWI e efici&#234;ncia de TM (p = 0,04), sem diferen&#231;as significativas entre os grupos considerando os valores de <italic>strain</italic> circunferencial, <italic>strain</italic> radial, <italic>twist</italic> ou tor&#231;&#227;o.</p>
          <p>Os par&#226;metros de deforma&#231;&#227;o mioc&#225;rdica tamb&#233;m foram bastante estudados como &#237;ndices progn&#243;sticos na AC pela sua capacidade em fornecer dados quantitativos e pela sua alta sensibilidade e reprodutibilidade. Em estudo de Ternacle et al., foram preditores independentes de eventos cardiovascular maiores em um seguimento m&#233;dio de 11 meses: SL apical m&#233;dio (ponto de corte: -14,5%), NT-pro-BNP elevado e classe funcional NYHA III ou IV.<sup><xref ref-type="bibr" rid="B198">198</xref></sup> Em outro estudo, o &#237;ndice RELAPS se associou de forma independente com o desfecho composto de morte ou transplante card&#237;aco em 5 anos (<italic>hazard ratio</italic> 2,45; p = 0,003), mantendo o valor preditivo desse desfecho prim&#225;rio mesmo na an&#225;lise multivariada (p = 0,018).<sup><xref ref-type="bibr" rid="B217">217</xref></sup></p>
          <p>Em um grande estudo publicado por Buss et al. incluindo 206 pacientes com AC AL, foi demonstrado que o SL baseado no Doppler e o SLG tiveram forte associa&#231;&#227;o com os n&#237;veis de NT-proBNP e com a sobrevida (melhor ponto de corte: -11,78%), sendo que, na an&#225;lise multivariada, apenas a DD e o SLG permaneceram como preditores independentes de sobrevida.<sup><xref ref-type="bibr" rid="B218">218</xref></sup></p>
          <p>Em trabalho recente, Liu et al. inclu&#237;ram 40 pacientes portadores de mieloma m&#250;ltiplo com FE preservada antes do in&#237;cio de tratamento com bortezomibe, medindo SLG e par&#226;metros de TM na linha de base.<sup><xref ref-type="bibr" rid="B219">219</xref></sup> Os autores observaram que efici&#234;ncia de TM global (<italic>global MW efficiency</italic>, GMWE) tinha associa&#231;&#227;o significativa com eventos adversos card&#237;acos ap&#243;s 6 meses de quimioterapia, com ASC = 0,896 (IC95% 0,758&#8211;0,970; p &lt; 0,05). O SL do VD tamb&#233;m foi associado a progn&#243;stico em pacientes com AC. Huntjens et al., estudando 136 pacientes com AC, demonstraram que valores de <italic>strain</italic> de todas as cavidades tinham associa&#231;&#227;o significativa com sobrevida em um seguimento m&#233;dio de 5 anos.<sup><xref ref-type="bibr" rid="B220">220</xref></sup> O SL de pico do AE e o <italic>strain</italic> m&#233;dio de parede livre do VD mantiveram associa&#231;&#227;o independente com progn&#243;stico na an&#225;lise multivariada. Como vari&#225;vel independente, o <italic>strain</italic> de pico do AE teve a associa&#231;&#227;o mais robusta com a sobrevida (p &lt; 0,001), e combinando <italic>strain</italic> do AE com SLG e <italic>strain</italic> m&#233;dio de parede livre do VD, foi obtida a maior capacidade de predi&#231;&#227;o progn&#243;stica (p &lt; 0,001).</p>
        </sec>
      </sec>
    </sec>
    <sec>
      <title>8.2. Doen&#231;a de Fabry</title>
      <p>A doen&#231;a de Anderson-Fabry &#233; a doen&#231;a de dep&#243;sito glicog&#234;nico mais comum, acometendo 1 a cada 50.000 indiv&#237;duos.<sup><xref ref-type="bibr" rid="B221">221</xref></sup> &#201; uma doen&#231;a recessiva ligada ao X, portanto, afeta comumente mais indiv&#237;duos masculinos, sendo as mulheres carreadoras da muta&#231;&#227;o, e caracteriza-se pela aus&#234;ncia da atividade da alfa-galactosidade. Com isso, ocorre um ac&#250;mulo progressivo de globotriaosilceramida nos rins, cora&#231;&#227;o e nervos. Clinicamente, os pacientes manifestam-se com altera&#231;&#245;es cut&#226;neas (angioqueratomas), neuropatia perif&#233;rica, insufici&#234;ncia renal e IC decorrente de uma CMP restritiva com aumento da espessura mioc&#225;rdica. Essas manifesta&#231;&#245;es cl&#237;nicas podem ocorrer na inf&#226;ncia, por&#233;m, &#233; mais comum que surjam ap&#243;s a terceira d&#233;cada de vida.<sup><xref ref-type="bibr" rid="B222">222</xref></sup></p>
      <p>A an&#225;lise morfol&#243;gica do acometimento ventricular apresenta a caracter&#237;stica de aumento da espessura do VE, podendo evoluir para uma redu&#231;&#227;o de sua complac&#234;ncia e IC com FE preservada por uma CMP restritiva. Outros achados interessantes que podem somar como <italic>red flags</italic> s&#227;o a presen&#231;a de hipertrofia do m&#250;sculo papilar, sinal do duplo contorno do endoc&#225;rdio e obstru&#231;&#227;o din&#226;mica na via de sa&#237;da do VE.<sup><xref ref-type="bibr" rid="B223">223</xref></sup> Esse fen&#243;tipo semelhante da CMPH &#233; descrito em 6% dos homens<sup><xref ref-type="bibr" rid="B224">224</xref></sup> e em 12% das mulheres, com o diagn&#243;stico na faixa et&#225;ria mais tardia.<sup><xref ref-type="bibr" rid="B225">225</xref></sup> Por outro lado, a an&#225;lise param&#233;trica disposta pelo <italic>bull&#8217;s eye</italic> da deforma&#231;&#227;o longitudinal do VE tem um papel relevante na diferencia&#231;&#227;o das CMPs que cursam com aumento da espessura mioc&#225;rdica, principalmente quando h&#225; um fen&#243;tipo assim&#233;trico da hipertrofia ventricular esquerda (HVE), em que h&#225; a possibilidade etiol&#243;gica de uma CMPH, amiloidose (principalmente por transtirretina), doen&#231;a de Fabry e cardiopatia hipertensiva no idoso.</p>
      <p>Caracteristicamente, a CMPH apresenta os valores segmentares mais reduzidos nas por&#231;&#245;es em que ocorre maior espessura; a CMP amiloid&#243;tica ocorre um padr&#227;o de poupar o &#225;pice e acometer mais as regi&#245;es m&#233;dio-basais do VE, a cardiopatia hipertensiva pode se apresentar com discreta redu&#231;&#227;o SLG. Por&#233;m, curiosamente, a doen&#231;a de Fabry, apresenta um padr&#227;o singular em que, apesar do aumento assim&#233;trico da espessura ventricular, a regi&#227;o mais acometida pela deforma&#231;&#227;o longitudinal &#233; a por&#231;&#227;o basal da parede &#237;nfero-lateral (<xref ref-type="fig" rid="f20">Figura 8.6</xref>), e ocorre um padr&#227;o decremental progressivo &#224; medida que a doen&#231;a evolui sem tratamento. Existe uma boa correla&#231;&#227;o entre o acometimento descrito pela an&#225;lise de deforma&#231;&#227;o longitudinal do VE e o realce tardio pela RM nas diferentes fases da doen&#231;a.<sup><xref ref-type="bibr" rid="B222">222</xref></sup> Al&#233;m desse papel discriminat&#243;rio, um estudo avaliou doentes com Fabry sem altera&#231;&#245;es morfol&#243;gicas com um grupo-controle saud&#225;vel. Nesse estudo, foi analisado o <italic>strain</italic> longitudinal do VE, VD e do AE com diferen&#231;a entre os grupos (18,1 &#177; 4,0, 21,4 &#177; 4,9 e 29,7 &#177; 9,9 vs. 21,6 &#177; 2,2, 25,2 &#177; 4,0 e 44,8 &#177; 11,1%, p &lt; 0,001). Interessantemente, al&#233;m dessa diferen&#231;a entre os grupos, as altera&#231;&#245;es da deforma&#231;&#227;o apresentaram boa correla&#231;&#227;o com a gravidade dos sintomas.<sup><xref ref-type="bibr" rid="B226">226</xref></sup></p>
      <p>
        <fig id="f20">
          <label>Figura 8.6</label>
          <caption>
            <title>&#8211; Strain global longitudinal, em paciente com doen&#231;a de Fabry, mostrando, no bull&#8217;s eye, os valores mais reduzidos nas por&#231;&#245;es basais da parede &#237;nfero-lateral do ventr&#237;culo esquerdo.</title>
          </caption>
          <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf19.tif"/></fig>
      </p>
      <p>O tratamento j&#225; &#233; disponibilizado, e &#233; poss&#237;vel apresentar mudan&#231;as morfol&#243;gicas do cora&#231;&#227;o a partir de um ano de tratamento, como a redu&#231;&#227;o de sua espessura.<sup><xref ref-type="bibr" rid="B227">227</xref>,<xref ref-type="bibr" rid="B228">228</xref></sup> Sendo assim, &#233; esperado que ocorra uma melhora da deforma&#231;&#227;o longitudinal do VE mais precocemente, mesmo antes da redu&#231;&#227;o da massa ventricular. Por&#233;m, a literatura ainda carece de publica&#231;&#245;es sobre a resposta terap&#234;utica e o padr&#227;o do SLG ao longo do tratamento.</p>
      <p>A an&#225;lise da deforma&#231;&#227;o mioc&#225;rdica &#233; uma importante ferramenta no diagn&#243;stico das hipertrofias ventriculares sem etiologia, principalmente dentro de um contexto cl&#237;nico coerente e com boa janela ecocardiogr&#225;fica, acompanhamento dos familiares que n&#227;o tiveram acesso ao estudo gen&#233;tico e avalia&#231;&#227;o de resposta terap&#234;utica (<xref ref-type="fig" rid="f20">Figura 8.6</xref>).</p>
    </sec>
    <sec>
      <title>9. <italic>Strain</italic> na Hipertens&#227;o Arterial Sist&#234;mica</title>
      <sec>
        <title>9.1. Introdu&#231;&#227;o</title>
        <p>Nesta sess&#227;o, ser&#227;o discutidas as principais vantagens e desvantagens do uso do <italic>strain</italic> em casos de HAS, com e sem crit&#233;rios para CMP hipertensiva (presen&#231;a ou n&#227;o de HVE), e o seu valor cl&#237;nico atual.</p>
      </sec>
      <sec>
        <title>9.2. Hipertens&#227;o Arterial Sist&#234;mica sem Crit&#233;rios para Hipertrofia Ventricular Esquerda</title>
        <p>A HAS provoca, ao longo de sua evolu&#231;&#227;o cl&#237;nica, altera&#231;&#245;es da contratilidade mioc&#225;rdica comprovada com a redu&#231;&#227;o do <italic>strain</italic> longitudinal em resposta &#224; p&#243;s-carga e ao estresse sist&#243;lico de parede elevados, com significado progn&#243;stico comprovado. A queda do SLG traduz a disfun&#231;&#227;o mioc&#225;rdica subcl&#237;nica antes mesmo do surgimento da HVE e queda de FE detectada pela medida tradicional, sendo essa medida do <italic>strain</italic> a &#250;nica a se alterar em HAS est&#225;gio A do desenvolvimento de IC.<sup><xref ref-type="bibr" rid="B229">229</xref>-<xref ref-type="bibr" rid="B239">239</xref></sup>A redu&#231;&#227;o do SLG acontece, inicialmente, na regi&#227;o basal do septo interventricular (SIV), estendendo-se para as regi&#245;es basal e m&#233;dia de outras paredes, e isso se deve &#224; prov&#225;vel maior sobrecarga do SIV ao estresse sist&#243;lico de parede nos est&#225;gios iniciais da s&#237;ndrome hipertensiva.<sup><xref ref-type="bibr" rid="B240">240</xref>,<xref ref-type="bibr" rid="B241">241</xref></sup> (<xref ref-type="fig" rid="f21">Figura 9.1</xref>) As fibras longitudinais da camada subendoc&#225;rdica est&#227;o precocemente acometidas nessa fase inicial juntamente com o mesoc&#225;rdio, ao contr&#225;rio do epic&#225;rdio, como demonstrado em alguns estudos.<sup><xref ref-type="bibr" rid="B242">242</xref></sup></p>
        <p>
          <fig id="f21">
            <label>Figura 9.1</label>
            <caption>
              <title>&#8211; Exemplos de mapa polar do strain longitudinal global (SLG) com as curvas do strain de pico sist&#243;lico obtidas em 4C, 2C e 3C. (A) Paciente saud&#225;vel n&#227;o hipertenso com SLG preservado; (B) Paciente hipertenso sem hipertrofia ventricular esquerda (HVE) com SLG no limite inferior da normalidade com altera&#231;&#227;o regional da deforma&#231;&#227;o mioc&#225;rdica em septo basal; (C) Paciente hipertenso com HVE com SLG reduzido e com maior altera&#231;&#227;o da deforma&#231;&#227;o mioc&#225;rdica nos segmentos basais e m&#233;dios do que nos apicais.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf20.tif"/></fig>
        </p>
        <p>Entretanto, a altera&#231;&#227;o do <italic>strain</italic> longitudinal da camada epic&#225;rdica foi a &#250;nica vari&#225;vel preditora de eventos CVs em outra publica&#231;&#227;o, indicando que seu acometimento pode corresponder &#224; les&#227;o mais severa e cr&#244;nica.<sup><xref ref-type="bibr" rid="B243">243</xref></sup> Todavia, na grande maioria dos equipamentos dispon&#237;veis atualmente a an&#225;lise por camadas do mioc&#225;rdio n&#227;o &#233; poss&#237;vel. Por outro lado, os <italic>strains</italic> radial e circunferencial, que usam toda a espessura mioc&#225;rdica em sua an&#225;lise, t&#234;m uma tend&#234;ncia a permanecerem inalterados ou at&#233; mesmo aumentados como uma prov&#225;vel tentativa de compensa&#231;&#227;o mec&#226;nica &#224; redu&#231;&#227;o do SLG<sup><xref ref-type="bibr" rid="B60">60</xref>,<xref ref-type="bibr" rid="B236">236</xref></sup> e, quando o componente circunferencial se altera, pode traduzir disfun&#231;&#227;o mioc&#225;rdica mais severa.<sup><xref ref-type="bibr" rid="B244">244</xref></sup></p>
        <p>As principais explica&#231;&#245;es para a redu&#231;&#227;o do SLG est&#227;o associadas a um aumento da s&#237;ntese de col&#225;geno, culminando com a fibrose, marcador contundente de disfun&#231;&#227;o mioc&#225;rdica. O SLG reduzido se correlaciona n&#227;o somente com marcadores plasm&#225;ticos de fibrose, como a eleva&#231;&#227;o do inibidor tecidual de metaloproteinase, mas tamb&#233;m com a fibrose detectada com realce tardio pelo gadol&#237;neo em estudos de RM em pacientes hipertensos.<sup><xref ref-type="bibr" rid="B231">231</xref>,<xref ref-type="bibr" rid="B234">234</xref>,<xref ref-type="bibr" rid="B238">238</xref>,<xref ref-type="bibr" rid="B239">239</xref></sup> Redu&#231;&#245;es do SLG foram tamb&#233;m observadas em pacientes com hipertens&#227;o dos tipos mascarada e &#8220;jaleco branco&#8221;<sup><xref ref-type="bibr" rid="B245">245</xref>,<xref ref-type="bibr" rid="B246">246</xref></sup>, com correla&#231;&#227;o dessas quedas com marcadores ecocardiogr&#225;ficos convencionais de DD<sup><xref ref-type="bibr" rid="B240">240</xref></sup>, al&#233;m de maior deteriora&#231;&#227;o a longo prazo em indiv&#237;duos que interromperam tratamento anti-hipertensivo.<sup><xref ref-type="bibr" rid="B247">247</xref></sup></p>
      </sec>
      <sec>
        <title>9.3. Hipertens&#227;o Arterial Sist&#234;mica com Crit&#233;rios para Hipertrofia Ventricular Esquerda</title>
        <p>As consequ&#234;ncias mioc&#225;rdicas da doen&#231;a hipertensiva cr&#244;nica incluem a hipertrofia de mi&#243;citos, al&#233;m de fibrose mioc&#225;rdica e espessamento medial das art&#233;rias coron&#225;rias intramioc&#225;rdicas.<sup><xref ref-type="bibr" rid="B248">248</xref></sup> Consequentemente, a HAS e as modifica&#231;&#245;es do remodelamento mioc&#225;rdico s&#227;o fatores de risco para o desenvolvimento de eventos card&#237;acos maiores, tais como o risco de desenvolvimento de IC e morte prematura. Assim o uso do <italic>strain</italic> nesses casos tem o objetivo principal de detectar altera&#231;&#245;es sutis da fun&#231;&#227;o sist&#243;lica, antes mesmo do comprometimento da FE obtida de forma convencional, selecionando casos de ICFEP para a ado&#231;&#227;o de tratamento adequado.</p>
        <p>Os tipos de remodelamento do VE podem apresentar altera&#231;&#245;es dos v&#225;rios tipos de <italic>strain</italic>. Assim, na hipertrofia conc&#234;ntrica, &#233; poss&#237;vel encontrar valores reduzidos do SLG com queda progressiva de acordo com a evolu&#231;&#227;o dos tipos geom&#233;tricos, desde o remodelamento conc&#234;ntrico at&#233; a hipertrofia exc&#234;ntrica com dilata&#231;&#227;o do VE.<sup><xref ref-type="bibr" rid="B249">249</xref>-<xref ref-type="bibr" rid="B251">251</xref></sup> O <italic>strain</italic> global circunferencial e o <italic>strain</italic> global radial encontram-se com valores preservados na maioria dos estudos<sup><xref ref-type="bibr" rid="B252">252</xref></sup> ou at&#233; mesmo reduzidos em algumas s&#233;ries<sup><xref ref-type="bibr" rid="B249">249</xref></sup> e tendem a permanecer normais nas camadas epic&#225;rdicas em indiv&#237;duos com HAS e HVE.<sup><xref ref-type="bibr" rid="B250">250</xref></sup> O comportamento da tor&#231;&#227;o e do <italic>twisting</italic> tamb&#233;m pode ser vari&#225;vel, com valores normais ou reduzidos de acordo com o tipo de geometria ventricular.<sup><xref ref-type="bibr" rid="B249">249</xref>,<xref ref-type="bibr" rid="B253">253</xref></sup> Quando se considera o uso da t&#233;cnica tridimensional do <italic>strain</italic>, o SLG 3D tende a se deteriorar de acordo com o grau de hipertrofia e di&#226;metro da cavidade do VE na HAS.<sup><xref ref-type="bibr" rid="B62">62</xref>,<xref ref-type="bibr" rid="B250">250</xref></sup></p>
        <p>Al&#233;m da correla&#231;&#227;o do SLG reduzido com os diferentes padr&#245;es de HVE, o <italic>strain</italic> pode ser usado para auxiliar no esclarecimento da causa da hipertrofia e &#233; frequentemente mais reduzido em casos de CMPH quando comparado com HVE por HAS.<sup><xref ref-type="bibr" rid="B254">254</xref></sup></p>
      </sec>
      <sec>
        <title>9.4. Tratamento Cl&#237;nico</title>
        <p>O SLG apresenta queda paralela com a piora da classe funcional<sup><xref ref-type="bibr" rid="B241">241</xref></sup> e melhora com o tratamento a longo prazo, como demonstrado em uma an&#225;lise de seguimento de 3 anos ap&#243;s tratamento anti-hipertensivo<sup><xref ref-type="bibr" rid="B255">255</xref></sup> e em casos de tratamento anti-hipertensivo no ambiente de atendimento em emerg&#234;ncia.<sup><xref ref-type="bibr" rid="B256">256</xref></sup> O SLG reduzido tamb&#233;m se correlacionou com a MAPA anormal em pacientes em tratamento, mesmo ap&#243;s ajuste de outras vari&#225;veis cl&#237;nicas como idade, presen&#231;a de diabetes melito e &#237;ndice de massa do VE.<sup><xref ref-type="bibr" rid="B257">257</xref></sup></p>
      </sec>
      <sec>
        <title>9.5. Conclus&#227;o</title>
        <p>Existem evid&#234;ncias suficientes para recomendar o uso do <italic>strain</italic> em pacientes com HAS, independentemente da presen&#231;a de HVE, tanto para a identifica&#231;&#227;o precoce das altera&#231;&#245;es estruturais subcl&#237;nicas, como para os quadros de ICFEP visando a ado&#231;&#227;o de tratamento otimizado. Por outro lado, h&#225; a necessidade de estudos mais robustos para nortear o uso sistem&#225;tico do <italic>strain</italic> nessa popula&#231;&#227;o.</p>
      </sec>
    </sec>
    <sec>
      <title>10. <italic>Strain</italic> em Atletas</title>
      <p>A atividade f&#237;sica regular e intensa &#233; respons&#225;vel por uma s&#233;rie de profundas altera&#231;&#245;es el&#233;tricas, estruturais e funcionais adaptativas, usualmente referidas como &#8220;cora&#231;&#227;o de atleta&#8221;.<sup><xref ref-type="bibr" rid="B258">258</xref></sup> A an&#225;lise dessa condi&#231;&#227;o &#233; importante para uma melhor compreens&#227;o dos mecanismos de adequa&#231;&#227;o card&#237;aca e melhoria da <italic>performance</italic> e do rendimento, orientando o treinamento otimizado. Al&#233;m disso, permite a diferencia&#231;&#227;o de patologias que podem ter caracter&#237;sticas morfol&#243;gicas semelhantes &#224;quelas induzidas pelo treinamento.</p>
      <p>Atletas de alto rendimento e que apresentam grandes volumes do VE parecem pertencer ao espectro da fisiologia saud&#225;vel t&#237;pica do &#8220;cora&#231;&#227;o de atleta&#8221;. Alguns trabalhos demonstram que o SLG se encontra discretamente reduzido nos atletas em repouso, quando comparado com sedent&#225;rios; em outros, essa medida mostra-se superior aos controles.<sup><xref ref-type="bibr" rid="B259">259</xref>,<xref ref-type="bibr" rid="B260">260</xref></sup> Entretanto, na maioria dos estudos, n&#227;o foi identificada diferen&#231;a significativa.<sup><xref ref-type="bibr" rid="B261">261</xref></sup> Essa varia&#231;&#227;o pode estar relacionada ao impacto de diferentes fatores como pr&#233;- e p&#243;s-carga, massa mioc&#225;rdica e bradicardia sinusal. Por esse motivo, a presen&#231;a de valores reduzidos de SLG em atletas com fun&#231;&#227;o diast&#243;lica do VE normal ou supranormal pode ser determinante para a distin&#231;&#227;o entre as adapta&#231;&#245;es secund&#225;rias aos exerc&#237;cios e &#224;s patologias card&#237;acas. Valores absolutos iguais ou superiores a 18% s&#227;o considerados ainda dentro da normalidade. A redu&#231;&#227;o desses &#237;ndices &#233; muito mais acentuada em portadores de CMPH e HAS.<sup><xref ref-type="bibr" rid="B262">262</xref></sup> No entanto, o <italic>strain</italic> circunferencial global e o <italic>strain</italic> radial n&#227;o demonstraram altera&#231;&#245;es significativas em rela&#231;&#227;o ao grupo-controle.<sup><xref ref-type="bibr" rid="B261">261</xref></sup> A representa&#231;&#227;o param&#233;trica em <italic>bull&#8217;s-eye</italic> pode fornecer subs&#237;dios para diferenciar o cora&#231;&#227;o do atleta de outras doen&#231;as que cursam com hipertrofias.<sup><xref ref-type="bibr" rid="B263">263</xref></sup></p>
      <p>Quando os atletas s&#227;o categorizados de acordo com o tipo e intensidade dos exerc&#237;cios praticados em est&#225;tico e din&#226;mico, surgem diferen&#231;as predominantemente em aspectos mec&#226;nicos do VE. Um estudo recente mostrou que a tor&#231;&#227;o card&#237;aca foi maior em atletas com din&#226;mica baixa, est&#225;tica alta (levantamento de peso, artes marciais), est&#225;tica baixa e din&#226;mica alta (maratona, futebol) em rela&#231;&#227;o aos controles. Contrariamente, a tor&#231;&#227;o foi menor em atletas com din&#226;mica alta, est&#225;tica moderada (nata&#231;&#227;o, polo aqu&#225;tico), o que pode ser explicado por altera&#231;&#245;es na rota&#231;&#227;o apical, mas n&#227;o na basal. O pico de <italic>untwisting</italic> foi maior em atletas com predomin&#226;ncia de exerc&#237;cios com componentes din&#226;mico baixo e est&#225;tico alto, enquanto picos menores foram encontrados em atletas praticantes de esportes com componentes din&#226;mico alto e est&#225;tico alto.<sup><xref ref-type="bibr" rid="B261">261</xref></sup> Estudos utilizando o <italic>speckle tacking</italic> para quantificar a deforma&#231;&#227;o mioc&#225;rdica t&#234;m mostrado que atletas competitivos de resist&#234;ncia (<italic>endurance</italic>) apresentam valores normais ou aumentados do <italic>strain</italic>.<sup><xref ref-type="bibr" rid="B264">264</xref>-<xref ref-type="bibr" rid="B268">268</xref></sup></p>
      <p>Em rela&#231;&#227;o ao VD, os &#237;ndices de deforma&#231;&#227;o mioc&#225;rdica, obtidos tanto pelo Doppler tecidual quanto pelo <italic>speckle tracking,</italic> podem estar discretamente reduzidos nos segmentos basal e m&#233;dio da parede livre do VD, notadamente em atletas de resist&#234;ncia em compara&#231;&#227;o aos controles.<sup><xref ref-type="bibr" rid="B269">269</xref></sup> Ainda &#233; controverso se tal redu&#231;&#227;o da deforma&#231;&#227;o mioc&#225;rdica do VD &#233; apenas uma resposta adaptativa ao exerc&#237;cio ou se &#233; uma altera&#231;&#227;o subcl&#237;nica por les&#227;o mioc&#225;rdica.<sup><xref ref-type="bibr" rid="B270">270</xref></sup> Alguns autores sup&#245;em que tal achado pode ser explicado pelas mudan&#231;as na curvatura entre o &#225;pice e base do VD, resultando nessa diferen&#231;a do <italic>strain</italic> entre os segmentos.</p>
      <p>Ainda s&#227;o iniciais os estudos da fun&#231;&#227;o atrial em atletas com a t&#233;cnica do <italic>speckle tracking</italic> e apresentam resultados conflitantes. Um estudo mostrou que a contra&#231;&#227;o atrial avaliada pelo SLG do AE diminuiu significativamente ap&#243;s treino.<sup><xref ref-type="bibr" rid="B271">271</xref></sup> Outro estudo n&#227;o mostrou diferen&#231;as no <italic>strain</italic> atrial entre atletas e sedent&#225;rios.<sup><xref ref-type="bibr" rid="B272">272</xref></sup></p>
      <p>A medida do <italic>strain</italic> tamb&#233;m se faz importante na avalia&#231;&#227;o da fun&#231;&#227;o diast&#243;lica. O exerc&#237;cio din&#226;mico leva a um relaxamento ventricular mais efetivo, al&#233;m da dilata&#231;&#227;o biventricular, entretanto, o exerc&#237;cio est&#225;tico pode estar relacionado ao de aumento da espessura mioc&#225;rdica e hipertrofia conc&#234;ntrica do VE, podendo levar a algum grau de comprometimento da fun&#231;&#227;o diast&#243;lica.<sup><xref ref-type="bibr" rid="B273">273</xref></sup> Al&#233;m disso, o uso de drogas il&#237;citas para o aumento da <italic>performance</italic> pode levar &#224; deteriora&#231;&#227;o da fun&#231;&#227;o ventricular, sist&#243;lica ou diast&#243;lica; a ecocardiografia com <italic>speckle tracking</italic> pode detectar precocemente essas altera&#231;&#245;es.<sup><xref ref-type="bibr" rid="B274">274</xref></sup></p>
      <p>Por isso, &#233; fundamental que, na avalia&#231;&#227;o da fun&#231;&#227;o ventricular dos atletas profissionais e/ou amadores, utilizemos todas as ferramentas dispon&#237;veis no arsenal da ecocardiografia. O <italic>strain</italic> &#233; capaz de detectar altera&#231;&#245;es incipientes da fun&#231;&#227;o sist&#243;lica muito antes que ocorra qualquer altera&#231;&#227;o da contratilidade ao estudo bidimensional ou diminui&#231;&#227;o da FE.</p>
      <p>A ecocardiografia com <italic>speckle tracking</italic> tem se mostrado bastante promissora para complementar a ecocardiografia bidimensional de rotina na avalia&#231;&#227;o de atletas. O SLG nessa popula&#231;&#227;o (diferentemente da popula&#231;&#227;o sedent&#225;ria) pode ser considerado normal com valores absolutos superiores a 16%, valores inferiores devem levantar suspeita de patologia, principalmente se diante de outros sinais sugestivos como hipertrofia ou dilata&#231;&#227;o ventricular significativas.<sup><xref ref-type="bibr" rid="B275">275</xref></sup></p>
    </sec>
    <sec>
      <title>11. <italic>Strain</italic> na Ecocardiografia com Estresse</title>
      <p>A <xref ref-type="table" rid="t7">Tabela 11.1</xref> mostra as principais aplica&#231;&#245;es do <italic>strain</italic> na ecocardiografia com estresse.</p>
      <p>
        <table-wrap id="t7">
          <label>Tabela 11.1</label>
          <caption>
            <title>&#8211; Aplica&#231;&#245;es do strain na ecocardiografia com estresse</title>
          </caption>
          <table frame="hsides" rules="groups">
            <colgroup width="50%">
              <col/>
              <col/>
            </colgroup>
            <thead>
              <tr>
                <th align="left">Cen&#225;rio cl&#237;nico</th>
                <th align="left">Conceito</th>
              </tr>
            </thead>
            <tbody>
              <tr>
                <td>Detec&#231;&#227;o de isquemia<sup>189,276-280</sup></td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;SL regional detecta isquemia endoc&#225;rdica.</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;SC &#233; &#250;til para a diferencia&#231;&#227;o entre infarto transmural e n&#227;o transmural.</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;O aumento do tempo at&#233; o pico de SL &#233; &#250;til para a detec&#231;&#227;o precoce de isquemia.</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;Encurtamento p&#243;s-sist&#243;lico (sens&#237;vel, mas n&#227;o espec&#237;fico para detec&#231;&#227;o de isquemia).</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;SRL sist&#243;lico (menor depend&#234;ncia de carga e FC em rela&#231;&#227;o ao <italic>strain</italic>).</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;Par&#226;metros de deforma&#231;&#227;o diast&#243;lica.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Avalia&#231;&#227;o da viabilidade<sup>281-285</sup></td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;SL e SRL aumentam a acur&#225;cia para a detec&#231;&#227;o de viabilidade em paciente com IM tratados com ATC em baixas doses de dobutamina.</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;SL &#233; o melhor preditor de melhora da fun&#231;&#227;o ap&#243;s CRM.</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;Aus&#234;ncia de resposta &#224; dobutamina prediz com acur&#225;cia a aus&#234;ncia de melhora ap&#243;s CRM.</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;Diferencia&#231;&#227;o entre mioc&#225;rdio atordoado e hibernante (SL e SRL diminu&#237;dos e encurtamento p&#243;s-sist&#243;lico presente).</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Estenose a&#243;rtica<sup>286,287</sup></td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;SLG na avalia&#231;&#227;o da estenose a&#243;rtica baixo fluxo baixo gradiente.</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;Pacientes com SLG &gt; 10%, ap&#243;s uso da dobutamina, apresentam maior sobrevida.</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;SLG de estresse apresentou maior acur&#225;cia do que ao repouso.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Miocardiopatia hipertensiva<sup>288</sup></td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;D&#233;ficit de SL e SR mais evidente ao estresse do que ao repouso nas fases iniciais, possibilitando medidas de preven&#231;&#227;o.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Miocardiopatia diab&#233;tica<sup>289,290</sup></td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;SRL diminu&#237;do nos segmentos m&#233;dios e basais durante ESD</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;Velocidades mioc&#225;rdicas diminu&#237;das precocemente em pacientes assintom&#225;ticos com resist&#234;ncia &#224; insulina durante ESD.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Cardiomiopatias<sup>132,291-293</sup></td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;Diminui&#231;&#227;o da reserva funcional sist&#243;lica detectada ao SL e SR ap&#243;s estresse.</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;Aus&#234;ncia de melhora de par&#226;metros de fun&#231;&#227;o diast&#243;lica.</p>
                    </list-item>
                    <list-item>
                      <p><italic>&#8226;Time-to-peak</italic> aumentado na CMPH associado &#224; dissincronia.</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;Baixos valores do SL do VD na displasia arritmog&#234;nica n&#227;o melhora significativamente com estresse.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Cora&#231;&#227;o de atleta<sup>294,295</sup></td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>&#8226;Valores do SL discretamente reduzidos com reserva mioc&#225;rdica preservada ou supranormal.</p>
                    </list-item>
                    <list-item>
                      <p>&#8226;O uso do SLG de estresse ajuda a diferenciar o cora&#231;&#227;o de atleta de uma cardiomiopatia.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
            </tbody>
          </table>
          <table-wrap-foot>
            <attrib>
              <italic>ATC: angioplastia transluminal coron&#225;ria; CMPH: cardiomiopatia hipertr&#243;fica; CRM: cirurgia de revasculariza&#231;&#227;o mioc&#225;rdica; ESD: ecocardiografia de estresse com dobutamina; FC: frequ&#234;ncia card&#237;aca; IM: infarto do mioc&#225;rdio; SC: strain circunferencial; SL: strain longitudinal; SR: strain radial, SLG: strain longitudinal global; SRL: strain regional longitudinal; VD: ventr&#237;culo direito.</italic>
            </attrib>
          </table-wrap-foot>
        </table-wrap>
      </p>
      <p>Em breve, um artigo de revis&#227;o mais completo sobre ecocardiografia de estresse ser&#225; publicado neste peri&#243;dico.</p>
    </sec>
    <sec>
      <title>12. <italic>Strain</italic> nas Cardiopatias Cong&#234;nitas</title>
      <p>Alguns estudos j&#225; demonstraram o elevado valor progn&#243;stico do <italic>strain</italic> obtido pelo <italic>speckle tracking</italic>, refor&#231;ando sua utilidade tanto em patologias cong&#234;nitas como adquiridas.<sup><xref ref-type="bibr" rid="B9">9</xref></sup>No entanto, o <italic>strain</italic> mioc&#225;rdico est&#225; sujeito a varia&#231;&#245;es fisiol&#243;gicas causadas por idade, sexo, frequ&#234;ncia card&#237;aca, pr&#233;-carga, press&#227;o arterial e superf&#237;cie corp&#243;rea, al&#233;m do tipo de <italic>software</italic> utilizado para an&#225;lise.<sup><xref ref-type="bibr" rid="B296">296</xref></sup> Um esfor&#231;o cont&#237;nuo vem sendo realizado no sentido de estabelecer valores normais do <italic>strain</italic> que possam ser utilizados como refer&#234;ncia universal em pediatria, para que a avalia&#231;&#227;o da deforma&#231;&#227;o mioc&#225;rdica seja adotada na rotina cl&#237;nica.<sup><xref ref-type="bibr" rid="B297">297</xref>-<xref ref-type="bibr" rid="B299">299</xref></sup></p>
      <p>Apresentaremos, nas tabelas a seguir, os valores de <italic>strain</italic> mioc&#225;rdico j&#225; apresentados na literatura, em crian&#231;as normais (<xref ref-type="table" rid="t8">Tabelas 12.1</xref> <xref ref-type="table" rid="t19"/> a <xref ref-type="table" rid="t20">12.3</xref>) e em algumas cardiopatias cong&#234;nitas, com recomenda&#231;&#245;es de valores de corte (<xref ref-type="table" rid="t9">Tabela 12.4</xref>).</p>
      <p>
        <table-wrap id="t8">
          <label>Tabela 12.1</label>
          <caption>
            <title>&#8211; Valores normais de strain de ventr&#237;culo esquerdo, segundo as faixas et&#225;rias<bold>298</bold></title>
          </caption>
          <table frame="hsides" rules="groups">
            <colgroup width="14%">
              <col/>
              <col/>
              <col/>
              <col/>
              <col/>
              <col/>
              <col/>
            </colgroup>
            <thead>
              <tr>
                <th align="left">Idade em anos</th>
                <th><italic>Strain</italic> global de pico sist&#243;lico longitudinal</th>
                <th><italic>Strain</italic> de pico sist&#243;lico longitudinal corte apical 4 c&#226;maras</th>
                <th><italic>Strain</italic> global de pico sist&#243;lico circunferencial</th>
                <th><italic>Strain</italic> de pico sist&#243;lico circunferencial ao n&#237;vel dos m&#250;sculos papilares</th>
                <th><italic>Strain</italic> global de pico sist&#243;lico radial</th>
                <th><italic>Strain</italic> de pico sist&#243;lico radial ao n&#237;vel dos m&#250;sculos papilares</th>
              </tr>
            </thead>
            <tbody>
              <tr>
                <td>0-1</td>
                <td align="center">18,7% (20,8; 16,7)</td>
                <td align="center">19,4% (22,2; 16,6)</td>
                <td align="center">_____</td>
                <td align="center">18,2% (22,6; 13,7)</td>
                <td align="center">_____</td>
                <td align="center">44,4% (36,6; 52,1)</td>
              </tr>
              <tr>
                <td>2-9</td>
                <td align="center">21,7% (23,0; 20,5)</td>
                <td align="center">21,0% (21,8; 20,2)</td>
                <td align="center">24,5% (27,2; 21,7)</td>
                <td align="center">20,3% (21,4; 19,1)</td>
                <td align="center">48,0% (33,3; 62,8)</td>
                <td align="center">50,8% (47,4; 54,1)</td>
              </tr>
              <tr>
                <td>10-13</td>
                <td align="center">20% (20,8; 19,1)</td>
                <td align="center">20,5% (21,7; 19,2)</td>
                <td align="center">21,9% (26,5; 17,4)</td>
                <td align="center">21,5% (23,1; 19,8)</td>
                <td align="center">43,7% (33,0; 54,5)</td>
                <td align="center">52,1% (48,5; 55,8)</td>
              </tr>
              <tr>
                <td>14-21</td>
                <td align="center">19,9 (20,6; 19,2)</td>
                <td align="center">19,9% (21,2; 18,6)</td>
                <td align="center">16,4% (23,3; 9,6)</td>
                <td align="center">16,4% (23,3; 9,6)</td>
                <td align="center">44,0% (41,6; 46,4)</td>
                <td align="center">46,4% (39,7; 53,1)</td>
              </tr>
              <tr>
                <td>Geral</td>
                <td align="center">20,2% (20,8; 19,6)</td>
                <td align="center">20,4% (21,1; 19,8)</td>
                <td align="center">22,3% (19,9; 24,6)</td>
                <td align="center">20,4% (21,1; 19,8)</td>
                <td align="center">45,2% (38,8; 51,7)</td>
                <td align="center">49,4% (47,2; 51,6)</td>
              </tr>
            </tbody>
          </table>
          <table-wrap-foot>
            <attrib>
              <italic>Valores expressos como m&#233;dia e intervalo de confian&#231;a de 95%.</italic>
            </attrib>
          </table-wrap-foot>
        </table-wrap>
      </p>
      <p>
        <table-wrap id="t19">
          <label>Tabela 12.2</label>
          <caption>
            <title>&#8211; Valores normais de <italic>strain</italic> de ventr&#237;culo direito, segundo as faixas et&#225;rias300</title>
          </caption>
          <table frame="hsides" rules="groups">
            <colgroup width="20%">
              <col/>
              <col/>
              <col/>
              <col/>
              <col/>
            </colgroup>
            <thead>
              <tr>
                <th align="left" style="font-weight:normal"> </th>
                <th>31 dias a 24 meses</th>
                <th>2 a 5 anos</th>
                <th>5 a 11 anos</th>
                <th>11 a 18 anos</th>
              </tr>
            </thead>
            <tbody>
              <tr>
                <td>SLG VD %</td>
                <td align="center">25,4 &#177; 3,9</td>
                <td align="center">25,9 &#177; 4,0</td>
                <td align="center">25,8 &#177; 4,7</td>
                <td align="center">25,4 &#177; 4,1</td>
              </tr>
            </tbody>
          </table>
          <table-wrap-foot>
            <attrib>
              <italic>SLG: strain longitudinal global; VD: ventr&#237;culo direito. Valores expressos como m&#233;dia &#177; desvio padr&#227;o.</italic>
            </attrib>
          </table-wrap-foot>
        </table-wrap>
      </p>
      <p>
        <table-wrap id="t20">
          <label>Tabela 12.3</label>
          <caption>
            <title>&#8211; Valores normais de strain atrial direito e esquerdo, segundo as faixas et&#225;ria<bold>301</bold></title>
          </caption>
          <table frame="hsides" rules="groups">
            <colgroup width="20%">
              <col/>
              <col/>
              <col/>
              <col/>
              <col/>
            </colgroup>
            <thead>
              <tr>
                <th align="left">Medida</th>
                <th>31 dias a 24 meses</th>
                <th>2 a 5 anos</th>
                <th>5 a 11 anos</th>
                <th>11 a 18 anos</th>
              </tr>
            </thead>
            <tbody>
              <tr>
                <td>
                  <bold><italic>Strain</italic> AE (R) %</bold>
                </td>
                <td align="center">52,8 &#177; 10,1</td>
                <td align="center">55,7 &#177; 10,7</td>
                <td align="center">58,1 &#177; 10</td>
                <td align="center">57,6 &#177; 10,5</td>
              </tr>
              <tr>
                <td>
                  <bold><italic>Strain</italic> AE (C) %</bold>
                </td>
                <td align="center">14,2 &#177; 6,6</td>
                <td align="center">12,7 &#177; 6,1</td>
                <td align="center">14,0 &#177; 6,7</td>
                <td align="center">15,1 &#177; 7,0</td>
              </tr>
              <tr>
                <td>
                  <bold><italic>Strain</italic> AD (R) %</bold>
                </td>
                <td align="center">47,1 &#177; 9,6</td>
                <td align="center">49,6 &#177; 10,2</td>
                <td align="center">51,6 &#177; 10,7</td>
                <td align="center">52,0 &#177; 10,6</td>
              </tr>
              <tr>
                <td>
                  <bold>
                    <italic>Strain AD (C) %</italic>
                  </bold>
                </td>
                <td align="center">11,5 &#177; 6,0</td>
                <td align="center">11,9 &#177; 5,9</td>
                <td align="center">11,8 &#177; 6,3</td>
                <td align="center">12,8 &#177; 5,8</td>
              </tr>
            </tbody>
          </table>
          <table-wrap-foot>
            <attrib>
              <italic>AD: &#225;trio direito; AE: &#225;trio esquerdo; C: fase de contra&#231;&#227;o atrial; R: fase de reservat&#243;rio. Valores expressos como m&#233;dia &#177; desvio padr&#227;o.</italic>
            </attrib>
          </table-wrap-foot>
        </table-wrap>
      </p>
      <p>
        <table-wrap id="t9">
          <label>Tabela 12.4</label>
          <caption>
            <title>&#8211; Exemplos de estudos que avaliam o uso do strain na hipertens&#227;o pulmonar idiop&#225;tica e em cardiopatias cong&#234;nitas</title>
          </caption>
          <table frame="hsides" rules="groups">
            <colgroup width="17%">
              <col/>
              <col/>
              <col/>
              <col/>
              <col/>
              <col/>
            </colgroup>
            <thead>
              <tr>
                <th align="left" style="font-weight:normal"> </th>
                <th>Autores</th>
                <th>Par&#226;metro</th>
                <th>Ponto de corte</th>
                <th>Achado</th>
                <th>S/E</th>
              </tr>
            </thead>
            <tbody>
              <tr>
                <td>Hipertens&#227;o pulmonar idiop&#225;tica</td>
                <td align="center">Muntean et al.<sup>302</sup></td>
                <td align="center"><italic>Strain</italic> segmento m&#233;dio PL VD</td>
                <td align="center">18,5%</td>
                <td align="center">Preditor de piora cl&#237;nica</td>
                <td align="center">
                  <list list-type="simple">
                    <list-item>
                      <p>S: 91,7%</p>
                    </list-item>
                    <list-item>
                      <p>E: 30,8%</p>
                    </list-item>
                    <list-item>
                      <p>ASC = 0,88 &#177; 0,06</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Anomalia de Ebstein</td>
                <td align="center">K&#252;hn et al.<sup>303</sup></td>
                <td align="center">SLG VD (06 segmentos)</td>
                <td align="center">20,15%</td>
                <td align="center">Diagn&#243;stico de disfun&#231;&#227;o de VD (FE &lt; 50% &#224; RM)</td>
                <td align="center">
                  <list list-type="simple">
                    <list-item>
                      <p>S: 77%</p>
                    </list-item>
                    <list-item>
                      <p>E: 46%</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>VD sist&#234;mico (PO TGA Senning/Mustard)</td>
                <td align="center">Lipczy&#324;ska et al.<sup>304</sup></td>
                <td align="center">SLG VD (06 segmentos)</td>
                <td align="center">14,2%</td>
                <td align="center">Diagn&#243;stico de disfun&#231;&#227;o de VD (FE &lt; 45% &#224; RM)</td>
                <td align="center">
                  <list list-type="simple">
                    <list-item>
                      <p>S: 83%</p>
                    </list-item>
                    <list-item>
                      <p>E: 90%</p>
                    </list-item>
                    <list-item>
                      <p>ASC = 0,882</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>VD sist&#234;mico (TCCGA)</td>
                <td align="center">Kowalik et al.<sup>305</sup></td>
                <td align="center">SLG VD (06 segmentos)</td>
                <td> </td>
                <td align="center">Diagn&#243;stico de disfun&#231;&#227;o de VD (FE &lt; 45% &#224; RM)</td>
                <td align="center">
                  <list list-type="simple">
                    <list-item>
                      <p>S: 77,3%</p>
                    </list-item>
                    <list-item>
                      <p>E: 72,7%</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>PO OACE</td>
                <td align="center">Castaldi et al.<sup>306</sup></td>
                <td align="center"><italic>Strain</italic> segmentar de pico do VE</td>
                <td align="center">14,8%</td>
                <td align="center">Preditor de fibrose &#224; RM</td>
                <td align="center">
                  <list list-type="simple">
                    <list-item>
                      <p>S: 92,5%</p>
                    </list-item>
                    <list-item>
                      <p>E: 93,7%</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Fisiologia Univentricular (PO Fontan)</td>
                <td align="center">Park et al.<sup>307</sup></td>
                <td align="center"><italic>Strain rate</italic> circunferencial</td>
                <td align="center">-1,0s<sup>-1</sup></td>
                <td align="center">Preditor de interna&#231;&#227;o prolongada (&gt;14 dias) ap&#243;s anastomose CPT</td>
                <td align="center">
                  <list list-type="simple">
                    <list-item>
                      <p>S: 72%</p>
                    </list-item>
                    <list-item>
                      <p>E: 60%</p>
                    </list-item>
                  </list>
                </td>
              </tr>
            </tbody>
          </table>
          <table-wrap-foot>
            <attrib>
              <italic>ASC: &#225;rea sob a curva; CPT: cavopulmonar total; E: especificidade; FE: fra&#231;&#227;o de eje&#231;&#227;o; OACE: origem an&#244;mala de art&#233;ria coronariana esquerda; PL: parede livre; PO: p&#243;s-operat&#243;rio; RM: resson&#226;ncia magn&#233;tica; S: sensibilidade; SLG: strain longitudinal global; TCCGA: transposi&#231;&#227;o corrigida das grandes art&#233;rias; TGA: transposi&#231;&#227;o das grandes art&#233;rias; VD: ventr&#237;culo direito.</italic>
            </attrib>
          </table-wrap-foot>
        </table-wrap>
      </p>
      <p>Em breve, um artigo de revis&#227;o mais completo sobre o tema ser&#225; publicado neste peri&#243;dico.</p>
    </sec>
    <sec>
      <title>13. <italic>Strain</italic> do Ventr&#237;culo Direito</title>
      <sec>
        <title>13.1. Introdu&#231;&#227;o</title>
        <p>O VD tem importante papel na fisiopatologia das doen&#231;as cardiopulmonares. Um grande n&#250;mero de evid&#234;ncias tem demonstrado que a disfun&#231;&#227;o do VD &#233; um importante marcador independente de morbidade e mortalidade em v&#225;rias situa&#231;&#245;es cl&#237;nicas como: IC, doen&#231;as valvares, HP, embolia pulmonar (EP), cardiopatia isqu&#234;mica e na presen&#231;a de cardiopatia cong&#234;nita nos adultos.<sup><xref ref-type="bibr" rid="B308">308</xref>-<xref ref-type="bibr" rid="B313">313</xref></sup></p>
        <p>A RMC &#233; considerada o exame n&#227;o invasivo padr&#227;o-ouro para a obten&#231;&#227;o dos volumes, FE e avalia&#231;&#227;o estrutural do VD. Tem, por&#233;m, como principais limita&#231;&#245;es um custo elevado, maior tempo da aquisi&#231;&#227;o das imagens e pouca disponibilidade na maioria dos centros.<sup><xref ref-type="bibr" rid="B314">314</xref></sup> A ecocardiografia bidimensional (2D) &#233; o exame inicial mais utilizado na avalia&#231;&#227;o estrutural e funcional do VD, por ser mais dispon&#237;vel, de menor custo, n&#227;o invasiva e com menor tempo para aquisi&#231;&#227;o das imagens. Essa avalia&#231;&#227;o do VD pela 2D, entretanto, &#233; desafiadora, pela estrutura complexa da cavidade, pela posi&#231;&#227;o desfavor&#225;vel dentro da parede tor&#225;cica, pela intensa trabecula&#231;&#227;o mioc&#225;rdica, que impede a melhor visualiza&#231;&#227;o do endoc&#225;rdio, por possuir paredes mais finas e pela alta depend&#234;ncia das condi&#231;&#245;es de carga dos &#237;ndices mais utilizados da fun&#231;&#227;o sist&#243;lica.<sup><xref ref-type="bibr" rid="B315">315</xref></sup></p>
        <p>V&#225;rios par&#226;metros ecocardiogr&#225;ficos indicadores da fun&#231;&#227;o sist&#243;lica do VD s&#227;o utilizados na pr&#225;tica cl&#237;nica. Recentemente, a ecocardiografia 2D com <italic>strain</italic> pelo <italic>speckle tracking</italic> foi introduzida no cen&#225;rio cl&#237;nico como um indicador objetivo de contratilidade mioc&#225;rdica regional e global, inicialmente na avalia&#231;&#227;o do VE e, mais recentemente, do VD. Com a aplica&#231;&#227;o dessa nova metodologia, mais pesquisas e publica&#231;&#245;es t&#234;m chamado aten&#231;&#227;o das vantagens da sua utiliza&#231;&#227;o em rela&#231;&#227;o aos outros par&#226;metros convencionais ecocardiogr&#225;ficos.<sup><xref ref-type="bibr" rid="B316">316</xref></sup></p>
      </sec>
      <sec>
        <title>13.2. Caracter&#237;sticas Anat&#244;micas e Funcionais do Ventr&#237;culo Direito</title>
        <p>Na <xref ref-type="table" rid="t21">Tabela 13.1</xref>, podemos observar as principais caracter&#237;sticas que diferenciam os ventr&#237;culos.<sup><xref ref-type="bibr" rid="B317">317</xref>-<xref ref-type="bibr" rid="B319">319</xref></sup></p>
        <p>
          <table-wrap id="t21">
            <label>Tabela 13.1</label>
            <caption>
              <title>&#8211; Caracter&#237;sticas anat&#244;micas e funcionais dos ventr&#237;culos</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="33%">
                <col/>
                <col/>
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left" style="font-weight:normal"> </th>
                  <th>Ventr&#237;culo direito</th>
                  <th>Ventr&#237;culo esquerdo</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>Estrutura</td>
                  <td align="center">Via de entrada, regi&#227;o trabeculada, infund&#237;bulo.</td>
                  <td align="center">N&#227;o tem infund&#237;bulo, e a trabecula&#231;&#227;o &#233; limitada.</td>
                </tr>
                <tr>
                  <td>Forma</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>V&#225;rias bandas musculares</p>
                      </list-item>
                      <list-item>
                        <p>Triangular no plano coronal</p>
                      </list-item>
                      <list-item>
                        <p>Crescente no plano transversal</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">El&#237;ptica</td>
                </tr>
                <tr>
                  <td>Orienta&#231;&#227;o predominante das fibras mioc&#225;rdicas</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>Subepic&#225;rdio: circunferencial</p>
                      </list-item>
                      <list-item>
                        <p>Subendoc&#225;rdio: longitudinal</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>Subepic&#225;rdio: obl&#237;qua</p>
                      </list-item>
                      <list-item>
                        <p>Mesoc&#225;rdio: circunferencial</p>
                      </list-item>
                      <list-item>
                        <p>Subendoc&#225;rdio: longitudinal</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Disposi&#231;&#227;o das fibras na parede livre</td>
                  <td align="center">Predom&#237;nio transversalmente</td>
                  <td align="center">Predom&#237;nio obliquamente</td>
                </tr>
                <tr>
                  <td>Disposi&#231;&#227;o das fibras no SIV</td>
                  <td align="center">Obliquamente com extens&#227;o para a via de sa&#237;da</td>
                  <td align="center">Obliquamente</td>
                </tr>
                <tr>
                  <td>Contribui&#231;&#227;o do espessamento do SIV no eixo transversal e encurtamento no eixo longitudinal na s&#237;stole</td>
                  <td align="center">+++</td>
                  <td align="center">+++</td>
                </tr>
                <tr>
                  <td>Padr&#227;o de contra&#231;&#227;o</td>
                  <td align="center">Principalmente longitudinal da base para o &#225;pex</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>Subepic&#225;rdio e subendoc&#225;rdio: encurtamento longitudinal em dire&#231;&#245;es opostas</p>
                      </list-item>
                      <list-item>
                        <p>Mesoc&#225;rdio: dire&#231;&#227;o circunferencial</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Massa (g/m<sup>2</sup>)</td>
                  <td align="center">26 &#177; 5</td>
                  <td align="center">87 &#177; 12</td>
                </tr>
                <tr>
                  <td>Espessura da parede (mm)</td>
                  <td align="center">2 a 5</td>
                  <td align="center">7 a 11</td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>SIV: septo interventricular.</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
        <p>As fun&#231;&#245;es do VE e VD est&#227;o intimamente relacionadas, fen&#244;meno chamado de intera&#231;&#227;o ventricular sist&#243;lica, pois compartilham fibras musculares dispostas obliquamente no SIV. Elas t&#234;m vantagens mec&#226;nicas sobre as fibras transversais da parede livre do VD.<sup><xref ref-type="bibr" rid="B36">36</xref></sup> A continuidade dessas fibras musculares permite que a parede livre do VD seja tracionada quando ocorre a contra&#231;&#227;o do VE<italic>,</italic> sendo estimado que 20 a 40% do volume sist&#243;lico ejetado e da press&#227;o sist&#243;lica do VD resultem da contra&#231;&#227;o do VE.<sup><xref ref-type="bibr" rid="B318">318</xref>,<xref ref-type="bibr" rid="B319">319</xref></sup></p>
      </sec>
      <sec>
        <title>13.3. Ventr&#237;culo Direito e Par&#226;metros Ecocardiogr&#225;ficos na Avalia&#231;&#227;o da Fun&#231;&#227;o Sist&#243;lica</title>
        <p>Na avalia&#231;&#227;o da fun&#231;&#227;o sist&#243;lica do VD, v&#225;rios &#237;ndices s&#227;o utilizados rotineiramente como a mudan&#231;a fracional da &#225;rea (FAC), a excurs&#227;o sist&#243;lica do anel tric&#250;spide (TAPSE), a velocidade de pico sist&#243;lico do anel tric&#250;spide e o &#237;ndice de <italic>performance</italic> mioc&#225;rdica. Cada um deles tem vantagens e limita&#231;&#245;es, vari&#225;vel exequibilidade e reprodutibilidade, com discut&#237;vel efic&#225;cia diagn&#243;stica e progn&#243;stica.<sup><xref ref-type="bibr" rid="B35">35</xref>,<xref ref-type="bibr" rid="B36">36</xref></sup> Acredita-se que, no momento, nenhum deles seja, isoladamente, um bom indicador da fun&#231;&#227;o sist&#243;lica do VD. Uma vez que o vetor da contra&#231;&#227;o longitudinal &#233; o mais importante, pela orienta&#231;&#227;o das fibras musculares longitudinais predominantes do anel tric&#250;spide ao &#225;pex, d&#225;-se prefer&#234;ncia aos &#237;ndices que exploram a movimenta&#231;&#227;o no eixo longitudinal na avalia&#231;&#227;o da fun&#231;&#227;o longitudinal regional ou global do VD.<sup><xref ref-type="bibr" rid="B92">92</xref></sup></p>
        <p>A ecocardiografia 2DST &#233; uma modalidade de imagem que avalia a deforma&#231;&#227;o mioc&#225;rdica, propriedade intr&#237;nseca do mioc&#225;rdio, nas tr&#234;s dire&#231;&#245;es (longitudinal, circunferencial e radial), sendo a longitudinal a mais utilizada por sua boa reprodutibilidade, relevante informa&#231;&#227;o progn&#243;stica, valida&#231;&#227;o em estudo experimental<sup><xref ref-type="bibr" rid="B75">75</xref></sup> e em estudos cl&#237;nicos com RMC em v&#225;rias doen&#231;as CV.<sup><xref ref-type="bibr" rid="B320">320</xref>-<xref ref-type="bibr" rid="B323">323</xref></sup></p>
        <p>Assim<italic>,</italic> o 2DST do VD tem se mostrado um bom marcador da fun&#231;&#227;o sist&#243;lica, com valor progn&#243;stico em v&#225;rias doen&#231;as CV.<sup><xref ref-type="bibr" rid="B75">75</xref>,<xref ref-type="bibr" rid="B324">324</xref>-<xref ref-type="bibr" rid="B330">330</xref></sup></p>
      </sec>
      <sec>
        <title>13.4. Aquisi&#231;&#227;o e Limita&#231;&#245;es</title>
        <p>O SLGVD pelo 2DST deve ser obtido atrav&#233;s da janela apical 4 c&#226;maras modificada, focada no VD, com o transdutor deslocado mais lateralmente e direcionado para o ombro direito, o que permite a melhor visibiliza&#231;&#227;o da parede livre e reprodutibilidade das medidas (<xref ref-type="fig" rid="f22">Figura 13.1</xref>). &#201; importante otimizar a orienta&#231;&#227;o, a profundidade e o ganho e, com isso, maximizar o tamanho do VD e visualizar o seu &#225;pice durante todo o ciclo card&#237;aco.<sup><xref ref-type="bibr" rid="B36">36</xref></sup> Um outro cuidado na aquisi&#231;&#227;o &#233; n&#227;o anteriorizar ou posteriorizar o transdutor, evitando, respectivamente, o aparecimento da valva a&#243;rtica ou do seio coron&#225;rio, exibindo apenas o septo interatrial.<sup><xref ref-type="bibr" rid="B331">331</xref></sup> Uma vez que a visualiza&#231;&#227;o adequada for obtida, recomenda-se ajustar o aparelho para gravar tr&#234;s ciclos card&#237;acos e adquirir imagens com uma resolu&#231;&#227;o temporal de 50&#8211;80 quadros por segundo. Essa taxa de enquadramento pode ser obtida por ajustes indiretos, como por meio da profundidade da imagem e da abertura do feixe de ultrassom e resolu&#231;&#227;o, como tamb&#233;m por ajustes diretos permitidos pelo aparelho de ecocardiograma utilizado. Em alguns <italic>softwares</italic>, ainda se faz necess&#225;ria a defini&#231;&#227;o do in&#237;cio e do fim do tempo de eje&#231;&#227;o do VD por meio do Doppler pulsado registrado na via de sa&#237;da do VD.</p>
        <p>
          <fig id="f22">
            <label>Figura 13.1</label>
            <caption>
              <title>&#8211; Protocolo de imagem para medir a deforma&#231;&#227;o do ventr&#237;culo direito (VD) por meio da ecocardiografia speckle tracking na proje&#231;&#227;o apical 4 c&#226;maras. A) Janela apical 4 c&#226;maras (forma de aquisi&#231;&#227;o inadequada); B) Janela apical 4 c&#226;maras focada no VD (forma de aquisi&#231;&#227;o adequada). VD4CDL: strain global longitudinal do ventr&#237;culo direito; VDPLDL: strain de parede livre do ventr&#237;culo direito.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf21.tif"/></fig>
        </p>
        <p>A ROI &#233; definida pela borda endoc&#225;rdica incluindo a parede livre do VD e SIV, com o cuidado de n&#227;o incluir o peric&#225;rdio e ajustar a largura da ROI para n&#227;o ficar muito estreita, pois isso pode levar a resultados err&#244;neos. Aten&#231;&#227;o deve ser dada no posicionamento dos pontos de refer&#234;ncia basais, pois se estiver abaixo do ideal, ou seja, no lado atrial do anel tricusp&#237;deo, pode resultar em valores reduzidos da deforma&#231;&#227;o longitudinal.<sup><xref ref-type="bibr" rid="B332">332</xref></sup></p>
        <p>A ROI pode ser tra&#231;ada manualmente pelo usu&#225;rio ou gerada automaticamente. Se for gerada automaticamente, o usu&#225;rio deve ter permiss&#227;o para verificar e, eventualmente, edit&#225;-la de modo manual.<sup><xref ref-type="bibr" rid="B92">92</xref></sup> Depois de verificar a qualidade do rastreamento e sua aprova&#231;&#227;o final pelo operador, os valores de deforma&#231;&#227;o regional ser&#227;o exibidos. Pelas recomenda&#231;&#245;es atuais, o valor utilizado deve ser o maior valor modular alcan&#231;ado durante a s&#237;stole (<italic>strain</italic> de pico sist&#243;lico), sendo o tra&#231;ado do Doppler da valva pulmonar utilizado para determinar o final da di&#225;stole e da s&#237;stole.<sup><xref ref-type="bibr" rid="B92">92</xref></sup> Sempre que poss&#237;vel, deve-se utilizar um <italic>software</italic> apropriado, j&#225; que o algoritmo de detec&#231;&#227;o autom&#225;tica dos segmentos do VD reduz a necessidade de interven&#231;&#245;es por parte do operador, contribuindo, assim, para uma melhor reprodutibilidade dos resultados.</p>
        <p>A segmenta&#231;&#227;o da parede livre do VD entre o &#225;pice e a base inclui tr&#234;s segmentos (segmentos basal, m&#233;dio e apical). O SIV &#233; segmentado de maneira semelhante. O <italic>strain</italic> longitudinal da parede livre do VD (SL-PLVD) &#233; a m&#233;dia dos valores de deforma&#231;&#227;o dos seus tr&#234;s segmentos, enquanto o SLGVD &#233; a m&#233;dia dos valores do <italic>strain</italic> dos segmentos de sua parede livre e do SIV. O SL-PLVD &#233; o mais utilizado na pr&#225;tica e na pesquisa cl&#237;nica, uma vez que o SLGVD sofre interfer&#234;ncia da fun&#231;&#227;o ventricular esquerda pelo SIV, obtendo, assim, valores absolutos relativamente mais baixos.<sup><xref ref-type="bibr" rid="B333">333</xref></sup> Para fins de padroniza&#231;&#227;o, deve-se relatar como par&#226;metro padr&#227;o o SL-PLVD, sendo opcional o c&#225;lculo do SLGVD.<sup><xref ref-type="bibr" rid="B92">92</xref></sup></p>
        <p>Como limita&#231;&#245;es, al&#233;m de janelas ac&#250;sticas inadequadas, estudos experimentais e modelos matem&#225;ticos mostraram que a magnitude da deforma&#231;&#227;o mioc&#225;rdica &#233; influenciada pela frequ&#234;ncia card&#237;aca, al&#233;m da pr&#233;- e p&#243;s-carga. Com fun&#231;&#227;o sist&#243;lica preservada, estudos confirmaram que o <italic>strain</italic> pode aumentar com o aumento da pr&#233;-carga e da frequ&#234;ncia card&#237;aca e pode reduzir com o efeito contr&#225;rio dessas vari&#225;veis.<sup><xref ref-type="bibr" rid="B16">16</xref>,<xref ref-type="bibr" rid="B334">334</xref></sup></p>
      </sec>
      <sec>
        <title>13.5. Indica&#231;&#245;es/Valores de Normalidade</title>
        <p>A disfun&#231;&#227;o sist&#243;lica do VD &#233; bem estabelecida como um fator de progn&#243;stico ruim em v&#225;rias doen&#231;as CV, e o SLGVD &#233; um marcador progn&#243;stico independente nos pacientes com HP, IC, cardiopatia isqu&#234;mica e outras CMPs, assim como tem melhor correla&#231;&#227;o com a FE do VD pela RMC em compara&#231;&#227;o aos par&#226;metros tradicionais.<sup><xref ref-type="bibr" rid="B35">35</xref>,<xref ref-type="bibr" rid="B320">320</xref>-<xref ref-type="bibr" rid="B23">23</xref>,<xref ref-type="bibr" rid="B334">334</xref>-<xref ref-type="bibr" rid="B336">336</xref></sup></p>
        <p>Nos pacientes com HP, o SLGVD est&#225; diminu&#237;do, mostrando uma boa correla&#231;&#227;o com os par&#226;metros hemodin&#226;micos invasivos da <italic>performance</italic> do VD.<sup><xref ref-type="bibr" rid="B337">337</xref></sup> Al&#233;m disso, foi demonstrado que o SLGVD &#233; preditor independente de mortalidade por todas as causas e eventos relacionados &#224; HP. Com o objetivo de avaliar o valor progn&#243;stico do SLGVD nesses pacientes, uma metan&#225;lise recente mostrou que sua redu&#231;&#227;o relativa de 19% est&#225; associada a um maior risco de eventos relacionados &#224; HP, enquanto a redu&#231;&#227;o relativa de 22% do SLGVD est&#225; associada a um maior risco de morte por todas as causas.<sup><xref ref-type="bibr" rid="B324">324</xref></sup> A <xref ref-type="fig" rid="f23">Figura 13.2</xref> mostra um exemplo de <italic>strain</italic> de VD em um paciente com HP prim&#225;ria de longa data.</p>
        <p>
          <fig id="f23">
            <label>Figura 13.2</label>
            <caption>
              <title>&#8211; Exemplo de strain de ventr&#237;culo direito em paciente com hipertens&#227;o pulmonar prim&#225;ria de longa data. Software Tomtec. VD4CDL: strain global longitudinal do ventr&#237;culo direito; VDPLDL: strain de parede livre do ventr&#237;culo direito.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf22.tif"/></fig>
        </p>
        <p>Em pacientes com IC, o SLGVD tem elevada sensibilidade e acur&#225;cia no diagn&#243;stico da disfun&#231;&#227;o sist&#243;lica dessa c&#226;mara card&#237;aca.<sup><xref ref-type="bibr" rid="B338">338</xref></sup> Uma publica&#231;&#227;o recente evidenciou que valores absolutos &lt; 14,8% est&#227;o associados a eventos adversos como morte, transplante card&#237;aco e hospitaliza&#231;&#227;o, independentemente da FEVE e DD do VE.<sup><xref ref-type="bibr" rid="B19">19</xref></sup> Al&#233;m disso, o SLGVD e o SL-PLVD foram capazes de detectar anormalidades sutis da fun&#231;&#227;o sist&#243;lica do VD em pacientes com IC e FEVE reduzida e em menor grau nos com IC e FEVE preservada.<sup><xref ref-type="bibr" rid="B329">329</xref></sup> Quanto aos pacientes eleg&#237;veis para o implante de dispositivo de assist&#234;ncia ventricular esquerda, o SLGVD &#233; uma ferramenta &#250;til na estratifica&#231;&#227;o de risco de fal&#234;ncia do VD. Com uma sensibilidade de 68% e uma especificidade de 76%, o valor absoluto de SLGVD &lt; 9,6% foi capaz de identificar os pacientes que evolu&#237;ram com fal&#234;ncia do VD p&#243;s-procedimento, definida como necessidade de dispositivo de assist&#234;ncia ventricular direita ou uso de inotr&#243;picos por mais de 14 dias.<sup><xref ref-type="bibr" rid="B339">339</xref></sup> J&#225; em transplantados card&#237;acos, a combina&#231;&#227;o das medidas do SLGVE e o SL-PLVD pode ser &#250;til para excluir rejei&#231;&#227;o celular aguda e reduzir o n&#250;mero de bi&#243;psias de rotina.<sup><xref ref-type="bibr" rid="B340">340</xref></sup> As <xref ref-type="fig" rid="f24">Figuras 13.3</xref> e <xref ref-type="fig" rid="f25">13.4</xref> mostram exemplos de <italic>strain</italic> de VD em paciente com dispositivo de assist&#234;ncia ventricular e em paciente transplantado card&#237;aco, respectivamente.</p>
        <p>
          <fig id="f24">
            <label>Figura 13.3</label>
            <caption>
              <title>&#8211; Exemplo de strain de ventr&#237;culo direito em paciente em uso de dispositivo de assist&#234;ncia ventricular. Software Echopac GE. SLG: strain de parede livre do ventr&#237;culo direito.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf23.tif"/></fig>
        </p>
        <p>
          <fig id="f25">
            <label>Figura 13.4</label>
            <caption>
              <title>&#8211; Exemplo de strain de ventr&#237;culo direito em paciente transplantado card&#237;aco. Software Tomtec. RV4CDL: strain global longitudinal do ventr&#237;culo direito; RVFWSL: strain de parede livre do ventr&#237;culo direito.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf24.tif"/></fig>
        </p>
        <p>No IAM, o SLGVD &#233; o par&#226;metro ecocardiogr&#225;fico que tem melhor correla&#231;&#227;o com a fra&#231;&#227;o de eje&#231;&#227;o do ventr&#237;culo direito (FEVD) obtida pela RMC.<sup><xref ref-type="bibr" rid="B341">341</xref></sup> Somado a isso, esse par&#226;metro demonstrou ser preditor independente de morte, reinfarto e hospitaliza&#231;&#227;o por IC, confirmando seu papel fundamental na avalia&#231;&#227;o dessa popula&#231;&#227;o.<sup><xref ref-type="bibr" rid="B342">342</xref></sup>A avalia&#231;&#227;o de pacientes com displasia arritmog&#234;nica do VD &#233; discutida em outra sess&#227;o.</p>
        <p>Recentemente, o papel da disfun&#231;&#227;o sist&#243;lica do VD tem sido investigado em outras CMPs. Na CMPH, foram descritos valores de SLGVD reduzidos em rela&#231;&#227;o a um grupo-controle saud&#225;vel,<sup><xref ref-type="bibr" rid="B343">343</xref></sup> e tamb&#233;m diferenciou pacientes com CMPH e hipertrofia secund&#225;ria &#224; hipertens&#227;o, com alta sensibilidade e especificidade.<sup><xref ref-type="bibr" rid="B344">344</xref></sup></p>
        <p>A estenose mitral &#233; a doen&#231;a valvar card&#237;aca que mais acomete o VD, com altera&#231;&#227;o frequente dos par&#226;metros convencionais da sua avalia&#231;&#227;o. O SLGVD demonstra um padr&#227;o de altera&#231;&#227;o segmentar, com valores significativamente menores no SIV e na parede livre basal do VD e valores normais na parede livre m&#233;dia e apical.<sup><xref ref-type="bibr" rid="B345">345</xref>,<xref ref-type="bibr" rid="B346">346</xref></sup> Em pacientes com insufici&#234;ncia tric&#250;spide funcional importante, o SL-PLVD identificou, em maior propor&#231;&#227;o, os pacientes com disfun&#231;&#227;o do VD (84,9%) em compara&#231;&#227;o &#224; FAC (48,5%) e &#224; TAPSE (71,7%). Al&#233;m disso, o SL<italic>-</italic>PLVD esteve associado de maneira independente com a mortalidade por todas as causas e teve um valor progn&#243;stico incremental quando associado aos par&#226;metros tradicionais de avalia&#231;&#227;o do VD.<sup><xref ref-type="bibr" rid="B328">328</xref></sup></p>
        <p>Atualmente, falta um consenso em rela&#231;&#227;o aos valores normais de <italic>strain</italic> do VD devido &#224; escassez de estudos nessa &#225;rea. O &#250;ltimo documento de recomenda&#231;&#245;es para quantifica&#231;&#227;o das c&#226;maras card&#237;acas pela ecocardiografia em adultos da Sociedade Americana de Ecocardiografia e da Associa&#231;&#227;o Europeia de Imagem Cardiovascular sugere que valores, tanto do SLGVD quanto do SL-PLVD<italic>,</italic> inferiores a 20% sejam considerados como anormais.<sup><xref ref-type="bibr" rid="B35">35</xref></sup> No entanto, &#233; preciso cautela, pois os diferentes tipos de aparelho trazem <italic>softwares</italic> diferentes, com valores de refer&#234;ncia particulares e diferen&#231;as quanto ao n&#237;vel de mapeamento (endoc&#225;rdico, epic&#225;rdico ou abrangendo toda a parede mioc&#225;rdica).</p>
        <p>A <xref ref-type="table" rid="t22">Tabela 13.2</xref> resume as principais recomenda&#231;&#245;es da utiliza&#231;&#227;o do SLG na avalia&#231;&#227;o do VD.</p>
        <p>
          <table-wrap id="t22">
            <label>Tabela 13.2</label>
            <caption>
              <title>&#8211; Indica&#231;&#245;es da utiliza&#231;&#227;o do <italic>strain</italic> longitudinal global na avalia&#231;&#227;o do ventr&#237;culo direito</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="100%">
                <col/>
              </colgroup>
              <tbody>
                <tr>
                  <td align="left">
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Hipertens&#227;o pulmonar (incluindo pacientes com embolia pulmonar aguda ou cr&#244;nica)</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Insufici&#234;ncia card&#237;aca com fra&#231;&#227;o de eje&#231;&#227;o reduzida ou preservada</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Infarto agudo do mioc&#225;rdio</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Cardiomiopatias (DAVD, CMPH, CMD)</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Valvopatias (estenose mitral, insufici&#234;ncia tric&#250;spide funcional)</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Candidatos a implante de dispositivo de assist&#234;ncia ventricular</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Transplante card&#237;aco</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>CMPH: cardiomiopatia hipertr&#243;fica; CMD: Cardiomiopatia dilatada; DAVD: displasia arritmog&#234;nica de ventr&#237;culo direito.</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
      </sec>
    </sec>
    <sec>
      <title>14. <italic>Strain</italic> do &#193;trio Esquerdo e do &#193;trio Direito</title>
      <sec>
        <title>14.1. T&#233;cnica de Obten&#231;&#227;o e An&#225;lise do strain do &#193;trio Esquerdo</title>
        <p>A an&#225;lise da fun&#231;&#227;o do AE usando o <italic>strain</italic> permite que os tr&#234;s componentes da fun&#231;&#227;o do AE sejam analisados: AESr, que avalia a fun&#231;&#227;o reservat&#243;rio; AEScd, que avalia a fun&#231;&#227;o de conduto; e o AESct, que avalia a fun&#231;&#227;o contr&#225;til. Embora menos utilizada, tamb&#233;m h&#225; a taxa de deforma&#231;&#227;o ou <italic>strain rate</italic>, descrita como pAESRr (pico <italic>strain rate</italic> na fase reservat&#243;rio), pAESRcd (pico de <italic>strain rate</italic> na fase de conduto) e pAESRct (pico de <italic>strain rate</italic> durante contra&#231;&#227;o atrial).<sup><xref ref-type="bibr" rid="B92">92</xref>,<xref ref-type="bibr" rid="B347">347</xref></sup></p>
        <p>Para a an&#225;lise do <italic>strain</italic> do AE, usam-se imagens apicais 4 c&#226;maras e 2 c&#226;maras otimizadas para o AE e com frequ&#234;ncia de quadros alta, habitualmente entre 40 e 80 fps. Seleciona-se um ciclo card&#237;aco espec&#237;fico e faz-se manualmente o tra&#231;ado ponto a ponto a partir da borda endoc&#225;rdica do anel mitral at&#233; o anel mitral oposto, extrapolando-se a entrada das veias pulmonares e do ap&#234;ndice atrial esquerdo. O <italic>software</italic> cria a ROI, a qual &#233; ajustada para 03 mm de largura e deve cobrir da borda endoc&#225;rdica at&#233; a epic&#225;rdica. Caso a qualidade do <italic>tracking</italic> seja reprovada em dois ou mais segmentos, mesmo ap&#243;s ajuste manual, deve-se excluir essa incid&#234;ncia da an&#225;lise. Finalmente, o <italic>software</italic> calcula o SLG para cada uma das janelas apicais citadas acima.</p>
        <p>Na an&#225;lise do <italic>strain</italic> do AE, h&#225; dois m&#233;todos diferentes como ponto de refer&#234;ncia ou zero: o in&#237;cio da onda P do ECG<sup><xref ref-type="bibr" rid="B2">2</xref></sup> ou o pico da onda R do QRS.<sup><xref ref-type="bibr" rid="B348">348</xref></sup> O primeiro m&#233;todo permite o reconhecimento mais f&#225;cil dos componentes do <italic>strain</italic> do AE, sendo necess&#225;ria a soma dos valores absolutos de AEScd e AESct, para se obter o AESr. O segundo m&#233;todo oferece diretamente o valor do AESr, que &#233; o dado com maior valor progn&#243;stico, sendo que os demais componentes s&#227;o obtidos a partir do gr&#225;fico. O m&#233;todo que usa a onda R como refer&#234;ncia &#233; o mais recomendado, porque esse &#233; o ponto de menor volume do AE, sendo o AESr mais facilmente obtido. A maior parte dos trabalhos usa esse m&#233;todo.<sup><xref ref-type="bibr" rid="B92">92</xref></sup></p>
      </sec>
      <sec>
        <title>14.2. Valores de Normalidade</title>
        <p>O <italic>strain</italic> do AE apresenta grande heterogeneidade na literatura quanto aos valores de normalidade. A metan&#225;lise realizada por Pathan et al<italic>.</italic> &#233; a melhor evid&#234;ncia no momento: os valores m&#233;dios do AESr, AEScd e AESct foram, respectivamente: 39,4% (IC95% 38%&#8211;40,8%); 23% (IC95% 20,7%&#8211;25,2%) e 17,4% (IC95% 16,0%&#8211;19,0%).<sup><xref ref-type="bibr" rid="B37">37</xref></sup></p>
      </sec>
      <sec>
        <title>14.3. Aplicabilidade Cl&#237;nica do <italic>Strain</italic> do &#193;trio Esquerdo</title>
        <p>A avalia&#231;&#227;o do <italic>strain</italic> do AE demonstrou valor progn&#243;stico incremental em diversos contextos cl&#237;nicos, quando comparada &#224; mensura&#231;&#227;o volum&#233;trica isolada<sup><xref ref-type="bibr" rid="B349">349</xref></sup> (<xref ref-type="fig" rid="f26">Figura 14.1</xref>).</p>
        <p>
          <fig id="f26">
            <label>Figura 14.1</label>
            <caption>
              <title>&#8211; Mecanismos envolvidos na disfun&#231;&#227;o atrial esquerda avaliada pelo strain.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf25.tif"/></fig>
        </p>
        <sec>
          <title>14.3.1. Insufici&#234;ncia Card&#237;aca e Avalia&#231;&#227;o de Fun&#231;&#227;o Diast&#243;lica</title>
          <p>O <italic>strain</italic> do AE est&#225; deprimido na ICFEr e possui valor progn&#243;stico para previs&#227;o de morte por todas as causas ou de nova interna&#231;&#227;o por IC,<sup><xref ref-type="bibr" rid="B350">350</xref></sup> boa correla&#231;&#227;o com capacidade funcional<sup><xref ref-type="bibr" rid="B351">351</xref></sup> e press&#245;es de enchimento do VE,<sup><xref ref-type="bibr" rid="B352">352</xref></sup> al&#233;m de ser bom preditor de resposta &#224; terapia de ressincroniza&#231;&#227;o mioc&#225;rdica.<sup><xref ref-type="bibr" rid="B353">353</xref></sup> Na ICFEp, o <italic>strain</italic> do AE apresenta importante papel no diagn&#243;stico <sup><xref ref-type="bibr" rid="B354">354</xref></sup> e progn&#243;stico,<sup><xref ref-type="bibr" rid="B73">73</xref>,<xref ref-type="bibr" rid="B355">355</xref></sup> al&#233;m de ser capaz de predizer o risco de evolu&#231;&#227;o para FA.<sup><xref ref-type="bibr" rid="B98">98</xref></sup></p>
          <p>Cerca de 20% dos casos de ICFEp podem ter padr&#227;o indeterminado na avalia&#231;&#227;o da fun&#231;&#227;o diast&#243;lica do VE,<sup><xref ref-type="bibr" rid="B93">93</xref></sup> e o <italic>strain</italic> do AE &#233; capaz de recategorizar esses pacientes,<sup><xref ref-type="bibr" rid="B90">90</xref></sup> sendo que os tr&#234;s componentes da fun&#231;&#227;o atrial demonstraram boa acur&#225;cia em determinar aumento da press&#227;o atrial esquerda.<sup><xref ref-type="bibr" rid="B89">89</xref></sup></p>
        </sec>
        <sec>
          <title>14.3.2. Fibrila&#231;&#227;o Atrial</title>
          <p>Na FA, as fun&#231;&#245;es de reservat&#243;rio e conduto do AE est&#227;o deprimidas e a contr&#225;til &#233; ausente. O <italic>strain</italic> do AE &#233; capaz de prever FA nova em diversas patologias como ICFEr,<sup><xref ref-type="bibr" rid="B356">356</xref></sup> estenose mitral,<sup><xref ref-type="bibr" rid="B357">357</xref></sup> doen&#231;a de Chagas<sup><xref ref-type="bibr" rid="B358">358</xref></sup> e ap&#243;s implante de marca-passo,<sup><xref ref-type="bibr" rid="B359">359</xref></sup> al&#233;m de prever o risco de recorr&#234;ncia de FA ap&#243;s cardiovers&#227;o<sup><xref ref-type="bibr" rid="B360">360</xref></sup> ou abla&#231;&#227;o.<sup><xref ref-type="bibr" rid="B361">361</xref>-<xref ref-type="bibr" rid="B363">363</xref></sup> &#201; poss&#237;vel que a avalia&#231;&#227;o da fun&#231;&#227;o do AE pelo <italic>strain</italic> seja incorporada no processo decis&#243;rio da indica&#231;&#227;o de abla&#231;&#227;o de FA. O AESr tamb&#233;m est&#225; associado com ocorr&#234;ncia de AVCi independente de CHA2DS2-VASc escore, idade e uso de anticoagulante.<sup><xref ref-type="bibr" rid="B364">364</xref></sup></p>
        </sec>
        <sec>
          <title>14.3.3. Valvopatias</title>
          <p>O <italic>strain</italic> do AE pode sinalizar maior gravidade e evolu&#231;&#227;o desfavor&#225;vel na valvopatia mitral e a&#243;rtica.<sup><xref ref-type="bibr" rid="B365">365</xref>,<xref ref-type="bibr" rid="B366">366</xref></sup> Na IM prim&#225;ria grave, o AESr demonstrou ser preditor de hospitaliza&#231;&#227;o por IC ou morte por todas as causas, independentemente das indica&#231;&#245;es de interven&#231;&#227;o cir&#250;rgica.<sup><xref ref-type="bibr" rid="B367">367</xref>,<xref ref-type="bibr" rid="B368">368</xref></sup></p>
        </sec>
        <sec>
          <title>14.3.4. Doen&#231;a Arterial Coronariana</title>
          <p>A DAC associa-se &#224; disfun&#231;&#227;o atrial por dois mecanismos principais: DD do VE e isquemia direta do AE.<sup><xref ref-type="bibr" rid="B369">369</xref></sup> O <italic>strain</italic> do AE pode ter importante valor progn&#243;stico na s&#237;ndrome coronariana aguda, correlacionando-se com maior gravidade<sup><xref ref-type="bibr" rid="B370">370</xref></sup> e desfechos desfavor&#225;veis.<sup><xref ref-type="bibr" rid="B371">371</xref></sup></p>
        </sec>
      </sec>
    </sec>
    <sec>
      <title>14.4. <italic>Strain</italic> Atrial Direito</title>
      <p>O <italic>strain</italic> do AD carece de dados, mas um estudo recente avaliou 101 volunt&#225;rios saud&#225;veis e descreveu os seguintes valores utilizando o complexo QRS como refer&#234;ncia: reservat&#243;rio (37,6% &#177; 6,9), conduto (26,0% &#177; 7,1) e contra&#231;&#227;o (11,6% &#177; 4,4).<sup><xref ref-type="bibr" rid="B372">372</xref></sup> A avalia&#231;&#227;o da fun&#231;&#227;o do AD &#233; alvo de interesse em cardiopatias cong&#234;nitas,<sup><xref ref-type="bibr" rid="B301">301</xref>,<xref ref-type="bibr" rid="B373">373</xref></sup> valvopatia tric&#250;spide e HP.<sup><xref ref-type="bibr" rid="B374">374</xref></sup></p>
    </sec>
    <sec>
      <title>15. Avalia&#231;&#227;o da Tor&#231;&#227;o do Ventr&#237;culo Esquerdo</title>
      <sec>
        <title>15.1. Introdu&#231;&#227;o</title>
        <p>A fun&#231;&#227;o do VE &#233; determinada pelas intera&#231;&#245;es complexas entre a anatomia do tecido, a contratilidade mioc&#225;rdica e hemodin&#226;mica. No mioc&#225;rdio do VE, as fibras musculares possuem dire&#231;&#245;es diferentes. Na regi&#227;o subendoc&#225;rdica, as fibras s&#227;o quase paralelas &#224; parede e produzem um movimento de rota&#231;&#227;o do tipo direito (h&#233;lice de m&#227;o direita), o que gradualmente muda no subepic&#225;rdico para fibras anguladas a 60&#8211;70 graus, promovendo uma rota&#231;&#227;o do tipo esquerda (h&#233;lice de m&#227;o esquerda).<sup><xref ref-type="bibr" rid="B375">375</xref>,<xref ref-type="bibr" rid="B376">376</xref></sup></p>
        <p>A contra&#231;&#227;o das fibras subepic&#225;rdicas faz com que o &#225;pice do VE gire no sentido anti-hor&#225;rio e a sua base no sentido hor&#225;rio. Por outro lado, a contra&#231;&#227;o das fibras subendoc&#225;rdicas faz o &#225;pice e a base do VE girarem exatamente nas dire&#231;&#245;es opostas. Dado ao maior raio de rota&#231;&#227;o da camada epic&#225;rdica, a dire&#231;&#227;o das fibras subepic&#225;rdicas prevalece na dire&#231;&#227;o geral de rota&#231;&#227;o quando ambas as camadas se contraem simultaneamente. Isso resulta em rota&#231;&#227;o global do VE no sentido anti-hor&#225;rio pr&#243;xima ao &#225;pice e na rota&#231;&#227;o no sentido hor&#225;rio pr&#243;xima &#224; base do VE durante a eje&#231;&#227;o ventricular,<sup><xref ref-type="bibr" rid="B377">377</xref></sup> como ilustrado na <xref ref-type="fig" rid="f27">Figura 15.1</xref>.</p>
        <p>
          <fig id="f27">
            <label>Figura 15.1</label>
            <caption>
              <title>&#8211; Dire&#231;&#227;o da rota&#231;&#227;o das fibras subendoc&#225;rdicas (A); dire&#231;&#227;o da rota&#231;&#227;o das fibras subepic&#225;rdicas (B); e rota&#231;&#227;o resultante geral do ventr&#237;culo esquerdo com a contra&#231;&#227;o simult&#226;nea das fibras (C). Adaptado de St&#246;hr et al.<italic>384</italic></title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf26.tif"/></fig>
        </p>
        <p>Esse movimento de tor&#231;&#227;o do VE contribui para manter uma distribui&#231;&#227;o uniforme do encurtamento e do estresse das fibras ao longo de todas as paredes, produzindo, assim, uma FE relativamente elevada (~60%), a despeito de encurtamento limitado (~20%).<sup><xref ref-type="bibr" rid="B378">378</xref></sup> A tor&#231;&#227;o e o cisalhamento das fibras subendoc&#225;rdicas durante a eje&#231;&#227;o ventricular resultam no armazenamento de energia potencial, que &#233; subsequentemente usada para o desenrolar diast&#243;lico das fibras e, assim, destorcer as h&#233;lices, produzindo juntos a suc&#231;&#227;o diast&#243;lica.<sup><xref ref-type="bibr" rid="B379">379</xref>,<xref ref-type="bibr" rid="B380">380</xref></sup> As condi&#231;&#245;es de pr&#233;- e p&#243;s-carga e contratilidade alteram a extens&#227;o da tor&#231;&#227;o ventricular.<sup><xref ref-type="bibr" rid="B381">381</xref></sup> O aumento da pr&#233;-carga ou da contratilidade aumentam a tor&#231;&#227;o do VE, enquanto o aumento na p&#243;s-carga causa efeito inverso.</p>
        <p>V&#225;rias modalidades e t&#233;cnicas de imagem podem ser usadas para quantificar a mec&#226;nica da tor&#231;&#227;o ventricular: ecocardiografia (Doppler tecidual, ST2D e ST3D, imagem de velocidade vetorial [VVI]), RMC (<italic>tissue tagging</italic>) e sonomicrometria. Atualmente, n&#227;o existe um padr&#227;o-ouro para a avalia&#231;&#227;o da mec&#226;nica de tor&#231;&#227;o do VE, tendo as modalidades de imagem listadas acima boa concord&#226;ncia.<sup><xref ref-type="bibr" rid="B382">382</xref></sup> Devido &#224; sua seguran&#231;a, disponibilidade e melhor custo/efetividade, a ecocardiografia tem sido a modalidade de imagem mais empregada.</p>
      </sec>
      <sec>
        <title>15.2. Defini&#231;&#245;es e Nomenclaturas</title>
        <p>Tor&#231;&#227;o, <italic>twist, twist rate, untwist, untwist rate</italic> s&#227;o as terminologias comumente utilizadas para descrever os achados da rota&#231;&#227;o sist&#243;lica e a rota&#231;&#227;o diast&#243;lica reversa da base e do &#225;pice do VE, como vistos pelo &#225;pex. As defini&#231;&#245;es desses termos podem ser encontradas nas <xref ref-type="table" rid="t23">Tabelas 15.1</xref> e <xref ref-type="table" rid="t24">15.2</xref>.</p>
        <p>
          <table-wrap id="t23">
            <label>Tabela 15.1</label>
            <caption>
              <title>&#8211; Defini&#231;&#245;es e par&#226;metros utilizados para avalia&#231;&#227;o do mecanismo de <italic>twist</italic> do ventr&#237;culo esquerdo na s&#237;stole</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="50%">
                <col/>
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left">Par&#226;metro</th>
                  <th align="left">Defini&#231;&#227;o</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>Rota&#231;&#227;o apical (&#186;)</td>
                  <td>Pico da rota&#231;&#227;o sist&#243;lica no sentido anti-hor&#225;rio da regi&#227;o apical do VE (medido em graus)</td>
                </tr>
                <tr>
                  <td>Taxa de rota&#231;&#227;o apical (&#186;/s)</td>
                  <td>Pico de velocidade de rota&#231;&#227;o apical no sentido anti-hor&#225;rio (medido em graus/segundo)</td>
                </tr>
                <tr>
                  <td>Rota&#231;&#227;o basal (&#186;)</td>
                  <td>Pico da rota&#231;&#227;o sist&#243;lica no sentido hor&#225;rio da regi&#227;o basal do VE (medido em graus)</td>
                </tr>
                <tr>
                  <td>Taxa de rota&#231;&#227;o basal (&#186;/s)</td>
                  <td>Pico de velocidade de rota&#231;&#227;o basal no sentido hor&#225;rio (medido em graus/segundo)</td>
                </tr>
                <tr>
                  <td><italic>Twist</italic> VE (&#186;)</td>
                  <td>Diferen&#231;a do pico das rota&#231;&#245;es sist&#243;licas do &#225;pice e da base do VE (medido em graus)</td>
                </tr>
                <tr>
                  <td>Tor&#231;&#227;o do VE (&#186;/cm)</td>
                  <td><italic>Twist</italic> normalizado: raz&#227;o do &#226;ngulo do twist pela dist&#226;ncia entre a base e o &#225;pice na s&#237;stole (medido em graus/cent&#237;metro)</td>
                </tr>
                <tr>
                  <td><italic>Twist</italic> rate (&#186;/s)</td>
                  <td>Velocidade de pico do <italic>twist</italic> do VE (medido em graus/segundo)</td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>(o): graus; (o/s): graus por segundo; (&#186;/cm): graus por cent&#237;metro; VE: ventr&#237;culo esquerdo.</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
        <p>
          <table-wrap id="t24">
            <label>Tabela 15.2</label>
            <caption>
              <title>&#8211; Defini&#231;&#245;es e par&#226;metros utilizados para avalia&#231;&#227;o do mecanismo de twist do ventr&#237;culo esquerdo na di&#225;stole</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="50%">
                <col/>
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left">Par&#226;metro</th>
                  <th align="left">Defini&#231;&#227;o</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>Rota&#231;&#227;o reversa apical (&#186;)</td>
                  <td>Pico da rota&#231;&#227;o diast&#243;lica no sentido hor&#225;rio da regi&#227;o apical do VE (medido em graus)</td>
                </tr>
                <tr>
                  <td>Taxa de rota&#231;&#227;o reversa apical (&#186;/s)</td>
                  <td>Pico de velocidade da rota&#231;&#227;o reversa apical no sentido hor&#225;rio (medido em graus/segundo)</td>
                </tr>
                <tr>
                  <td>Rota&#231;&#227;o reversa basal (&#186;)</td>
                  <td>Pico da rota&#231;&#227;o diast&#243;lica no sentido anti-hor&#225;rio da regi&#227;o basal do VE (medido em graus)</td>
                </tr>
                <tr>
                  <td>Taxa de rota&#231;&#227;o reversa basal (&#186;/s)</td>
                  <td>Pico de velocidade da rota&#231;&#227;o basal (medido em graus/segundo)</td>
                </tr>
                <tr>
                  <td><italic>Untwist</italic> (&#186;)</td>
                  <td>Diferen&#231;a do pico das rota&#231;&#245;es diast&#243;licas reversas do &#225;pice e da base do VE (medido em graus)</td>
                </tr>
                <tr>
                  <td><italic>Untwist</italic> rate (&#186;/s)</td>
                  <td>Velocidade de pico do untwist do VE (medido em graus/segundo)</td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>(o): graus; (o/s): graus por segundo; VE: ventr&#237;culo esquerdo.</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
      </sec>
      <sec>
        <title>15.3. Passo a Passo da Avalia&#231;&#227;o da Tor&#231;&#227;o Ventricular pelo Ecocardiograma com <italic>Speckle Tracking</italic></title>
        <p>Para avalia&#231;&#227;o do mecanismo de rota&#231;&#227;o, s&#227;o obtidas imagens paraesternais do eixo curto do VE ao n&#237;vel basal (valva mitral) e apical (abaixo dos m&#250;sculos papilares) (<xref ref-type="fig" rid="f28">Figura 15.2</xref>). &#201; importante obter a imagem apical do VE onde n&#227;o apare&#231;a o VD ou apenas uma parte deste, em geral um a dois espa&#231;os intercostais abaixo da posi&#231;&#227;o habitual. A maioria dos erros de avalia&#231;&#227;o ocorre devido &#224; sele&#231;&#227;o inapropriada dos planos basal e apical e do ajuste da ROI.</p>
        <p>
          <fig id="f28">
            <label>Figura 15.2</label>
            <caption>
              <title>&#8211; Planos de obten&#231;&#227;o das imagens para medida da rota&#231;&#227;o basal e apical. Imagens cedidas pelo Dr. Marcio Lima.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf27.tif"/></fig>
        </p>
        <p>Por conven&#231;&#227;o, quando a rota&#231;&#227;o &#233; hor&#225;ria, o tra&#231;ado &#233; registrado abaixo da linha de base e, quando a rota&#231;&#227;o &#233; anti-hor&#225;ria, o tra&#231;ado &#233; inscrito acima da linha de base (<xref ref-type="fig" rid="f29">Figura 15.3</xref>).</p>
        <p>
          <fig id="f29">
            <label>Figura 15.3</label>
            <caption>
              <title>&#8211; Registro das rota&#231;&#245;es hor&#225;ria (abaixo da linha de base) e anti-hor&#225;ria (acima da linha de base). Imagens cedidas pelo Dr. Marcio Lima.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf28.tif"/></fig>
        </p>
        <p>O valor normal do <italic>twist</italic> global &#233; de 9,7&#176; &#177; 4,1&#176;. Para a tor&#231;&#227;o, h&#225; poucos valores de refer&#234;ncia na literatura, sendo estimada em 1,35&#176;/cm &#177; 0,54&#176;/cm.<sup><xref ref-type="bibr" rid="B383">383</xref></sup></p>
      </sec>
      <sec>
        <title>15.4. Aplica&#231;&#245;es Cl&#237;nicas</title>
        <p>Os par&#226;metros de tor&#231;&#227;o do VE t&#234;m sido usados principalmente para avaliar as altera&#231;&#245;es na mec&#226;nica ventricular que ocorrem em patologias com FEVE reduzida (CMP isqu&#234;mica e dilatada) ou preservada (ICFEp, hipertens&#227;o, CMPH, EA, IAo e IM), bem como na avalia&#231;&#227;o de disfun&#231;&#227;o mioc&#225;rdica subcl&#237;nica causada por quimioter&#225;picos.</p>
        <p>A medida do <italic>twist</italic> e da tor&#231;&#227;o, embora sejam bons par&#226;metros para ajudar na an&#225;lise da fun&#231;&#227;o sist&#243;lica global, tem limita&#231;&#245;es quanto &#224; reprodutibilidade, em especial devido &#224; falta de par&#226;metros anat&#244;micos para o corte apical. Os achados de altera&#231;&#245;es no <italic>twist</italic> e tor&#231;&#227;o ventricular n&#227;o s&#227;o espec&#237;ficos, mas podem contribuir para o entendimento da fisiopatologia de diferentes CMPs, auxiliando na diferencia&#231;&#227;o entre elas (<xref ref-type="table" rid="t25">Tabela 15.3</xref>).</p>
        <p>
          <table-wrap id="t25">
            <label>Tabela 15.3</label>
            <caption>
              <title>&#8211; Twist do ventr&#237;culo esquerdo em diferentes doen&#231;as cardiovasculares</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="33%">
                <col/>
                <col/>
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left">Doen&#231;a cardiovascular</th>
                  <th><italic>Twist</italic> do VE</th>
                  <th align="left">Achados</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>Cardiomiopatia isqu&#234;mica</td>
                  <td align="center">Diminu&#237;do</td>
                  <td><underline><italic>Twist</italic></underline> diminui dependendo da localiza&#231;&#227;o e extens&#227;o da isquemia.</td>
                </tr>
                <tr>
                  <td>Cardiomiopatia dilatada</td>
                  <td align="center">Diminu&#237;do</td>
                  <td>Diminui&#231;&#227;o do <italic>twist</italic> proporcional &#224; queda da fra&#231;&#227;o de eje&#231;&#227;o</td>
                </tr>
                <tr>
                  <td>Cardiomiopatia hipertr&#243;fica</td>
                  <td align="center">Aumentado</td>
                  <td>Aumento do <italic>twist</italic> em especial se houver obstru&#231;&#227;o da via de sa&#237;da do VE</td>
                </tr>
                <tr>
                  <td>Estenose a&#243;rtica</td>
                  <td align="center">Aumentado</td>
                  <td>Aumento do <italic>twist</italic> em caso de aumento da p&#243;s-carga do VE.</td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>VE: ventr&#237;culo esquerdo.</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
      </sec>
    </sec>
    <sec>
      <title>16. <italic>Strain</italic> na An&#225;lise da Dissincronia Ventricular</title>
      <sec>
        <title>16.1. Introdu&#231;&#227;o</title>
        <p>A terapia de ressincroniza&#231;&#227;o card&#237;aca (TRC) &#233; uma op&#231;&#227;o terap&#234;utica com indica&#231;&#245;es j&#225; estabelecidas em diretrizes nacionais e internacionais e redu&#231;&#227;o expressiva comprovada em morbidade e mortalidade. Ela &#233; recomendada como classe I para pacientes com CMP dilatada, sintom&#225;ticos, em tratamento cl&#237;nico otimizado, ECG com padr&#227;o de BRE, dura&#231;&#227;o do QRS &#8805; 150 ms e FEVE abaixo de 35% (n&#237;vel de evid&#234;ncia: A).<sup><xref ref-type="bibr" rid="B385">385</xref></sup></p>
        <p>Essas diretrizes empregam a presen&#231;a de BRE com dura&#231;&#227;o &#8805; 150 ms ao ECG como marcador de dissincronia devido &#224; aus&#234;ncia de evid&#234;ncias da utilidade da avalia&#231;&#227;o ecocardiogr&#225;fica da sincronia at&#233; o momento. Entretanto, o ECG tamb&#233;m apresenta limita&#231;&#245;es como marcador de dissincronia. Assim, atualmente, a avalia&#231;&#227;o ecocardiogr&#225;fica da dissincronia para a sele&#231;&#227;o da TRC deve ser realizada de maneira individualizada e criteriosa por um examinador com treinamento adequado e interpretada juntamente aos dados cl&#237;nicos do paciente. Tamb&#233;m &#233; importante lembrar que o papel da ecocardiografia engloba n&#227;o apenas a avalia&#231;&#227;o da sincronia card&#237;aca na sele&#231;&#227;o dos pacientes, mas tamb&#233;m o aux&#237;lio na escolha do melhor local para o implante do eletrodo VE, al&#233;m de avalia&#231;&#227;o da resposta e remodelamento reverso e, mais recentemente, a identifica&#231;&#227;o do risco de arritmias ventriculares.<sup><xref ref-type="bibr" rid="B385">385</xref></sup></p>
      </sec>
      <sec>
        <title>16.2. Avalia&#231;&#227;o da Dissincronia na Sele&#231;&#227;o dos Pacientes para a Terapia de Ressincroniza&#231;&#227;o Card&#237;aca</title>
        <p>A avalia&#231;&#227;o da dissincronia pelo <italic>strain</italic>, isoladamente, n&#227;o indica a TRC, nem a an&#225;lise de sua efici&#234;ncia. Entretanto, reconhece-se que, mesmo com a indica&#231;&#227;o precisa, a chance de sucesso, isto &#233;, melhora cl&#237;nica, funcional e/ou de vari&#225;veis obtidas por m&#233;todos de imagem, fica em torno de 60&#8211;70% dos casos. A taxa de resposta &#224; TRC pode ser estimada e at&#233; melhorada com o emprego da ecocardiografia. Nesse panorama, a medida de valores da deforma&#231;&#227;o mioc&#225;rdica se destaca.</p>
        <p>A an&#225;lise inicial da dissincronia pelo <italic>strain</italic> radial descreveu a diferen&#231;a de tempo entre a deforma&#231;&#227;o m&#225;xima radial dos segmentos m&#233;dios anterosseptal e inferolateral. Uma medida com valor superior a 130 ms caracteriza pacientes com maior taxa de resposta,<sup><xref ref-type="bibr" rid="B386">386</xref></sup> como mostrado na <xref ref-type="fig" rid="f30">Figura 16.1</xref>.</p>
        <p>
          <fig id="f30">
            <label>Figura 16.1</label>
            <caption>
              <title>&#8211; Imagem de strain radial com curvas dos segmentos m&#233;dios das paredes anterosseptal e inferolateral. O intervalo acima de 130 ms correlaciona-se com uma maior taxa de resposta &#224; terapia de ressincroniza&#231;&#227;o card&#237;aca; nesse caso, 340 ms.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf29.tif"/></fig>
        </p>
        <p>Al&#233;m da dissincronia radial, a identifica&#231;&#227;o de um padr&#227;o de estiramento rebote da parede septal (SRS, <italic>septal rebound stretch</italic>) pela t&#233;cnica de <italic>speckle tracking</italic> demonstrou-se um preditor independente de progn&#243;stico em longo prazo, al&#233;m de remodelamento reverso ventricular esquerdo com valor incremental &#224; presen&#231;a de BRE e de <italic>apical rocking</italic> detectada pela an&#225;lise visual. Esse padr&#227;o reflete &#224; incoordena&#231;&#227;o da contra&#231;&#227;o card&#237;aca com resultante redu&#231;&#227;o da <italic>performance</italic> mioc&#225;rdica. Assim, estudos recentes indicam que a presen&#231;a de SRS pode melhorar a sele&#231;&#227;o dos pacientes na TRC, especialmente no subgrupo de pacientes sem BRE definido.<sup><xref ref-type="bibr" rid="B387">387</xref></sup> A denomina&#231;&#227;o desse padr&#227;o cl&#225;ssico &#233; feita por meio de tr&#234;s elementos obtidos pelo padr&#227;o de deforma&#231;&#227;o longitudinal dos segmentos (frequentemente basais) inferosseptal e anterolateral: 1) oposi&#231;&#227;o de pico das curvas septal (negativa), lateral (positiva) inicialmente; 2) pico de deforma&#231;&#227;o negativa do septo em at&#233; 70% do tempo de eje&#231;&#227;o; 3) pico de deforma&#231;&#227;o negativa de parede lateral ap&#243;s fechamento da valva a&#243;rtica,<sup><xref ref-type="bibr" rid="B388">388</xref></sup> conforme demonstrado na <xref ref-type="fig" rid="f31">Figura 16.2</xref>.</p>
        <p>
          <fig id="f31">
            <label>Figura 16.2</label>
            <caption>
              <title>&#8211; Imagem do strain longitudinal com curvas dos segmentos basais inferosseptal (amarela) e anterolateral (vermelha) com padr&#227;o de bloqueio de ramo esquerdo t&#237;pico: 1) oposi&#231;&#227;o do pico das curvas septal (negativa) e lateral (positiva), inicialmente; 2) pico de deforma&#231;&#227;o negativa do septo em at&#233; 70% do tempo de eje&#231;&#227;o, com o encurtamento sendo interrompido durante a s&#237;stole, isto &#233;, antes do fechamento da valva a&#243;rtica (AVC), resultando em estiramento sist&#243;lico; 3) pico de deforma&#231;&#227;o negativa de parede lateral ap&#243;s o fechamento da valva a&#243;rtica.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf30.tif"/></fig>
        </p>
        <p>Recentemente, a an&#225;lise da efici&#234;ncia do TM global ventricular esquerdo (GLVMWE, <italic>global left ventricular myocardial work efficiency</italic>) tem se mostrado promissora no contexto da TRC. O GLVMWE pode ser quantificado de maneira n&#227;o invasiva a partir das curvas de <italic>strain</italic> mioc&#225;rdico e medidas da press&#227;o arterial. Valores reduzidos de GLVMWE estiveram associados, de maneira independente, a melhor progn&#243;stico em longo prazo.<sup><xref ref-type="bibr" rid="B389">389</xref></sup> Na <xref ref-type="fig" rid="f32">Figura 16.3</xref>, exemplificam-se as modifica&#231;&#245;es ocorridas no <italic>strain, myocardial work</italic> e <italic>myocardial efficiency</italic> em paciente submetido a TRC com sucesso.</p>
        <p>
          <fig id="f32">
            <label>Figura 16.3</label>
            <caption>
              <title>&#8211; Mapas polares comparativos pr&#233;- e p&#243;s-procedimento do strain longitudinal (A), do myocardial work (B), myocardial efficiency (C) em paciente submetido a terapia de ressincroniza&#231;&#227;o com sucesso.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf31.tif"/></fig>
        </p>
      </sec>
      <sec>
        <title>16.3. Avalia&#231;&#227;o de Viabilidade Mioc&#225;rdica</title>
        <p>Outra aplica&#231;&#227;o da deforma&#231;&#227;o mioc&#225;rdica no contexto da TRC refere-se &#224; correla&#231;&#227;o da presen&#231;a de fibrose mioc&#225;rdica com valores reduzidos de <italic>strain</italic>. Valores de <italic>strain</italic> global radial reduzidos correlacionam-se a maior grau de fibrose (detectados por RMC) e, assim, identificam pacientes com chance reduzida de recupera&#231;&#227;o da fun&#231;&#227;o ventricular. A redu&#231;&#227;o da deforma&#231;&#227;o longitudinal em pacientes com cardiopatia isqu&#234;mica tamb&#233;m pode ser empregada para essa finalidade.</p>
      </sec>
      <sec>
        <title>16.4. Orienta&#231;&#227;o do Local de Implante dos Eletrodos</title>
        <p>T&#227;o importante como a caracteriza&#231;&#227;o da fibrose total do VE, a presen&#231;a de valores comprometidos em segmentos no local de implante do eletrodo do VE tem se relacionado &#224; menor taxa de pacientes respondedores &#224; TRC.</p>
        <p>Estudos demonstram que o posicionamento do eletrodo do VE no segmento que apresenta maior atraso da contra&#231;&#227;o mec&#226;nica resulta em maiores taxas de sucesso &#224; TRC. A identifica&#231;&#227;o do segmento a ser estimulado pode ser realizada pela t&#233;cnica de <italic>speckle tracking</italic>. No estudo TARGET, o posicionamento do eletrodo do VE guiado pela t&#233;cnica de ST2D resultou em melhor resposta cl&#237;nica e menores taxas de morte e hospitaliza&#231;&#245;es por IC.<sup><xref ref-type="bibr" rid="B390">390</xref>,<xref ref-type="bibr" rid="B391">391</xref></sup></p>
      </sec>
      <sec>
        <title>16.5. Avalia&#231;&#227;o Progn&#243;stica ap&#243;s a Terapia de Ressincroniza&#231;&#227;o Card&#237;aca</title>
        <p>A an&#225;lise da dissincronia pelo <italic>strain</italic> longitudinal ap&#243;s a TRC foi um preditor forte de arritmias ventriculares. A persist&#234;ncia ou o aumento da dispers&#227;o mec&#226;nica 6 meses ap&#243;s a TRC, avaliada pelo <italic>speckle tracking,</italic> est&#225; associada a pior progn&#243;stico. Al&#233;m disso, a resposta &#224; TRC evidenciada pelo remodelamento reverso foi dependente da melhora tanto da fun&#231;&#227;o longitudinal quanto da circunferencial ap&#243;s a TRC.<sup><xref ref-type="bibr" rid="B392">392</xref></sup></p>
      </sec>
      <sec>
        <title>16.6. Ajuste nos Par&#226;metros de Ressincroniza&#231;&#227;o</title>
        <p>Cerca de 30% dos pacientes submetidos a TRC s&#227;o considerados n&#227;o respondedores devido &#224; aus&#234;ncia de melhora cl&#237;nica e/ou funcional, al&#233;m da aus&#234;ncia de remodelamento reverso evidenciada pela redu&#231;&#227;o das dimens&#245;es ventriculares e o aumento da FE.<sup><xref ref-type="bibr" rid="B393">393</xref></sup> Nesse grupo de pacientes, ajustes dos intervalos atrioventricular, interventricular e intraventricular esquerdo podem melhorar a resposta individual &#224; TRC. Alguns estudos t&#234;m demonstrado que a <italic>speckle tracking</italic> pode ser empregada como guia para ajuste dos par&#226;metros da TRC, com melhora significativa da classe funcional e da FE em pacientes n&#227;o respondedores.<sup><xref ref-type="bibr" rid="B394">394</xref></sup></p>
      </sec>
    </sec>
    <sec>
      <title>17. <italic>Myocardial Work</italic> (Trabalho Mioc&#225;rdico)</title>
      <sec>
        <title>17.1. Introdu&#231;&#227;o</title>
        <p>Uma nova ferramenta ecocardiogr&#225;fica chamada <italic>myocardial work</italic> (MW) surgiu recentemente visando incrementar informa&#231;&#245;es acerca da fun&#231;&#227;o ventricular, adicionando o efeito da p&#243;s-carga do VE &#224; medida do <italic>strain</italic> longitudinal.</p>
        <p>Com o trabalho experimental de Suga et al. em 1979,<sup><xref ref-type="bibr" rid="B395">395</xref></sup> demonstrando que a &#225;rea sob a curva press&#227;o-volume adquirida de forma invasiva com um cateter de condut&#226;ncia intraventricular refletia o trabalho mioc&#225;rdico (TM) regional e o consumo de oxig&#234;nio por batimento, crescia o interesse dos m&#233;todos de imagem em tornar essa an&#225;lise fact&#237;vel de forma n&#227;o invasiva.<sup><xref ref-type="bibr" rid="B396">396</xref>,<xref ref-type="bibr" rid="B397">397</xref></sup></p>
        <p>Russell et al.,<sup><xref ref-type="bibr" rid="B398">398</xref></sup> em 2012, validaram a al&#231;a press&#227;o-deforma&#231;&#227;o (PD) do VE obtida de forma totalmente n&#227;o invasiva, integrando a press&#227;o arterial sist&#243;lica (PAS) no momento do exame com o <italic>strain</italic> longitudinal utilizando o <italic>speckle tracking</italic>, o que gera, quando interpretadas por um <italic>software</italic> pr&#243;prio, al&#231;as PD global e por segmento (<xref ref-type="fig" rid="f33">Figura 17.1</xref>). A &#225;rea sob a curva representa o TM e obteve excelente correla&#231;&#227;o com as medidas diretas intraventriculares. Al&#233;m disso o TM foi capaz de refletir o metabolismo mioc&#225;rdico regional de oxig&#234;nio, quando comparado &#224; medida pela tomografia por emiss&#227;o de p&#243;sitrons com (18<sup>F</sup>) fluorodesoxiglicose.<sup><xref ref-type="bibr" rid="B399">399</xref>-<xref ref-type="bibr" rid="B401">401</xref></sup></p>
        <p>
          <fig id="f33">
            <label>Figura 17.1</label>
            <caption>
              <title>&#8211; Al&#231;a press&#227;o vs. deforma&#231;&#227;o do ventr&#237;culo esquerdo. Em vermelho: al&#231;a press&#227;o vs. deforma&#231;&#227;o global do ventr&#237;culo esquerdo. Em verde: al&#231;a press&#227;o-deforma&#231;&#227;o do segmento basal da parede &#237;nfero-lateral. LVP: press&#227;o do ventr&#237;culo esquerdo estimada pela press&#227;o arterial sist&#243;lica; AVO: abertura da v&#225;lvula a&#243;rtica; AVC: fechamento da v&#225;lvula a&#243;rtica; MVO: abertura da v&#225;lvula mitral; MVC: fechamento da v&#225;lvula mitral.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf32.tif"/></fig>
        </p>
        <p>Aumentos modestos na press&#227;o arterial podem gerar redu&#231;&#227;o de at&#233; 9% no SLG, podendo levar a uma err&#244;nea interpreta&#231;&#227;o de redu&#231;&#227;o de contratilidade, quando, na verdade, o TM permanece preservado, refletindo apenas uma eleva&#231;&#227;o da p&#243;s-carga. Nesse sentido, o TM &#233; considerado um avan&#231;o na compreens&#227;o da mec&#226;nica ventricular.<sup><xref ref-type="bibr" rid="B398">398</xref>,<xref ref-type="bibr" rid="B402">402</xref></sup> As principais diferen&#231;as entre o TM e o <italic>strain</italic> do VE s&#227;o demonstrados na <xref ref-type="table" rid="t26">Tabela 17.1</xref>.</p>
        <p>
          <table-wrap id="t26">
            <label>Tabela 17.1</label>
            <caption>
              <title>&#8211; Principais diferen&#231;as entre o trabalho mioc&#225;rdico e o <italic>strain</italic> do ventr&#237;culo esquerdo</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="33%">
                <col/>
                <col/>
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left" style="font-weight:normal"> </th>
                  <th>
                    <italic>Strain</italic>
                  </th>
                  <th>Trabalho mioc&#225;rdico</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>Utiliza AFI<sup>&#174;</sup></td>
                  <td align="center">Sim</td>
                  <td align="center">Sim</td>
                </tr>
                <tr>
                  <td>Medida realizada</td>
                  <td align="center">AVO-AVC</td>
                  <td align="center">TCIV+ Tej + TRIV</td>
                </tr>
                <tr>
                  <td>Integra com PA</td>
                  <td align="center">N&#227;o</td>
                  <td align="center">Sim</td>
                </tr>
                <tr>
                  <td>Valor</td>
                  <td align="center">%</td>
                  <td align="center">mmHg%</td>
                </tr>
                <tr>
                  <td>Incorpora p&#243;s carga</td>
                  <td align="center">N&#227;o</td>
                  <td align="center">Sim</td>
                </tr>
                <tr>
                  <td>Medida de efici&#234;ncia</td>
                  <td align="center">N&#227;o</td>
                  <td align="center">Sim</td>
                </tr>
                <tr>
                  <td>Estima consumo mioc&#225;rdico de oxig&#234;nio</td>
                  <td align="center">N&#227;o</td>
                  <td align="center">Sim</td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>AVO: abertura da v&#225;lvula a&#243;rtica; AVC: fechamento da v&#225;lvula a&#243;rtica; TCIV: tempo de contra&#231;&#227;o isovolum&#233;trico; Tej: tempo de eje&#231;&#227;o; TRIV: tempo de relaxamento isovolum&#233;trico.</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
      </sec>
      <sec>
        <title>17.2. Aquisi&#231;&#227;o do Trabalho Mioc&#225;rdico</title>
        <p>Para a obten&#231;&#227;o de resultados reprodut&#237;veis e com boa acur&#225;cia, &#233; importante o uso de t&#233;cnica adequada para o c&#225;lculo do TM, n&#227;o s&#243; para a aquisi&#231;&#227;o das imagens, mas tamb&#233;m para o p&#243;s-processamento e a an&#225;lise dos par&#226;metros. Essa tecnologia atualmente est&#225; apenas dispon&#237;vel em esta&#231;&#245;es de trabalho (<italic>workstations</italic>) ou embarcadas em aparelhos com <italic>software</italic> desenvolvido por apenas um fabricante (GE Healthcare, Horten, Norway). As an&#225;lises podem ser realizadas diretamente no aparelho ou p&#243;s-processadas nas <italic>workstations</italic> a partir de imagens previamente adquiridas.</p>
        <p>O protocolo de obten&#231;&#227;o de imagens para o c&#225;lculo do TM segue os mesmos pr&#233;-requisitos t&#233;cnicos necess&#225;rios para a an&#225;lise do SLG, abordados em cap&#237;tulo espec&#237;fico. Ap&#243;s a realiza&#231;&#227;o das an&#225;lises de <italic>strain</italic> bidimensional, utilizando imagens adquiridas nas tr&#234;s proje&#231;&#245;es apicais atrav&#233;s da t&#233;cnica do AFI (<italic>automated functional imaging</italic>), o <italic>software</italic> permite que seja selecionada a an&#225;lise do TM (<xref ref-type="fig" rid="f34">Figura 17.2</xref>). Como passo inicial, devemos inserir manualmente os valores de press&#227;o arterial n&#227;o invasiva (PNI) medidos no momento do exame, e isso pode ser realizado a qualquer momento do exame na tela de identifica&#231;&#227;o do paciente ou posteriormente, na pr&#243;pria tela de c&#225;lculo de TM (<xref ref-type="fig" rid="f35">Figura 17.3</xref>). Essas medidas de PNI ser&#227;o automaticamente integralizadas no c&#225;lculo de curva de press&#227;o vs. deforma&#231;&#227;o.</p>
        <p>
          <fig id="f34">
            <label>Figura 17.2</label>
            <caption>
              <title>&#8211; Ap&#243;s a realiza&#231;&#227;o da an&#225;lise de strain bidimensional longitudinal do ventr&#237;culo esquerdo pelo m&#233;todo AFI (automated functional imaging), tendo processado as tr&#234;s janelas apicais, o software oferece a op&#231;&#227;o de c&#225;lculo do trabalho mioc&#225;rdico (myocardial work) &#8211; seta.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf33.tif"/></fig>
        </p>
        <p>
          <fig id="f35">
            <label>Figura 17.3</label>
            <caption>
              <title>&#8211; Tela inicial de c&#225;lculo do trabalho mioc&#225;rdico. Podemos inserir manualmente, nessa etapa, o valor da press&#227;o arterial n&#227;o invasiva aferida (seta) e reavaliar ou realizar a marca&#231;&#227;o de eventos card&#237;acos, como a abertura e fechamento das valvas mitral e a&#243;rtica (setas).</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf34.tif"/></fig>
        </p>
        <p>Para que seja poss&#237;vel obter a indexa&#231;&#227;o temporal dos valores obtidos, &#233; necess&#225;rio que sejam feitas as marca&#231;&#245;es de eventos do ciclo card&#237;aco, identificando a abertura e fechamento das valvas mitral e a&#243;rtica, o que pode ser realizado atrav&#233;s do Doppler espectral dos fluxos mitral e a&#243;rtico, ou ao bidimensional, na an&#225;lise da proje&#231;&#227;o apical 3 c&#226;maras, em que podemos evidenciar a abertura e fechamento de ambas as valvas (<xref ref-type="fig" rid="f36">Figura 17.4</xref>). Essas marca&#231;&#245;es tamb&#233;m podem ser realizadas na pr&#243;pria tela de c&#225;lculo do TM, modificando quadro a quadro (&#8220;<italic>frame</italic>&#8221;) a imagem do apical 3 c&#226;maras, selecionando qual o momento exato de cada evento (<xref ref-type="fig" rid="f37">Figura 17.5</xref>). Ap&#243;s aprovar as imagens e marca&#231;&#245;es realizadas (&#8220;<italic>aprove</italic>&#8221;), o <italic>software</italic> realiza os c&#225;lculos e disp&#245;e lado a lado o mapa polar (<italic>bull&#8217;s eye</italic>) com valores de SLG e <italic>strain</italic> de pico por segmento e, &#224; direita o mapa polar com o &#237;ndice de TM por segmento, dispondo na parte inferior os valores de &#237;ndice de TM global (GWI) e GMWE. Ao selecionarmos, &#224; direita, a tecla &#8220;<italic>work efficiency</italic>&#8221; o <italic>software</italic> disp&#245;e no mapa polar os valores de GMWE por segmento (<xref ref-type="fig" rid="f38">Figura 17.6</xref>). Quando selecionamos a tecla &#8220;<italic>advanced</italic>&#8221;, s&#227;o geradas as an&#225;lises por curvas e gr&#225;ficos, nas quais &#233; poss&#237;vel observar as al&#231;as de press&#227;o do VE (<italic>left ventricular pressure</italic>, LVP) vs. <italic>strain</italic> ao longo do ciclo card&#237;aco, al&#233;m de um gr&#225;fico de barras que demonstra a participa&#231;&#227;o do TM construtivo e do TM desperdi&#231;ado (<xref ref-type="fig" rid="f39">Figura 17.7</xref>).</p>
        <p>
          <fig id="f36">
            <label>Figura 17.4</label>
            <caption>
              <title>&#8211; Marca&#231;&#227;o de eventos card&#237;acos com o uso do Doppler espectral. Em A, observamos a marca&#231;&#227;o de abertura (MVO) e o fechamento da valva mitral (MVC) atrav&#233;s do influxo mitral. Em B, observamos a marca&#231;&#227;o de abertura (AVO) e o fechamento da valva a&#243;rtica (AVC) atrav&#233;s do fluxo da via de sa&#237;da do ventr&#237;culo esquerdo.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf35.tif"/></fig>
        </p>
        <p>
          <fig id="f37">
            <label>Figura 17.5</label>
            <caption>
              <title>&#8211; A marca&#231;&#227;o de eventos card&#237;acos tamb&#233;m pode ser realizada na pr&#243;pria tela de c&#225;lculo do trabalho mioc&#225;rdico (myocardial work), modificando quadro a quadro (&#8220;frame&#8221;) a imagem do apical 3 c&#226;maras, selecionando o momento exato de cada evento, clicando nos campos &#224; direita (setas).</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf36.tif"/></fig>
        </p>
        <p>
          <fig id="f38">
            <label>Figura 17.6</label>
            <caption>
              <title>&#8211; Ap&#243;s a aprova&#231;&#227;o dos dados obtidos, a marca&#231;&#227;o adequada de eventos e o preenchimento de press&#227;o n&#227;o invasiva, o software disp&#245;e os valores de strain longitudinal global e por segmento &#224; esquerda (setas brancas) e os mapas polares com valores de &#237;ndice de trabalho mioc&#225;rdico (A &#8211; seta amarela) e de efici&#234;ncia de trabalho mioc&#225;rdico (B &#8211; seta azul).</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf37.tif"/></fig>
        </p>
        <p>
          <fig id="f39">
            <label>Figura 17.7</label>
            <caption>
              <title>&#8211; Quando selecionamos a tecla &#8220;advanced&#8221;, s&#227;o geradas as an&#225;lises por curvas e gr&#225;ficos, onde &#233; poss&#237;vel observar as al&#231;as de press&#227;o do ventr&#237;culo esquerdo (left ventricular pressure, LVP) vs. strain ao longo do ciclo card&#237;aco (seta amarela), al&#233;m de um gr&#225;fico de barras que demonstra a participa&#231;&#227;o do trabalho mioc&#225;rdico construtivo e do trabalho mioc&#225;rdico desperdi&#231;ado (seta azul).</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf38.tif"/></fig>
        </p>
        <p>Os seguintes par&#226;metros s&#227;o fornecidos pelo <italic>software</italic>:</p>
        <p>1. &#205;ndice de TM global (ITMG/GWI): corresponde ao trabalho total dentro da &#225;rea sob a curva PD, sendo calculado a partir do fechamento da v&#225;lvula mitral at&#233; a abertura da valva mitral. Um <italic>bull&#8217;s eye</italic> com valores de TM segmentar e global &#233; fornecido (<xref ref-type="fig" rid="f38">Figura 17.6</xref>).</p>
        <p>2. TM construtivo (TMC/GCW): &#233; o trabalho que contribui para a eje&#231;&#227;o do VE durante a s&#237;stole, sendo obtido considerando-se o encurtamento dos mi&#243;citos durante a s&#237;stole, adicionando o alongamento dos mi&#243;citos durante o relaxamento isovolum&#233;trico (<xref ref-type="fig" rid="f39">Figura 17.7</xref>).</p>
        <p>3. TM desperdi&#231;ado (TMD/GWW): &#233; o trabalho que n&#227;o contribui para a eje&#231;&#227;o do VE, sendo obtido considerando-se o alongamento dos mi&#243;citos (em vez de encurtamento) durante a s&#237;stole, somado ao encurtamento durante a fase de relaxamento isovolum&#233;trico (encurtamento p&#243;s-sist&#243;lico) (<xref ref-type="fig" rid="f39">Figura 17.7</xref>).</p>
        <p>4. Efici&#234;ncia do TM (ETM/GMWE): &#233; obtido por meio da f&#243;rmula: <inline-formula><mml:math><mml:mtext> TM construtivo/(TM construtivo </mml:mtext><mml:mo>+</mml:mo><mml:mrow><mml:mi>T</mml:mi><mml:mi>M</mml:mi></mml:mrow><mml:mtext> desperdi&#231;ado) </mml:mtext></mml:math></inline-formula>. Seu valor &#233; dado em porcentagem de 0 a 100% de efici&#234;ncia (<xref ref-type="fig" rid="f38">Figura 17.6</xref>).</p>
      </sec>
      <sec>
        <title>17.3. Valores de Normalidade</title>
        <p>Devido &#224; valida&#231;&#227;o recente do TM e de suas vari&#225;veis para o uso cl&#237;nico, n&#227;o h&#225; ensaios multic&#234;ntricos com n&#250;mero adequado de pacientes para gerar valores de normalidade definitivos.</p>
        <p>Manganaro et al. recentemente analisaram os dados do estudo NORRE visando estabelecer limites de refer&#234;ncia normais para o TM. Esse foi um estudo multic&#234;ntrico e prospectivo europeu formado por 226 pacientes oriundos de 22 laborat&#243;rios de ecocardiografia, que forneceu valores de refer&#234;ncia para a maioria dos dados ecocardiogr&#225;ficos 2D e 3D.<sup><xref ref-type="bibr" rid="B403">403</xref></sup> A m&#233;dia ou mediana com o desvio padr&#227;o e o intervalo de confian&#231;a das vari&#225;veis do TM foram, respectivamente, 1.896 + 308 mmHg% (1.292&#8211;2.505) para o GWI, 2.232 &#177; 331 mmHg% (1.582&#8211;2.881) para o GCW, 79 mmHg% (53&#8211;122) para o GWW e 96% (94&#8211;97) para a GMWE.<sup><xref ref-type="bibr" rid="B403">403</xref></sup></p>
        <p>O GWI e GCW foram maiores em mulheres acima de 40 anos, e existe forte correla&#231;&#227;o no aumento do GWI e GCW com o aumento da press&#227;o arterial sist&#243;lica.<sup><xref ref-type="bibr" rid="B404">404</xref></sup></p>
      </sec>
      <sec>
        <title>17.4. Potencial Uso Cl&#237;nico</title>
        <p>A grande limita&#231;&#227;o para a democratiza&#231;&#227;o do uso do TM &#233; o fato de apenas uma empresa ser detentora do <italic>software</italic> (GE Healthcare). Al&#233;m disso, o c&#225;lculo do TM usa basicamente a press&#227;o sist&#243;lica aferida manualmente como medida de p&#243;s-carga em sua valida&#231;&#227;o. &#201; importante tamb&#233;m levar em considera&#231;&#227;o situa&#231;&#245;es cl&#237;nicas em que h&#225; um aditivo da p&#243;s-carga al&#233;m da PAS, como na EA, CMPH obstrutiva e em algumas cardiopatias cong&#234;nitas. Apesar de se tratar de uma nova ferramenta bastante promissora, &#224; luz do conhecimento cient&#237;fico atual, ainda &#233; restrita ao campo da pesquisa.</p>
        <p>Existem algumas publica&#231;&#245;es que j&#225; v&#234;m ganhando notoriedade da aplica&#231;&#227;o do uso do TM na pr&#225;tica cl&#237;nica, uma delas &#233; na sele&#231;&#227;o de pacientes para ressincroniza&#231;&#227;o mioc&#225;rdica. Algumas vezes, a an&#225;lise do bloqueio do ramo esquerdo pode gerar d&#250;vidas na interpreta&#231;&#227;o (<xref ref-type="fig" rid="f40">Figura 17.8</xref>). Por outro lado, atrav&#233;s da an&#225;lise visual e quantitativa do TM, tornou-se mais f&#225;cil o reconhecimento dos casos que t&#234;m um ECG com alargamento do QRS e que talvez n&#227;o tenha um dissincronismo mec&#226;nico associado (<xref ref-type="fig" rid="f41">Figura 17.9</xref>). Al&#233;m da an&#225;lise visual, tem-se valorizado o valor do trabalho construtivo para identificar os respondedores &#224; terapia de ressincroniza&#231;&#227;o, sendo um equivalente de reserva contr&#225;til.<sup><xref ref-type="bibr" rid="B405">405</xref></sup> Outro dado interessante para identificar os pacientes que se beneficiam com a ressincroniza&#231;&#227;o &#233; a an&#225;lise do trabalho perdido do septo.<sup><xref ref-type="bibr" rid="B406">406</xref></sup> Portanto, a an&#225;lise do TM nos pacientes com BRE pode ajudar a melhorar a estratifica&#231;&#227;o pela an&#225;lise visual, assim como a quantifica&#231;&#227;o do trabalho construtivo e o trabalho perdido.</p>
        <p>
          <fig id="f40">
            <label>Figura 17.8</label>
            <caption>
              <title>&#8211; Casos 1 e 2 com morfologias bem semelhantes de bloqueio de ramo esquerdo.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf39.tif"/></fig>
        </p>
        <p>
          <fig id="f41">
            <label>Figura 17.9</label>
            <caption>
              <title>&#8211; Caso 1 n&#227;o apresenta altera&#231;&#227;o na mec&#226;nica mioc&#225;rdica visualizado pela linha verde em que o trabalho mioc&#225;rdico na al&#231;a press&#227;o-strain &#233; semelhante ao valor global em vermelho. J&#225; no Caso 2, o &#8220;verdadeiro&#8221; bloqueio de ramo esquerdo, note que na mesma por&#231;&#227;o septal a curva em verde adquire um formato t&#237;pico de 8.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf40.tif"/></fig>
        </p>
        <p>Outro campo interessante na avalia&#231;&#227;o do TM &#233; na doen&#231;a coronariana obstrutiva. Ele tem demonstrado sua capacidade de detec&#231;&#227;o em repouso de doen&#231;a coron&#225;ria obstrutiva sendo superior ao SLGVE, mesmo naqueles com FE preservada e sem altera&#231;&#227;o da contratilidade segmentar.<sup><xref ref-type="bibr" rid="B407">407</xref></sup> A sua aplica&#231;&#227;o tamb&#233;m tem demonstrado identificar aqueles pacientes com infarto agudo que ir&#227;o apresentar mais complica&#231;&#245;es hospitalares e predizer aqueles com recupera&#231;&#227;o da fun&#231;&#227;o mioc&#225;rdica<sup><xref ref-type="bibr" rid="B408">408</xref></sup> e determinar complica&#231;&#245;es a longo prazo em pacientes com IAM com supradesn&#237;vel de ST.<sup><xref ref-type="bibr" rid="B409">409</xref></sup></p>
        <p>Al&#233;m das duas situa&#231;&#245;es cl&#237;nicas descritas, &#233; promissora sua aplica&#231;&#227;o na CMP dilatada, CMPH e amiloidose. Provavelmente, quando houver mais praticidade do <italic>software</italic> e mais evid&#234;ncia na literatura, a aplica&#231;&#227;o do TM ser&#225; incorporada na pr&#225;tica cl&#237;nica.</p>
      </sec>
    </sec>
    <sec>
      <title>18. <italic>Strain</italic> no 3D: O Que Pode Acrescentar ao Exame</title>
      <sec>
        <title>18.1. Introdu&#231;&#227;o</title>
        <p>A avalia&#231;&#227;o tridimensional (3D) da deforma&#231;&#227;o mioc&#225;rdica das c&#226;maras card&#237;acas atrav&#233;s da t&#233;cnica de rastreamento dos <italic>&#8220;speckles&#8221;</italic> tem in&#250;meras vantagens em rela&#231;&#227;o &#224; avalia&#231;&#227;o bidimensional (2D). Considerando que o mioc&#225;rdio ventricular esquerdo &#233; composto por tr&#234;s camadas de fibras, que est&#227;o dispostas em dire&#231;&#245;es diferentes (longitudinal, circunferencial e transversal), os &#8220;<italic>speckles</italic>&#8221; acabam por apresentar uma trajet&#243;ria n&#227;o linear, fugindo do plano bidimensional da imagem por alguns momentos do ciclo card&#237;aco. Por mais que se realizem m&#250;ltiplas aquisi&#231;&#245;es longitudinais e transversais do mioc&#225;rdio ventricular esquerdo, a avalia&#231;&#227;o dos &#8220;<italic>speckles</italic>&#8221; no ciclo card&#237;aco se faz por interpola&#231;&#227;o, n&#227;o sendo t&#227;o precisa quanto o 3D, que permite acompanh&#225;-los durante todo o ciclo card&#237;aco nas m&#250;ltiplas dimens&#245;es. Assim, as medidas do <italic>strain</italic> 3D n&#227;o s&#227;o impactadas pela &#8220;<italic>out-of-plane</italic>&#8221;, pela tors&#227;o mioc&#225;rdica ou encurtamento apical.<sup><xref ref-type="bibr" rid="B410">410</xref></sup></p>
        <p>Em rela&#231;&#227;o ao VD, a metodologia 3D &#233; a &#250;nica que permite a an&#225;lise global de todo o mioc&#225;rdio da c&#226;mara, ao passo que, no 2D, apenas a septo e/ou parede livre &#233; avaliada. Ademais, a avalia&#231;&#227;o do <italic>strain</italic> 3D &#233; mais fidedigna e fisiol&#243;gica, pois a an&#225;lise dos diferentes componentes da deforma&#231;&#227;o mioc&#225;rdica ocorre de forma simult&#226;nea em um &#250;nico <italic>dataset</italic> ou ciclo card&#237;aco. Dessa forma, o <italic>strain</italic> 3D &#233; uma aplica&#231;&#227;o promissora para uma avalia&#231;&#227;o quantitativa, objetiva, compreensiva e reprodutiva da fun&#231;&#227;o mec&#226;nica do mioc&#225;rdio. Contudo, essa metodologia apresenta forte depend&#234;ncia da uma boa janela ac&#250;stica e de um ritmo card&#237;aco regular, fatores que s&#227;o os principais limitantes para a incorpora&#231;&#227;o rotineira e sistem&#225;tica do <italic>strain</italic> 3D.<sup><xref ref-type="bibr" rid="B411">411</xref></sup> A aplica&#231;&#227;o cl&#237;nica tamb&#233;m &#233; limitada devido a diferen&#231;as nos algoritmos para acompanhamento dos &#8220;<italic>speckles</italic>&#8221; e o c&#225;lculo (<italic>cut-off</italic>) da deforma&#231;&#227;o mioc&#225;rdica, que n&#227;o est&#225; padronizado entre os diferentes fabricantes de <italic>softwares</italic>.<sup><xref ref-type="bibr" rid="B412">412</xref>,<xref ref-type="bibr" rid="B413">413</xref></sup></p>
        <p>Uma vez que as medidas do <italic>strain</italic> 3D obtidas por diferentes fabricantes e <italic>softwares</italic> n&#227;o s&#227;o intercambi&#225;veis, a incorpora&#231;&#227;o cl&#237;nica em avalia&#231;&#245;es sequenciais requer que as aquisi&#231;&#245;es basais e no acompanhamento do paciente, bem como as an&#225;lises, sejam obtidas usando o mesmo equipamento, e a interpreta&#231;&#227;o dos resultados deve considerar os valores da normalidade espec&#237;ficos para o equipamento em quest&#227;o.<sup><xref ref-type="bibr" rid="B410">410</xref>,<xref ref-type="bibr" rid="B412">412</xref></sup> Os valores de refer&#234;ncia da normalidade tamb&#233;m diferem entre as metodologias bidimensional e tridimensional, havendo apenas uma correla&#231;&#227;o modesta entre os valores do <italic>strain</italic> longitudinal. Por fim, ainda se fazem necess&#225;rias pesquisas cl&#237;nicas para avaliar a acur&#225;cia e o valor progn&#243;stico do <italic>strain</italic> 3D.</p>
      </sec>
      <sec>
        <title>18.2. <italic>Strain</italic> Ventricular Esquerdo</title>
        <p>O ST3D (ou <italic>strain</italic> tridimensional) apresenta um princ&#237;pio melhor quando comparado ao ST2D por n&#227;o ser limitado a um plano de corte e por permitir dados vetorizados em tr&#234;s planos ortogonais para uma an&#225;lise. Do ponto de vista de implementa&#231;&#227;o do m&#233;todo, sabemos que o <italic>strain</italic> bidimensional precisa de resolu&#231;&#227;o temporal muito elevada (34&#8211;50 vps), porque os &#8220;<italic>speckles</italic>&#8221; ficam pouco tempo (alguns milissegundos) no plano de corte, o que n&#227;o ocorre no modo tridimensional. Al&#233;m disso, para o ST3D, o ideal &#233; a obten&#231;&#227;o de seis batimentos card&#237;acos (&#8220;<italic>6 beat acquisition</italic>&#8221;), com a maior densidade de linhas e com 44 vps na frequ&#234;ncia de 2 a 4 Mhz (pois foi o que apresentou maior acur&#225;cia quando comparado a RM). N&#227;o se recomenda a aquisi&#231;&#227;o com volumes &#250;nicos, e o aumento da resolu&#231;&#227;o temporal no equipamento diminui a qualidade da imagem e o <italic>tracking</italic> por reduzir a densidade das linhas.<sup><xref ref-type="bibr" rid="B414">414</xref></sup></p>
        <p>A factibilidade geral &#233; em torno de 85%, e as limita&#231;&#245;es para a implementa&#231;&#227;o da t&#233;cnica s&#227;o: janela ac&#250;stica desfavor&#225;vel, arritmias card&#237;acas (impedem aquisi&#231;&#245;es em m&#250;ltiplos batimentos), visualiza&#231;&#227;o incompleta dos seguimentos apicais do VE e VD, problemas de <italic>tracking</italic> dos <italic>speckles</italic> nos seguimentos basais (distantes do transdutor) e determina&#231;&#227;o dos valores de normalidade e de progn&#243;stico cl&#237;nico.</p>
      </sec>
      <sec>
        <title>18.3. <italic>Strain</italic> Ventricular Direito</title>
        <p>A an&#225;lise da contra&#231;&#227;o do VD &#233; importante especialmente para entender o mecanismo dessa c&#226;mara diante das doen&#231;as cong&#234;nitas e adquiridas. Por&#233;m, ao contr&#225;rio do VE, a estimativa do VD &#233; mais dif&#237;cil devido &#224; forma complexa que o VD apresenta e devido &#224; parede fina que possui. Apesar disso, imagens de RM e <italic>speckle tracking</italic> pelo ecocardiograma t&#234;m sido promissoras na an&#225;lise ventricular direita. No entanto, os valores obtidos pelo ST3D para o VD ainda n&#227;o est&#227;o bem estabelecidos.<sup><xref ref-type="bibr" rid="B415">415</xref></sup> Persistem problemas t&#233;cnicos para a an&#225;lise do <italic>strain</italic> 3D quando o objetivo &#233; analisar as c&#226;maras direitas, uma vez que o <italic>software</italic> foi criado para a an&#225;lise do VE e ainda &#233; adaptado para o VD na maioria das m&#225;quinas. Apesar de o <italic>strain</italic> 3D permitir a an&#225;lise global de todo mioc&#225;rdio direito, a tecnologia tridimensional para essa c&#226;mara ainda est&#225; em andamento, n&#227;o havendo valores de corte bem definidos para o <italic>strain</italic> 3D do VD at&#233; o momento.</p>
        <sec>
          <title>18.3.1. Aquisi&#231;&#227;o e An&#225;lise do <italic>Full-volume</italic> 3D</title>
          <p>Usando imagem harm&#244;nica, idealmente se obt&#233;m quatro batimentos <italic>triggados</italic> na captura. A profundidade deve ser adequada para que somente o VD, suas paredes e o anel tric&#250;spide preencham o volume, e geralmente &#233; o pico sist&#243;lico do <italic>strain</italic> que &#233; usado para an&#225;lise.</p>
        </sec>
      </sec>
    </sec>
    <sec>
      <title>18.4. <italic>Strain</italic> Atrial Esquerdo</title>
      <p>O sistema de ultrassom na avalia&#231;&#227;o do <italic>strain</italic> 3D do AE (assim como dos ventr&#237;culos) &#233; capaz de adquirir os dados volum&#233;tricos do &#225;trio em tempo real e pode medir todos os componentes do <italic>strain</italic>. Contudo, o <italic>tracking</italic> em tr&#234;s dimens&#245;es &#233; um grande desafio, e a resolu&#231;&#227;o temporal e espacial do 3D &#233; inferior &#224; do 2D, o que torna a an&#225;lise tridimensional complexa e mais demorada, pois a alta qualidade de imagem &#233; necess&#225;ria para a aquisi&#231;&#227;o do <italic>strain</italic> 3D.</p>
      <p>Outro ponto em discuss&#227;o, &#233; a variabilidade inter e intraobservador na avalia&#231;&#227;o da mec&#226;nica card&#237;aca.<sup><xref ref-type="bibr" rid="B414">414</xref></sup> Sabe-se que tanto a fase de reservat&#243;rio como a de conduto e a de bomba atrial podem ser bem analisadas pelo <italic>strain</italic> 2D, e h&#225; valores m&#233;dios de corte relativamente definidos para o <italic>strain</italic> 2D em cada uma dessas fases. Contudo, ainda n&#227;o temos valores de refer&#234;ncia para o <italic>strain</italic> 3D. As principais aplica&#231;&#245;es do m&#233;todo nessa c&#226;mara, em que a an&#225;lise do <italic>strain</italic> torna-se relevante s&#227;o: IC com FE preservada,<sup><xref ref-type="bibr" rid="B7">7</xref></sup> avalia&#231;&#227;o das press&#245;es de enchimento intracavit&#225;rias,<sup><xref ref-type="bibr" rid="B95">95</xref></sup> fun&#231;&#227;o atrial do atleta de elite<sup><xref ref-type="bibr" rid="B416">416</xref></sup> e CMPs,<sup><xref ref-type="bibr" rid="B417">417</xref></sup> mas os estudos corroboram mais os dados do <italic>strain</italic> 2D do que do <italic>strain</italic> 3D.</p>
    </sec>
    <sec>
      <title>19. O papel da Resson&#226;ncia e Tomografia Card&#237;acas na Avalia&#231;&#227;o do <italic>Strain</italic></title>
      <sec>
        <title>19.1. Introdu&#231;&#227;o</title>
        <p>A RMC, com sua alta resolu&#231;&#227;o espacial e temporal e natureza n&#227;o invasiva, tornou-se uma importante modalidade para a avalia&#231;&#227;o da fun&#231;&#227;o global e segmentar dos ventr&#237;culos. A avalia&#231;&#227;o do <italic>strain</italic> &#233; uma medida estabelecida e confi&#225;vel de quantifica&#231;&#227;o de disfun&#231;&#227;o contr&#225;til regional e global e possui a capacidade de detectar disfun&#231;&#227;o card&#237;aca subcl&#237;nica sendo, portanto, uma ferramenta &#250;til para a avalia&#231;&#227;o da fun&#231;&#227;o mioc&#225;rdica. O ecocardiograma &#233;, atualmente, o m&#233;todo mais dispon&#237;vel e de menor custo para a avalia&#231;&#227;o do <italic>strain,</italic> por&#233;m a an&#225;lise pode ser prejudicada em pacientes com limita&#231;&#227;o de janela ac&#250;stica.</p>
      </sec>
      <sec>
        <title>19.2. M&#233;todos de Aquisi&#231;&#227;o do <italic>Strain</italic> pela Resson&#226;ncia Magn&#233;tica Card&#237;aca</title>
        <p>O <italic>tagging</italic> mioc&#225;rdico (&#8220;marca&#231;&#227;o mioc&#225;rdica&#8221;) &#233; a t&#233;cnica mais validada em estudos e consiste em uma fase de prepara&#231;&#227;o em que &#8220;<italic>tags</italic>&#8221; magn&#233;ticos (linhas pretas, <italic>tags</italic>) s&#227;o ortogonalmente sobrepostas ao mioc&#225;rdio no in&#237;cio de uma sequ&#234;ncia de cine.<sup><xref ref-type="bibr" rid="B12">12</xref>,<xref ref-type="bibr" rid="B418">418</xref></sup> Outra alternativa ao <italic>tagging</italic> que proporciona an&#225;lise direta do <italic>strain</italic> mioc&#225;rdico pela RMC s&#227;o as t&#233;cnicas de SENC (<italic>strain-encoded)</italic> e DENSE <italic>(displacement encoding with stimulated echoes).</italic><sup><xref ref-type="bibr" rid="B419">419</xref></sup> Recentemente, foi desenvolvido o m&#233;todo de <italic>feature tracking</italic> (FT), que permite a quantifica&#231;&#227;o da deforma&#231;&#227;o do mioc&#225;rdio nas imagens tradicionais de cine RMC sem a necessidade de aquisi&#231;&#245;es adicionais ou longa an&#225;lise.<sup><xref ref-type="bibr" rid="B420">420</xref>,<xref ref-type="bibr" rid="B421">421</xref></sup></p>
        <p>Em todas as t&#233;cnicas de an&#225;lise do <italic>strain</italic>, os par&#226;metros de <italic>strain</italic> circunferencial e longitudinal globais foram mais reprodut&#237;veis e consistentes do que os regionais.<sup><xref ref-type="bibr" rid="B422">422</xref></sup> Mais detalhes sobre os m&#233;todos de aquisi&#231;&#227;o do <italic>strain</italic> pela RMC podem ser obtidos nas refer&#234;ncias.<sup><xref ref-type="bibr" rid="B12">12</xref>,<xref ref-type="bibr" rid="B418">418</xref>-<xref ref-type="bibr" rid="B422">422</xref></sup></p>
      </sec>
      <sec>
        <title>19.3. <italic>Strain</italic> do Ventr&#237;culo Direito pela Resson&#226;ncia Magn&#233;tica Card&#237;aca</title>
        <p>A medida do <italic>strain</italic> mioc&#225;rdico &#233; um m&#233;todo preciso e pr&#225;tico de avalia&#231;&#227;o da fun&#231;&#227;o do VD, por se tratar de um marcador mais sens&#237;vel e precoce de disfun&#231;&#227;o contr&#225;til do que outros m&#233;todos dispon&#237;veis, como a FE. Estudos t&#234;m demonstrado o potencial do <italic>strain</italic> do VD, avaliado pela RMC, em fornecer informa&#231;&#245;es aditivas e progn&#243;sticas independentes.<sup><xref ref-type="bibr" rid="B423">423</xref>-<xref ref-type="bibr" rid="B428">428</xref></sup> Existem alguns estudos publicados nos quais os autores analisaram o <italic>strain</italic> do VD em indiv&#237;duos saud&#225;veis e tamb&#233;m em grupos-controle sem cardiopatia.<sup><xref ref-type="bibr" rid="B423">423</xref>,<xref ref-type="bibr" rid="B426">426</xref>,<xref ref-type="bibr" rid="B429">429</xref>,<xref ref-type="bibr" rid="B430">430</xref></sup></p>
        <p>As patologias que mais acometem o VD, como cardiopatias cong&#234;nitas, HP e displasia arritmog&#234;nica (DAVD) foram as que tiveram maior aplicabilidade na an&#225;lise do <italic>strain</italic> do VD. O FT&#8211;RMC (<italic>feature tracking</italic> pela RMC) foi utilizado em pacientes com tetralogia de Fallot corrigida, e os valores de <italic>strain</italic> estavam reduzidos nesses pacientes e estavam relacionados com par&#226;metros de fun&#231;&#227;o sist&#243;lica (FE biventricular) e tamb&#233;m capacidade funcional no teste cardiopulmonar.<sup><xref ref-type="bibr" rid="B425">425</xref></sup></p>
        <p>A avalia&#231;&#227;o das fun&#231;&#245;es globais e segmentares do VD &#233; fundamental para o diagn&#243;stico multiparam&#233;trico de DAVD, e o <italic>strain</italic> do VD provou ser uma ferramenta extremamente &#250;til.<sup><xref ref-type="bibr" rid="B428">428</xref>,<xref ref-type="bibr" rid="B431">431</xref></sup> Os <italic>strains</italic> global e segmentar do VD est&#227;o significativamente reduzidos em pacientes com DAVD, independente das dimens&#245;es e fun&#231;&#227;o do VD, de modo que o comprometimento da deforma&#231;&#227;o do VD pode representar um marcador precoce da doen&#231;a.<sup><xref ref-type="bibr" rid="B428">428</xref></sup></p>
        <p>A <xref ref-type="fig" rid="f42">Figura 19.1</xref> apresenta exemplos de <italic>strain</italic> do VD em paciente normal e paciente com HP.</p>
        <p>
          <fig id="f42">
            <label>Figura 19.1</label>
            <caption>
              <title>&#8211; An&#225;lise do strain longitudinal global pelo m&#233;todo de feature tracking em paciente com hipertens&#227;o pulmonar (acima) e sem hipertens&#227;o pulmonar (abaixo). O paciente com hipertens&#227;o pulmonar apresentou strain de 4,26% e o sem hipertens&#227;o pulmonar de 26,46%.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf41.tif"/></fig>
        </p>
      </sec>
      <sec>
        <title>19.4. <italic>Strain</italic> do Ventr&#237;culo Esquerdo pela Resson&#226;ncia Magn&#233;tica Card&#237;aca</title>
        <p>Os valores m&#233;dios em indiv&#237;duos saud&#225;veis dos tipos de <italic>strain</italic> do VE (SCG, SRG, SLG) foram pesquisados na &#250;ltima d&#233;cada atrav&#233;s do FT&#8211;RMC,<sup><xref ref-type="bibr" rid="B419">419</xref>-<xref ref-type="bibr" rid="B423">423</xref></sup> incluindo uma importante metan&#225;lise.<sup><xref ref-type="bibr" rid="B424">424</xref></sup> Os maiores e mais recentes estudos em SCG e SR pelo FT-RMC aplicaram a an&#225;lise da m&#233;dia de tr&#234;s cortes do eixo curto. A maior parte do SLGVE foi calculada atrav&#233;s de um corte 4 c&#226;maras, enquanto algumas publica&#231;&#245;es mais recentes trazem avalia&#231;&#245;es da m&#233;dia de tr&#234;s cortes longitudinais. Os valores do SLG e do SCG flutuam dentro de uma margem restrita, enquanto os valores de SRG tiveram intervalos de confian&#231;a mais amplos. Especula-se que a movimenta&#231;&#227;o atrav&#233;s do plano e a grande variabilidade pessoal podem explicar parcialmente esse fen&#244;meno. Entretanto, a real causa ainda permanece incerta.<sup><xref ref-type="bibr" rid="B424">424</xref></sup></p>
        <p>Observa-se uma forte rela&#231;&#227;o dos graus de deforma&#231;&#227;o mioc&#225;rdica com a presen&#231;a de realce tardio (RT) mioc&#225;rdico, em especial o SCG, mas tamb&#233;m o SLG derivados do FT-RMC. Ademais, observa-se boa correla&#231;&#227;o entre as t&#233;cnicas derivadas entre a ecocardiografia e a RMC.<sup><xref ref-type="bibr" rid="B425">425</xref></sup></p>
        <p>Na CMP dilatada, a presen&#231;a de um SLG acentuadamente reduzido se relacionou fortemente com pior sobrevida, mesmo naqueles com FE muito reduzida, independentemente da classe funcional e outros achados da RMC.<sup><xref ref-type="bibr" rid="B426">426</xref></sup> O FT-RMC pode identificar o subgrupo de portadores de IC com FE preservada e DD atrav&#233;s do SLG alterado em compara&#231;&#227;o a indiv&#237;duos saud&#225;veis.<sup><xref ref-type="bibr" rid="B427">427</xref></sup></p>
        <p>Na diferencia&#231;&#227;o entre pericardite constritiva (PC) e CMP restritiva, o SLG derivado da RMC apresentou valor diagn&#243;stico similar ao do ecocardiograma, al&#233;m de apresentar alto valor discriminat&#243;rio entre essas patologias. Os valores de SLG s&#227;o significativamente menores na CMP restritiva, enquanto na pericardite s&#227;o pr&#243;ximos dos valores encontrados em controles normais.<sup><xref ref-type="bibr" rid="B428">428</xref></sup> Os componentes longitudinal e circunferencial do <italic>strain</italic> s&#227;o alterados tamb&#233;m em casos de miocardite.<sup><xref ref-type="bibr" rid="B429">429</xref></sup></p>
        <p>Publica&#231;&#245;es que exploraram a capacidade do <italic>strain</italic> derivado pela resson&#226;ncia usando <italic>tagging</italic> mioc&#225;rdico demonstraram alta capacidade em determinar portadores de amiloidose com presen&#231;a de RT, sendo potencialmente mais sens&#237;vel que a pr&#243;pria sequencia p&#243;s-contraste.<sup><xref ref-type="bibr" rid="B430">430</xref></sup> A perda do gradiente base-&#225;pice do <italic>strain</italic> circunferencial parece representar um achado precoce das altera&#231;&#245;es observadas na doen&#231;a de Fabry, j&#225; as modalidades de <italic>strain</italic> longitudinal e circunferencial n&#227;o apresentaram varia&#231;&#227;o significativa entre os controles sadios.<sup><xref ref-type="bibr" rid="B431">431</xref></sup></p>
        <p>Usando o FT-RMC, foi observado que pacientes com CMPH t&#234;m redu&#231;&#227;o do SLG, SRG e SCG comparados com controles sadios, sendo o SLG e o SRG preditores de eventos adversos,<sup><xref ref-type="bibr" rid="B432">432</xref></sup> assim como j&#225; foi demonstrado que o SLG &#233; significativamente superior em pacientes portadores de HAS do que em portadores de CMPH.<sup><xref ref-type="bibr" rid="B433">433</xref></sup></p>
        <p>O diagn&#243;stico da doen&#231;a coronariana isqu&#234;mica pela RMC pode ser aperfei&#231;oado se adicionada a an&#225;lise com FT-RMC, sendo poss&#237;vel detectar pequenas altera&#231;&#245;es no <italic>strain</italic> circunferencial ap&#243;s o estresse por dobutamina, podendo o SLG ser &#250;til na detec&#231;&#227;o de infarto e avalia&#231;&#227;o de viabilidade.<sup><xref ref-type="bibr" rid="B434">434</xref></sup> Os tr&#234;s tipos de <italic>strain</italic> est&#227;o reduzidos em pacientes que sofreram IAM com supradesnivelamento do segmento ST, sendo preditores independentes de eventos cardiovasculares adversos.<sup><xref ref-type="bibr" rid="B435">435</xref></sup></p>
        <p>Pacientes portadores de EA importante t&#234;m SLG e SCG reduzidos em rela&#231;&#227;o aos controles sadios, a despeito dos sintomas apresentados.<sup><xref ref-type="bibr" rid="B436">436</xref></sup> Em pacientes portadores de valva a&#243;rtica bic&#250;spide e FE preservada, foram observados ind&#237;cios de DD atrav&#233;s de altera&#231;&#245;es no <italic>strain</italic> circunferencial.<sup><xref ref-type="bibr" rid="B437">437</xref></sup> A cardiotoxicidade induzida por quimioterapia apresenta anormalidades no SLG e SCG muito antes do decl&#237;nio da FEVE.<sup><xref ref-type="bibr" rid="B438">438</xref></sup></p>
        <p>Recentemente, foi reportado que o SLG pelo FT-RMC apresenta associa&#231;&#227;o mais intensa com mortalidade do que os observados pela combina&#231;&#227;o da FEVE e pelo RT mioc&#225;rdico. At&#233; o momento, essa foi a maior experi&#234;ncia em avaliar o valor progn&#243;stico do SLG avaliado pelo FT-RMC. Ajustado para fatores de risco cl&#225;ssicos, incluindo FEVE e RT, a piora de 1% no SLG foi associada a um aumento de 89% no risco de morte em pacientes isqu&#234;micos e n&#227;o isqu&#234;micos.<sup><xref ref-type="bibr" rid="B439">439</xref></sup></p>
      </sec>
      <sec>
        <title>19.5. <italic>Strain</italic> do &#193;trio Esquerdo pela Resson&#226;ncia Magn&#233;tica Card&#237;aca</title>
        <p>A avalia&#231;&#227;o da fun&#231;&#227;o do AE tem sido cada vez mais reconhecida como um fator crucial em uma diversidade de patologias card&#237;acas. Normalmente, sua altera&#231;&#227;o est&#225; associada a pior progn&#243;stico e precede o estabelecimento de IC.</p>
        <p>O AE tem a fun&#231;&#227;o de reservat&#243;rio para a drenagem das veias pulmonares, servindo de conduto para a passagem do fluxo at&#233; o VE por diferen&#231;a de press&#227;o causada pela abertura das c&#250;spides mitrais e por fim de fun&#231;&#227;o contr&#225;til, com a s&#237;stole atrial ocorrendo no final da di&#225;stole do VE.<sup><xref ref-type="bibr" rid="B440">440</xref></sup></p>
        <p>A an&#225;lise do <italic>strain</italic> atrial baseada em FT-RMC quantifica de forma confi&#225;vel o strain longitudinal do AE e o <italic>strain rate</italic>. Usando imagens cine-RM padr&#227;o, ela discrimina entre pacientes com relaxamento ventricular esquerdo alterados e pacientes saud&#225;veis, como podemos observar na <xref ref-type="table" rid="t27">Tabela 19.1</xref>.<sup><xref ref-type="bibr" rid="B441">441</xref></sup> Em um subestudo do MESA, a redu&#231;&#227;o no SLG atrial e altera&#231;&#227;o do volume indexado m&#237;nimo do AE foram fatores preditores independentes para a instala&#231;&#227;o de IC, mesmo ajustados para a massa do VE e pro-BNP.<sup><xref ref-type="bibr" rid="B442">442</xref></sup> Da mesma forma, a avalia&#231;&#227;o da fun&#231;&#227;o f&#225;sica do AE foi um preditor de risco independente para a admiss&#227;o por IC ou morte, mesmo ap&#243;s ajustar para o volume do AE e o remodelamento ventricular.<sup><xref ref-type="bibr" rid="B443">443</xref></sup></p>
        <p>
          <table-wrap id="t27">
            <label>Tabela 19.1</label>
            <caption>
              <title>&#8211; <italic>Strain</italic> do &#225;trio esquerdo</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="25%">
                <col/>
                <col/>
                <col/>
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left">Tipos</th>
                  <th>ICFEp</th>
                  <th>CMPH</th>
                  <th>Normais</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>Reservat&#243;rio</td>
                  <td align="center">16,3 &#177; 5,8</td>
                  <td align="center">22,1 &#177; 5,5</td>
                  <td align="center">29,1 &#177; 5,3</td>
                </tr>
                <tr>
                  <td>Conduto</td>
                  <td align="center">11,9 &#177; 4,0</td>
                  <td align="center">10,4 &#177; 3,9</td>
                  <td align="center">21,3 &#177; 5,1</td>
                </tr>
                <tr>
                  <td>Contr&#225;til</td>
                  <td align="center">4,5 &#177; 2,9</td>
                  <td align="center">11,7 &#177; 4,0</td>
                  <td align="center">7,8 &#177; 2,5</td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>CMPH: cardiomiopatia hipertr&#243;fica; ICFep: insufici&#234;ncia card&#237;aca com fra&#231;&#227;o de eje&#231;&#227;o preservada.</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
      </sec>
      <sec>
        <title>19.6. <italic>Strain</italic> pela Tomografia Card&#237;aca</title>
        <p>A avalia&#231;&#227;o do <italic>strain</italic> pela tomografia card&#237;aca (TC) pode ser realizada utilizando-se o m&#233;todo <italic>feature tracking</italic> (FT-TC) nas aquisi&#231;&#245;es contrastadas e trigadas, com reconstru&#231;&#245;es funcionais do ciclo card&#237;aco. Os dados ainda s&#227;o escassos, mas a sua aplicabilidade foi testada em algumas publica&#231;&#245;es recentes em pacientes portadores de EAo importante, submetidos a implante de pr&#243;tese a&#243;rtica transcut&#226;nea. Os resultados demonstram valores similares do SLG entre a FT-TC e a derivada pelo ECO,<sup><xref ref-type="bibr" rid="B444">444</xref>,<xref ref-type="bibr" rid="B445">445</xref></sup> assim como alta reprodutibilidade intraobservador e intraclasse para SLG FT-TC do VE, apesar de aparentemente subestimar os valores.<sup><xref ref-type="bibr" rid="B444">444</xref></sup></p>
        <p>Outra publica&#231;&#227;o explorou a rela&#231;&#227;o do <italic>strain</italic> FT-TC com a doen&#231;a isqu&#234;mica do cora&#231;&#227;o em portadores de les&#227;o significativa na art&#233;ria descendente anterior. Observou-se uma redu&#231;&#227;o do <italic>strain</italic> longitudinal nos segmentos do territ&#243;rio da art&#233;ria descendente anterior, a despeito de volumes diast&#243;lico, sist&#243;lico e FE normais.<sup><xref ref-type="bibr" rid="B446">446</xref></sup></p>
        <p>No momento, as limita&#231;&#245;es para a utiliza&#231;&#227;o do <italic>strain</italic> pela RMC e TC se devem &#224; escassa disponibilidade e ao elevado custo de <italic>softwares</italic> de p&#243;s-processamento.</p>
      </sec>
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        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0009-0008-1958-1825</contrib-id>
          <name>
            <surname>Santo</surname>
            <given-names>Thais Harada Campos Espirito</given-names>
          </name>
          <xref ref-type="aff" rid="aff13001">
            <sup>13</sup>
          </xref>
          <xref ref-type="aff" rid="aff14001">
            <sup>14</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-9983-6438</contrib-id>
          <name>
            <surname>Silva</surname>
            <given-names>Tonnison de Oliveira</given-names>
          </name>
          <xref ref-type="aff" rid="aff15001">
            <sup>15</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-7152-1810</contrib-id>
          <name>
            <surname>Salemi</surname>
            <given-names>Vera Maria Cury</given-names>
          </name>
          <xref ref-type="aff" rid="aff3001">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-0625-1084</contrib-id>
          <name>
            <surname>Rocon</surname>
            <given-names>Camila</given-names>
          </name>
          <xref ref-type="aff" rid="aff16001">
            <sup>16</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-6110-2500</contrib-id>
          <name>
            <surname>Lima</surname>
            <given-names>M&#225;rcio Silva Miguel</given-names>
          </name>
          <xref ref-type="aff" rid="aff3001">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-0711-7995</contrib-id>
          <name>
            <surname>Barberato</surname>
            <given-names>Silvio Henrique</given-names>
          </name>
          <xref ref-type="aff" rid="aff17001">
            <sup>17</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-4500-5270</contrib-id>
          <name>
            <surname>Rodrigues</surname>
            <given-names>Ana Clara</given-names>
          </name>
          <xref ref-type="aff" rid="aff10001">
            <sup>10</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Rabschkowisky</surname>
            <given-names>Arnaldo</given-names>
          </name>
          <xref ref-type="aff" rid="aff18001">
            <sup>18</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-9131-0439</contrib-id>
          <name>
            <surname>Frota</surname>
            <given-names>Daniela do Carmo Rassi</given-names>
          </name>
          <xref ref-type="aff" rid="aff19001">
            <sup>19</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-0477-480X</contrib-id>
          <name>
            <surname>Gripp</surname>
            <given-names>Eliza de Almeida</given-names>
          </name>
          <xref ref-type="aff" rid="aff20001">
            <sup>20</sup>
          </xref>
          <xref ref-type="aff" rid="aff21001">
            <sup>21</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Barretto</surname>
            <given-names>Rodrigo Bellio de Mattos</given-names>
          </name>
          <xref ref-type="aff" rid="aff3001">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-3152-298X</contrib-id>
          <name>
            <surname>Silva</surname>
            <given-names>Sandra Marques e</given-names>
          </name>
          <xref ref-type="aff" rid="aff22001">
            <sup>22</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-1969-5135</contrib-id>
          <name>
            <surname>Cauduro</surname>
            <given-names>Sanderson Antonio</given-names>
          </name>
          <xref ref-type="aff" rid="aff23001">
            <sup>23</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-3466-7052</contrib-id>
          <name>
            <surname>Pinheiro</surname>
            <given-names>Aur&#233;lio Carvalho</given-names>
          </name>
          <xref ref-type="aff" rid="aff24001">
            <sup>24</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0009-0000-0121-2599</contrib-id>
          <name>
            <surname>Araujo</surname>
            <given-names>Salustiano Pereira de</given-names>
          </name>
          <xref ref-type="aff" rid="aff25001">
            <sup>25</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-5376-1802</contrib-id>
          <name>
            <surname>Tressino</surname>
            <given-names>Cintia Galhardo</given-names>
          </name>
          <xref ref-type="aff" rid="aff8001">
            <sup>8</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Silva</surname>
            <given-names>Carlos Eduardo Suaide</given-names>
          </name>
          <xref ref-type="aff" rid="aff26001">
            <sup>26</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Monaco</surname>
            <given-names>Claudia Gianini</given-names>
          </name>
          <xref ref-type="aff" rid="aff10001">
            <sup>10</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-8728-4357</contrib-id>
          <name>
            <surname>Paiva</surname>
            <given-names>Marcelo Goulart</given-names>
          </name>
          <xref ref-type="aff" rid="aff27001">
            <sup>27</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0009-0005-7507-6338</contrib-id>
          <name>
            <surname>Fisher</surname>
            <given-names>Cl&#225;udio Henrique</given-names>
          </name>
          <xref ref-type="aff" rid="aff10001">
            <sup>10</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-0794-7339</contrib-id>
          <name>
            <surname>Alves</surname>
            <given-names>Marco Stephan Lofrano</given-names>
          </name>
          <xref ref-type="aff" rid="aff28001">
            <sup>28</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-2758-4793</contrib-id>
          <name>
            <surname>Grau</surname>
            <given-names>Cl&#225;udia R. Pinheiro de Castro</given-names>
          </name>
          <xref ref-type="aff" rid="aff3001">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0009-0008-2038-5741</contrib-id>
          <name>
            <surname>Santos</surname>
            <given-names>Maria Veronica Camara dos</given-names>
          </name>
          <xref ref-type="aff" rid="aff29001">
            <sup>29</sup>
          </xref>
          <xref ref-type="aff" rid="aff30001">
            <sup>30</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-3367-5779</contrib-id>
          <name>
            <surname>Guimar&#227;es</surname>
            <given-names>Isabel Cristina Britto</given-names>
          </name>
          <xref ref-type="aff" rid="aff31001">
            <sup>31</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-5531-9647</contrib-id>
          <name>
            <surname>Morhy</surname>
            <given-names>Samira Saady</given-names>
          </name>
          <xref ref-type="aff" rid="aff10001">
            <sup>10</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-6600-2311</contrib-id>
          <name>
            <surname>Leal</surname>
            <given-names>Gabriela Nunes</given-names>
          </name>
          <xref ref-type="aff" rid="aff32001">
            <sup>32</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-8534-5934</contrib-id>
          <name>
            <surname>Soares</surname>
            <given-names>Andressa Mussi</given-names>
          </name>
          <xref ref-type="aff" rid="aff33001">
            <sup>33</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-2932-766X</contrib-id>
          <name>
            <surname>Cruz</surname>
            <given-names>Cecilia Beatriz Bittencourt Viana</given-names>
          </name>
          <xref ref-type="aff" rid="aff3001">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-8760-2052</contrib-id>
          <name>
            <surname>Guimar&#227;es</surname>
            <given-names>Fabio Villa&#231;a</given-names>
            <suffix>Filho</suffix>
          </name>
          <xref ref-type="aff" rid="aff34001">
            <sup>34</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-0384-348X</contrib-id>
          <name>
            <surname>Assun&#231;&#227;o</surname>
            <given-names>Bruna Morhy Borges Leal</given-names>
          </name>
          <xref ref-type="aff" rid="aff35001">
            <sup>35</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-1216-8316</contrib-id>
          <name>
            <surname>Fernandes</surname>
            <given-names>Rafael Modesto</given-names>
          </name>
          <xref ref-type="aff" rid="aff36001">
            <sup>36</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Saraiva</surname>
            <given-names>Roberto Magalh&#227;es</given-names>
          </name>
          <xref ref-type="aff" rid="aff37001">
            <sup>37</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Tsutsui</surname>
            <given-names>Jeane Mike</given-names>
          </name>
          <xref ref-type="aff" rid="aff38001">
            <sup>38</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-1632-212X</contrib-id>
          <name>
            <surname>Soares</surname>
            <given-names>F&#225;bio Luis de Jesus</given-names>
          </name>
          <xref ref-type="aff" rid="aff39001">
            <sup>39</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-0448-8667</contrib-id>
          <name>
            <surname>Falc&#227;o</surname>
            <given-names>Sandra N&#237;vea dos Reis Saraiva</given-names>
          </name>
          <xref ref-type="aff" rid="aff40001">
            <sup>40</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-9236-3815</contrib-id>
          <name>
            <surname>Hotta</surname>
            <given-names>Viviane Tiemi</given-names>
          </name>
          <xref ref-type="aff" rid="aff3001">
            <sup>3</sup>
          </xref>
          <xref ref-type="aff" rid="aff38001">
            <sup>38</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-3161-8922</contrib-id>
          <name>
            <surname>Armstrong</surname>
            <given-names>Anderson da Costa</given-names>
          </name>
          <xref ref-type="aff" rid="aff41001">
            <sup>41</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-8857-3094</contrib-id>
          <name>
            <surname>Hygidio</surname>
            <given-names>Daniel de Andrade</given-names>
          </name>
          <xref ref-type="aff" rid="aff42001">
            <sup>42</sup>
          </xref>
          <xref ref-type="aff" rid="aff43001">
            <sup>43</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-3314-9712</contrib-id>
          <name>
            <surname>Miglioranza</surname>
            <given-names>Marcelo Haertel</given-names>
          </name>
          <xref ref-type="aff" rid="aff44001">
            <sup>44</sup>
          </xref>
          <xref ref-type="aff" rid="aff45001">
            <sup>45</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-9291-1308</contrib-id>
          <name>
            <surname>Camarozano</surname>
            <given-names>Ana Cristina</given-names>
          </name>
          <xref ref-type="aff" rid="aff28001">
            <sup>28</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-7302-7448</contrib-id>
          <name>
            <surname>Lopes</surname>
            <given-names>Marly Maria Uellendahl</given-names>
          </name>
          <xref ref-type="aff" rid="aff46001">
            <sup>46</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-3913-7181</contrib-id>
          <name>
            <surname>Cerci</surname>
            <given-names>Rodrigo Julio</given-names>
          </name>
          <xref ref-type="aff" rid="aff47001">
            <sup>47</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-0298-8262</contrib-id>
          <name>
            <surname>Siqueira</surname>
            <given-names>Maria Eduarda Menezes de</given-names>
          </name>
          <xref ref-type="aff" rid="aff46001">
            <sup>46</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-3418-3226</contrib-id>
          <name>
            <surname>Torre&#227;o</surname>
            <given-names>Jorge Andion</given-names>
          </name>
          <xref ref-type="aff" rid="aff48001">
            <sup>48</sup>
          </xref>
          <xref ref-type="aff" rid="aff49001">
            <sup>49</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-4505-3344</contrib-id>
          <name>
            <surname>Rochitte</surname>
            <given-names>Carlos Eduardo</given-names>
          </name>
          <xref ref-type="aff" rid="aff3001">
            <sup>3</sup>
          </xref>
          <xref ref-type="aff" rid="aff16001">
            <sup>16</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-7046-8707</contrib-id>
          <name>
            <surname>Felix</surname>
            <given-names>Alex</given-names>
          </name>
          <xref ref-type="aff" rid="aff26001">
            <sup>26</sup>
          </xref>
          <xref ref-type="aff" rid="aff50001">
            <sup>50</sup>
          </xref>
        </contrib>
      </contrib-group>
      <aff id="aff1001">
        <label>1</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Santa Casa de Miseric&#243;rdia de Feira de Santana, Feira de Santana, BA &#8211; Brazil</institution>
      </aff>
      <aff id="aff2001">
        <label>2</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Universidade Federal da Para&#237;ba, Jo&#227;o Pessoa, PB &#8211; Brazil</institution>
      </aff>
      <aff id="aff3001">
        <label>3</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Instituto do Cora&#231;&#227;o da Faculdade de Medicina da Universidade de S&#227;o Paulo (Incor/FMUSP), S&#227;o Paulo, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff4001">
        <label>4</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Faculdade Ci&#234;ncias M&#233;dicas de Minas Gerais, Belo Horizonte, MG &#8211; Brazil</institution>
      </aff>
      <aff id="aff5001">
        <label>5</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Hospital Felicio Rocho, Belo Horizonte, MG &#8211; Brazil</institution>
      </aff>
      <aff id="aff6001">
        <label>6</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Escola de Ecografia de Pernambuco (ECOPE), Recife, PE &#8211; Brazil</institution>
      </aff>
      <aff id="aff7001">
        <label>7</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Benefic&#234;ncia Portuguesa de S&#227;o Paulo, S&#227;o Paulo, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff8001">
        <label>8</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Instituto Dante Pazzanese de Cardiologia, S&#227;o Paulo, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff9001">
        <label>9</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">DF Star, Rede D&#8217;Or S&#227;o Luiz, Bras&#237;lia, DF &#8211; Brazil</institution>
      </aff>
      <aff id="aff10001">
        <label>10</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Hospital Israelita Albert Einstein, S&#227;o Paulo, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff11001">
        <label>11</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Santa Casa de Feira de Santana, Feira de Santana, BA &#8211; Brazil</institution>
      </aff>
      <aff id="aff12001">
        <label>12</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Instituto de Cardiologia e Transplantes do DF, Bras&#237;lia, DF &#8211; Brazil</institution>
      </aff>
      <aff id="aff13001">
        <label>13</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Diagnoson, Grupo Fleury, Salvador, BA &#8211; Brazil</institution>
      </aff>
      <aff id="aff14001">
        <label>14</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Hospital da Bahia, Salvador, BA &#8211; Brazil</institution>
      </aff>
      <aff id="aff15001">
        <label>15</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Escola Bahiana de Medicina e Sa&#250;de P&#250;blica, Salvador, BA &#8211; Brazil</institution>
      </aff>
      <aff id="aff16001">
        <label>16</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Hospital do Cora&#231;&#227;o (HCor), S&#227;o Paulo, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff17001">
        <label>17</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">CardioEco Centro de Diagn&#243;stico Cardiovascular e Ecocardiografia, Curitiba, PR &#8211; Brazil</institution>
      </aff>
      <aff id="aff18001">
        <label>18</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">UnitedHealth Group, Rio de Janeiro, RJ &#8211; Brazil</institution>
      </aff>
      <aff id="aff19001">
        <label>19</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Faculdade de Medicina da Universidade Federal de Goi&#225;s, Goi&#226;nia, GO &#8211; Brazil</institution>
      </aff>
      <aff id="aff20001">
        <label>20</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Hospital Pr&#243;-Cardiaco, Rio de Janeiro, RJ &#8211; Brazil</institution>
      </aff>
      <aff id="aff21001">
        <label>21</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Hospital Universit&#225;rio Ant&#244;nio Pedro da Universidade Federal Fluminense (UFF), Rio de Janeiro, RJ &#8211; Brazil</institution>
      </aff>
      <aff id="aff22001">
        <label>22</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Secretaria de Estado de Sa&#250;de do Distrito Federal, Bras&#237;lia, DF &#8211; Brazil</institution>
      </aff>
      <aff id="aff23001">
        <label>23</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Cl&#237;nica Cardio &amp; Sa&#250;de, Curitiba, PR &#8211; Brazil</institution>
      </aff>
      <aff id="aff24001">
        <label>24</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Heart &amp; Mind Care Servi&#231;os M&#233;dicos (HMC), Manaus, AM &#8211; Brazil</institution>
      </aff>
      <aff id="aff25001">
        <label>25</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Cardiologia N&#227;o Invasiva, Cl&#237;nica CNI, Uberl&#226;ndia, MG &#8211; Brazil</institution>
      </aff>
      <aff id="aff26001">
        <label>26</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Diagn&#243;sticos da Am&#233;rica SA (DASA), S&#227;o Paulo, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff27001">
        <label>27</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Hospital 9 de Julho, S&#227;o Paulo, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff28001">
        <label>28</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Universidade Federal do Paran&#225; (UFPR), Curitiba, PR &#8211; Brazil</institution>
      </aff>
      <aff id="aff29001">
        <label>29</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Departamento de Cardiologia Pedi&#225;trica (DCC/CP) da Sociedade Brasileira de Cardiologia (SBC), S&#227;o Paulo, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff30001">
        <label>30</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Sociedade Brasileira de Oncologia Pedi&#225;trica, S&#227;o Paulo, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff31001">
        <label>31</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Universidade Federal da Bahia (UFBA), Salvador, BA &#8211; Brazil</institution>
      </aff>
      <aff id="aff32001">
        <label>32</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Instituto da Crian&#231;a e do Adolescente do Hospital das Clinicas Faculdade de Medicina da Universidade de S&#227;o Paulo (FMUSP), S&#227;o Paulo, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff33001">
        <label>33</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Hospital Evang&#233;lico, Cachoeiro de Itapemirim, ES &#8211; Brazil</institution>
      </aff>
      <aff id="aff34001">
        <label>34</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Instituto do Cora&#231;&#227;o de Mar&#237;lia (ICM), Mar&#237;lia, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff35001">
        <label>35</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Instituto do C&#226;ncer do Estado de S&#227;o Paulo (ICESP), S&#227;o Paulo, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff36001">
        <label>36</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Hospital Alian&#231;a Rede D&#8217;Or S&#227;o Luiz, Salvador, BA &#8211; Brazil</institution>
      </aff>
      <aff id="aff37001">
        <label>37</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Funda&#231;&#227;o Oswaldo Cruz (FIOCRUZ), Rio de Janeiro, RJ &#8211; Brazil</institution>
      </aff>
      <aff id="aff38001">
        <label>38</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Grupo Fleury, S&#227;o Paulo, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff39001">
        <label>39</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Hospital Cardio Pulmonar Rede D&#8217;or S&#227;o Luiz, Salvador, BA &#8211; Brazil</institution>
      </aff>
      <aff id="aff40001">
        <label>40</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Universidade Federal do Cear&#225;, Fortaleza, CE &#8211; Brazil</institution>
      </aff>
      <aff id="aff41001">
        <label>41</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Universidade Federal do Vale do S&#227;o Francisco (UNIVASF), Petrolina, PE &#8211; Brazil</institution>
      </aff>
      <aff id="aff42001">
        <label>42</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Hospital Nossa Senhora da Concei&#231;&#227;o, Tubar&#227;o, SC &#8211; Brazil</institution>
      </aff>
      <aff id="aff43001">
        <label>43</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Universidade do Sul de Santa Catarina (UNISUL), Tubar&#227;o, SC &#8211; Brazil</institution>
      </aff>
      <aff id="aff44001">
        <label>44</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">EcoHaertel - Hospital Mae de Deus, Porto Alegre, RS &#8211; Brazil</institution>
      </aff>
      <aff id="aff45001">
        <label>45</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Universidade Federal de Ci&#234;ncias da Sa&#250;de de Porto Alegre, Porto Alegre, RS &#8211; Brazil</institution>
      </aff>
      <aff id="aff46001">
        <label>46</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Universidade Federal de S&#227;o Paulo (UNIFESP), S&#227;o Paulo, SP &#8211; Brazil</institution>
      </aff>
      <aff id="aff47001">
        <label>47</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Quanta Diagn&#243;stico por Imagem, Curitiba, PR &#8211; Brazil</institution>
      </aff>
      <aff id="aff48001">
        <label>48</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Hospital Santa Izabel Salvador, BA &#8211; Brazil</institution>
      </aff>
      <aff id="aff49001">
        <label>49</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Santa Casa da Bahia, Salvador, BA &#8211; Brazil</institution>
      </aff>
      <aff id="aff50001">
        <label>50</label>
        <country country="BR">Brazil</country>
        <institution content-type="original">Instituto Nacional de Cardiologia (INC), Rio de Janeiro, RJ &#8211; Brazil</institution>
      </aff>
      <author-notes>
        <corresp id="c01001"><bold>Correspondence:</bold> Sociedade Brasileira de Cardiologia &#8211; Av. Marechal C&#226;mara, 360/330 &#8211; Centro &#8211; Rio de Janeiro, Brazil &#8211; Posta Code 20020-907. E-mail: diretrizes@cardiol.br </corresp>
        <fn fn-type="edited-by">
          <p><bold>Presidents of the Department of Cardiovascular Imaging:</bold> Carlos Eduardo Rochitte (2020/2021) and Andr&#233; Luiz Cerqueira de Almeida (2022/2023)</p>
          <p><bold>Coordinating Editors:</bold> Andr&#233; Luiz Cerqueira de Almeida, Marcelo Dantas Tavares de Melo, Alex dos Santos Felix and David Costa de Souza Le Bihan</p>
          <p><bold>Co-Editors:</bold> Marcelo Luiz Campos Vieira and Jos&#233; Luiz Barros Pena</p>
          <p><bold>SBC Clinical Practice Guidelines Committee:</bold> Carisi Anne Polanczyk (Coordinator), Humberto Graner Moreira, M&#225;rio de Seixas Rocha, Jose Airton de Arruda, Pedro Gabriel Melo de Barros e Silva &#8211; Period 2022-2024</p>
        </fn>
      </author-notes>
      <abstract abstract-type="graphical">
        <p>
          <fig id="f01001">
            <label>Central Illustration</label>
            <caption>
              <title>: Position Statement on the Use of Myocardial Strain in Cardiology Routines by the Brazilian Society of Cardiology&#8217;s Department Of Cardiovascular Imaging &#8211; 2023</title>
            </caption>
            <attrib>
              <italic>Proposal for including strain in the integrated diastolic function assessment algorithm, adapted from Nagueh et al.<sup><italic>67</italic></sup> Am: mitral A-wave duration; Ap: reverse pulmonary A-wave duration; DD: diastolic dysfunction; LA: left atrium; LASr: LA strain reserve; LVGLS: left ventricular global longitudinal strain; TI: tricuspid insufficiency. Confirm concentric remodeling with LVGLS. In LVEF, mitral E wave deceleration time &lt; 160 ms and pulmonary S-wave &lt; D-wave are also parameters of increased filling pressure. This algorithm does not apply to patients with atrial fibrillation (AF), mitral annulus calcification, &gt; mild mitral valve disease, left bundle branch block, paced rhythm, prosthetic valves, or severe primary pulmonary hypertension</italic>
            </attrib>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf01-en.tif"/></fig>
        </p>
      </abstract>
    </front-stub>
    <body>
      <p>
        <table-wrap id="t1001">
          <table frame="hsides" rules="groups">
            <colgroup width="50%">
              <col/>
              <col/>
            </colgroup>
            <thead>
              <tr>
                <th colspan="2">Position Statement on the Use of Myocardial Strain in Cardiology Routines by the Brazilian Society of Cardiology&#8217;s Department Of Cardiovascular Imaging &#8211; 2023</th>
              </tr>
              <tr>
                <th colspan="2">The report below lists declarations of interest as reported to the SBC by the experts during the period of the development of these statement, 2022/2023.</th>
              </tr>
              <tr>
                <th align="left">Expert</th>
                <th align="left">Type of relationship with industry</th>
              </tr>
            </thead>
            <tbody>
              <tr>
                <td>Adenalva Lima de Souza Beck</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Alex Felix</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Ana Clara Rodrigues</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Ana Cristina Camarozano</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Anderson da Costa Armstrong</td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>Financial declaration</p>
                    </list-item>
                    <list-item>
                      <p>A - Economically relevant payments of any kind made to (i) you, (ii) your spouse/partner or any other person living with you, (iii) any legal person in which any of these is either a direct or indirect controlling owner, business partner, shareholder or participant; any payments received for lectures, lessons, training instruction, compensation, fees paid for participation in advisory boards, investigative boards or other committees, etc. From the brazilian or international pharmaceutical, orthosis, prosthesis, equipment and implants industry:</p>
                    </list-item>
                    <list-item>
                      <p>- Amyloidosis: Anylam.</p>
                    </list-item>
                    <list-item>
                      <p>Other relationships Funding of continuing medical education activities, including travel, accommodation and registration in conferences and courses, from the brazilian or international pharmaceutical, orthosis, prosthesis, equipment and implants industry:</p>
                    </list-item>
                    <list-item>
                      <p>- Health area; CARDIOVASF.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Andr&#233; Luiz Cerqueira de Almeida</td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>Financial declaration</p>
                    </list-item>
                    <list-item>
                      <p>A - Economically relevant payments of any kind made to (i) you, (ii) your spouse/partner or any other person living with you, (iii) any legal person in which any of these is either a direct or indirect controlling owner, business partner, shareholder or participant; any payments received for lectures, lessons, training instruction, compensation, fees paid for participation in advisory boards, investigative boards or other committees, etc. From the brazilian or international pharmaceutical, orthosis, prosthesis, equipment and implants industry:</p>
                    </list-item>
                    <list-item>
                      <p>- Boston Scientific: Speaker.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Andressa Mussi Soares</td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>Financial declaration</p>
                    </list-item>
                    <list-item>
                      <p>A - Economically relevant payments of any kind made to (i) you, (ii) your spouse/partner or any other person living with you, (iii) any legal person in which any of these is either a direct or indirect controlling owner, business partner, shareholder or participant; any payments received for lectures, lessons, training instruction, compensation, fees paid for participation in advisory boards, investigative boards or other committees, etc. From the brazilian or international pharmaceutical, orthosis, prosthesis, equipment and implants industry:</p>
                    </list-item>
                    <list-item>
                      <p>- Bayer: Anticoagulation and heart failure; Pfizer: Anticoagulation and amyloidosis; Jannsen: Leukemia.</p>
                    </list-item>
                    <list-item>
                      <p>Other relationships</p>
                    </list-item>
                    <list-item>
                      <p>Funding of continuing medical education activities, including travel, accommodation and registration in conferences and courses, from the brazilian or international pharmaceutical, orthosis, prosthesis, equipment and implants industry:</p>
                    </list-item>
                    <list-item>
                      <p>- Bayer: Heart failure.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Arnaldo Rabischoffsky</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Aur&#233;lio Carvalho Pinheiro</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Bruna Morhy Borges Leal Assun&#231;&#227;o</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Camila Rocon</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Carlos Eduardo Suaide Silva</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Carlos Eduardo Rochitte</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Cecilia Beatriz Bittencourt Viana Cruz</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Cintia Galhardo Tressino</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Claudia Gianini Monaco</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Claudia R. Pinheiro de Castro Grau</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Cl&#225;udio Henrique Fischer</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Daniel de Andrade Hygidio</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Daniela do Carmo Rassi Frota</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>David Costa de Souza Le Bihan</td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>Financial declaration</p>
                    </list-item>
                    <list-item>
                      <p>A - Economically relevant payments of any kind made to (i) you, (ii) your spouse/partner or any other person living with you, (iii) any legal person in which any of these is either a direct or indirect controlling owner, business partner, shareholder or participant; any payments received for lectures, lessons, training instruction, compensation, fees paid for participation in advisory boards, investigative boards or other committees, etc. From the brazilian or international pharmaceutical, orthosis, prosthesis, equipment and implants industry:</p>
                    </list-item>
                    <list-item>
                      <p>- Edwards Lifescience; Abbott; GE Healthcare; Philips.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Eliza de Almeida Gripp</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>F&#225;bio Luis de Jesus Soares</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Fabio Villa&#231;a Guimar&#227;es Filho</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Gabriela Nunes Leal</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Henry Abensur</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Isabel Cristina Britto Guimar&#227;es</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Jeane Mike Tsutsui</td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>Other relationships</p>
                    </list-item>
                    <list-item>
                      <p>Any economically relevant equity interest in companies in the healthcare or education industry or in any companies competing with or supplying to SBC:</p>
                    </list-item>
                    <list-item>
                      <p>- Health area: Grupo Fleury.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Jorge Andion Torre&#227;o</td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>Other relationships</p>
                    </list-item>
                    <list-item>
                      <p>Any economically relevant equity interest in companies in the healthcare or education industry or in any companies competing with or supplying to SBC:</p>
                    </list-item>
                    <list-item>
                      <p>- Partner of an education company in the health sector.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Jorge Eduardo Assef</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Jos&#233; Luiz Barros Pena</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Jose Maria Del Castillo</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Marcelo Dantas Tavares de Melo</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Marcelo Goulart Paiva</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Marcelo Haertel Miglioranza</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Marcelo Luiz Campos Vieira</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>M&#225;rcio Silva Miguel Lima</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Marco Stephan Lofrano Alves</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Maria Eduarda Menezes de Siqueira</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Maria Estef&#226;nia Bosco Otto</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Maria Rosa Dantas</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Maria Veronica Camara dos Santos</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Marly Maria Uellendahl Lopes</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Rafael Bonafim Piveta</td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>Other relationships</p>
                    </list-item>
                    <list-item>
                      <p>Any economically relevant equity interest in companies in the healthcare or education industry or in any companies competing with or supplying to SBC:</p>
                    </list-item>
                    <list-item>
                      <p>- Partner at WavesMed (digital platform for continuing education/updates).</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Rafael Modesto Fernandes</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Renato de Aguiar Hortegal</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Roberto Magalh&#227;es Saraiva</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Rodrigo Bellio de Mattos Barretto</td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>Financial declaration</p>
                    </list-item>
                    <list-item>
                      <p>A - Economically relevant payments of any kind made to (i) you, (ii) your spouse/partner or any other person living with you, (iii) any legal person in which any of these is either a direct or indirect controlling owner, business partner, shareholder or participant; any payments received for lectures, lessons, training instruction, compensation, fees paid for participation in advisory boards, investigative boards or other committees, etc. From the brazilian or international pharmaceutical, orthosis, prosthesis, equipment and implants industry:</p>
                    </list-item>
                    <list-item>
                      <p>- GE; Abbot; Edwards.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Rodrigo Julio Cerci</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Salustiano Pereira de Araujo</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Samira Saady Morhy</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Sanderson Antonio Cauduro</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Sandra Marques e Silva</td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>Other relationships</p>
                    </list-item>
                    <list-item>
                      <p>Funding of continuing medical education activities, including travel, accommodation and registration in conferences and courses, from the brazilian or international pharmaceutical, orthosis, prosthesis, equipment and implants industry:</p>
                    </list-item>
                    <list-item>
                      <p>- Pfizer: Amyloidosis; Sanofi, Pint Pharma, Takeda and Chiesi: Fabry.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
              <tr>
                <td>Sandra N&#237;vea dos Reis Saraiva Falc&#227;o</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Silvio Henrique Barberato</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Thais Harada Campos Espirito Santo</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Tonnison de Oliveira Silva</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Vera Maria Cury Salemi</td>
                <td>Nothing to be declared</td>
              </tr>
              <tr>
                <td>Viviane Tiemi Hotta</td>
                <td>
                  <list list-type="simple">
                    <list-item>
                      <p>Financial declaration</p>
                    </list-item>
                    <list-item>
                      <p>B - Research funding under your direct/personal responsibility (directed to the department or institution) from the Brazilian or international pharmaceutical, orthosis, prosthesis, equipment and implants industry:</p>
                    </list-item>
                    <list-item>
                      <p>- Pfizer: Amyloidosis.</p>
                    </list-item>
                  </list>
                </td>
              </tr>
            </tbody>
          </table>
        </table-wrap>
      </p>
      <sec>
        <title>Table of contents</title>
        <p>1. Basic Concepts in Left Ventricular Strain 7</p>
        <p>1.1. Brief Introduction to the Physical Principles of Speckle Formation in Cardiovascular Imaging 7</p>
        <p>1.2. Definitions 7</p>
        <p><bold>1.2.1. Strain and Strain Rate</bold> 7</p>
        <p><bold>1.2.2. Longitudinal, Circumferential, and Radial Deformation</bold> 7</p>
        <p><bold>1.2.3. Timing Mechanical Events</bold> 8</p>
        <p><bold>1.2.4. Peak Measurements Extracted from Strain Curves</bold> 8</p>
        <p>1.3. Factors Affecting Strain Estimation 8</p>
        <p><bold>1.3.1 Image Quality</bold> 8</p>
        <p><bold>1.3.2. Cardiovascular Imaging Modality</bold> 8</p>
        <p><bold>1.3.3. Software Manufacturer and Version</bold> 8</p>
        <p><bold>1.3.4. Hemodynamic Conditions</bold> 8</p>
        <p>1.4. Global Longitudinal Strain 9</p>
        <p>2. General Recommendations for Using Strain: Clinical Applicability, Comparison with Ejection Fraction, and Adequate Description for Echocardiography Reports 10</p>
        <p>2.1. Prognostic Value, Parametric Patterns, and Subclinical Detection of Heart Disease Through Myocardial Strain 10</p>
        <p>2.2. Which is Better, Strain or Ejection Fraction? 11</p>
        <p>2.3. General Recommendations for Reporting Strain Results and Normality Values 12</p>
        <p>2.4. Conclusion 12</p>
        <p>3. Strain in Cardio-oncology 13</p>
        <p>4. Strain in Diastolic Dysfunction 15</p>
        <p>4.1. Introduction 15</p>
        <p>4.2. Left Ventricle Strain 15</p>
        <p>4.3. Left Atrial Strain 15</p>
        <p>4.4. Conclusion 16</p>
        <p>5. Strain in Cardiomyopathies 16</p>
        <p>5.1. Introduction 16</p>
        <p>5.2. Dilated Cardiomyopathy 16</p>
        <p>5.3. Arrhythmogenic Cardiomyopathy 16</p>
        <p>5.4. Hypertrophic Cardiomyopathy 17</p>
        <p>5.5. Endomyocardial Fibrosis 17</p>
        <p>5.6. Noncompacted Myocardium 17</p>
        <p>6. Strain in Valvular Heart Disease 18</p>
        <p>7. Strain in Ischemic Heart Disease 19</p>
        <p>7.1. Introduction 19</p>
        <p>7.2. Strain in Acute Coronary Syndrome 19</p>
        <p>7.3. Strain in Chronic Coronary Syndromes 20</p>
        <p>7.4. Right Ventricular Strain in Ischemic Heart Disease 20</p>
        <p>8. Strain Assessment in Systemic Diseases (Amyloidosis and Fabry Disease) 20</p>
        <p>8.1. Strain Assessment in Cardiac Amyloidosis 20</p>
        <p><bold>8.1.1. Myocardial Strain Assessment in the Diagnosis of Cardiac Amyloidosis</bold> 21</p>
        <p>8.2. Fabry Disease 23</p>
        <p>9. Strain in Hypertension 24</p>
        <p>9.1. Introduction 24</p>
        <p>9.2. Hypertension without Left Ventricular Hypertrophy Criteria 24</p>
        <p>9.3. Hypertension with Left Ventricular Hypertrophy Criteria 25</p>
        <p>9.4. Clinical Treatment 25</p>
        <p>9.5. Conclusion 25</p>
        <p>10. Strain in Athletes 25</p>
        <p>11. Strain in Stress Echocardiography 26</p>
        <p>12. Strain in Congenital Heart Disease 26</p>
        <p>13. Right Ventricle Strain 26</p>
        <p>13.1. Introduction 26</p>
        <p>13.2. Anatomical and Functional Characteristics of the Right Ventricle 28</p>
        <p>13.3. Right Ventricle and Echocardiographic Parameters in Systolic Function Assessment 28</p>
        <p>13.4. Acquisition and Limitations 28</p>
        <p>13.5. Indications/Normal Values 30</p>
        <p>14. Left and Right Atrial Strain 31</p>
        <p>14.1. Left Atrial Strain Assessment Techniques 31</p>
        <p>14.2. Normality Values 31</p>
        <p>14.3. Clinical Applicability of Left Atrial Strain 32</p>
        <p><bold>14.3.1. Left Atrial Strain and Diastolic Function in Heart Failure</bold> 32</p>
        <p><bold>14.3.2. Atrial Fibrillation</bold> 32</p>
        <p><bold>14.3.3. Valvular Heart Disease</bold> 32</p>
        <p><bold>14.3.4. Coronary Artery Disease</bold> 32</p>
        <p>14.4. Right Atrial Strain 32</p>
        <p>15. Assessing Left Ventricular Torsion 32</p>
        <p>15.1. Introduction 32</p>
        <p>15.2. Definitions and Nomenclature 33</p>
        <p>15.3. Step-by-step Assessment of Ventricular Torsion by Speckle Tracking Echocardiography 33</p>
        <p>16. Strain in Ventricular Dyssynchrony Analysis 34</p>
        <p>16.1. Introduction 34</p>
        <p>16.2. Dyssynchrony Assessment when Selecting Patients for Cardiac Resynchronization Therapy 35</p>
        <p>16.3. Myocardial Viability Assessment 35</p>
        <p>16.4. Electrode Implantation Site 35</p>
        <p>16.5. Prognostic Assessment after CRT 35</p>
        <p>16.6. Adjustment of Resynchronization Parameters 36</p>
        <p>17. Myocardial Work 36</p>
        <p><bold>17.1. Introduction</bold> 36</p>
        <p><bold>17.2. Calculating Myocardial Work</bold> 36</p>
        <p><bold>17.3. Normality Values</bold> 37</p>
        <p><bold>17.4. Potential Clinical Use</bold> 37</p>
        <p>18. Three-dimensional Strain Assessment: What can be Added 40</p>
        <p>18.1. Introduction 40</p>
        <p>18.2. Left Ventricular Strain 41</p>
        <p>18.3. Right Ventricular Strain 41</p>
        <p><bold>18.3.1. Full-volume 3D Acquisition and Analysis</bold> 41</p>
        <p>18.4. Left Atrial Strain 41</p>
        <p>19. The Role of Cardiac Resonance and Tomography in Strain Assessment 41</p>
        <p>19.1. Introduction 41</p>
        <p>19.2. Strain Acquisition Methods by Cardiac Magnetic Resonance Imaging 41</p>
        <p>19.3. Determining Right Ventricle Strain Through Cardiac Magnetic Resonance Imaging 42</p>
        <p>19.4. Determining Left Ventricular Strain Through Cardiac Magnetic Resonance Imaging 42</p>
        <p>19.5. Determining Left Atrial Strain Through Cardiac Magnetic Resonance Imaging 42</p>
        <p>19.6. Determining Strain Through Cardiac Tomography 43</p>
        <p>References 43</p>
      </sec>
      <sec>
        <title>1. Basic Concepts in Left Ventricular Strain</title>
        <sec>
          <title>1.1. Brief Introduction to the Physical Principles of Speckle Formation in Cardiovascular Imaging</title>
          <p>Optical coherence imaging systems such as laser, optical coherence tomography, or ultrasound produce grainy reflections known as speckle.<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B2">2</xref></sup> In echocardiography, an emitted ultrasound pulse moves in a straight line, interacting with the acoustic interfaces of the thoracic cavity until it reaches the heart. Some of the beam is reflected by different cardiac structures, producing an echo that is partially captured by the transducer, and the software uses it as an input to produce images. In this case, the beam&#8217;s wavelength is usually shorter than the structures that reflect it.</p>
          <p>However, when the wavelength is longer than the microstructures it interacts with, the beam is a scattered, radiating in all directions (diffuse scattering). This phenomenon is the result of an interference pattern in all wavefronts scattered by the different phenomena (eg, local differences in tissue density and compressibility). Some this diffuse scattering, or speckle, is captured by the transducer. Although speckle makes the B-mode image less clear for human operators, it should not be seen as noise, since it carries unique information, acting as a myocardial &#8220;fingerprint&#8221;.<sup><xref ref-type="bibr" rid="B1">1</xref></sup></p>
        </sec>
        <sec>
          <title>1.2. Definitions</title>
          <sec>
            <title>1.2.1. Strain and Strain Rate</title>
            <p>Strain is the amount that an object deforms compared to its original shape.<sup><xref ref-type="bibr" rid="B3">3</xref></sup> In cardiology, this concept is represented as the magnitude (%) of myocardial fiber contraction/relaxation in relation to its initial measurement. This concept can be applied to a single segment (regional strain) or to entire heart chambers (global strain), such as the left ventricle (LV). Strain rate indicates the rate of myocardial deformation (%) every second (s<sup>-<xref ref-type="bibr" rid="B1">1</xref></sup>), ie, the speed at which deformation occurs.<sup><xref ref-type="bibr" rid="B3">3</xref>-<xref ref-type="bibr" rid="B4">4</xref></sup></p>
          </sec>
          <sec>
            <title>1.2.2. Longitudinal, Circumferential, and Radial Deformation</title>
            <p>Through the concept of strain, the contraction/relaxation of the LV myocardium from its orientation in different axes can be studied. In fact, due to the helical arrangement of cardiac muscle fibers, LV systolic shortening is determined by the longitudinal and circumferential action of fibers,<sup><xref ref-type="bibr" rid="B5">5</xref></sup> the two active force vectors of strain (<xref ref-type="fig" rid="f02001">Figure 1.1</xref> A).</p>
            <p>
              <fig id="f02001">
                <label>Figure 1.1</label>
                <caption>
                  <title>&#8211; Myocardial strain in different axes. A) Strain can be measured in the longitudinal, circumferential, and radial directions.<italic>4</italic> A third vector results from the interaction of 2 of these force-vectors. B) Radial-circumferential shear strain. C) Longitudinal-circumferential shear strain (ie, ventricular twist/torsion). D) Radial-circumferential shear strain.</title>
                </caption>
                <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf02-en.tif"/></fig>
            </p>
            <p>When longitudinal and circumferential forces are applied to a material with low compressibility, such as myocardial tissue, the myocardium is thickened radially (passive deformation component).<sup><xref ref-type="bibr" rid="B6">6</xref></sup> Ultimately, this accounts for radial shrinkage of the ventricular cavity.<sup><xref ref-type="bibr" rid="B4">4</xref></sup>The deformation process is much more complex than we can measure, since for each interaction between the force vectors, a new vector arises from the shear between the different deformations, called shear strain (<xref ref-type="fig" rid="f02001">Figure 1.1</xref> B, C and D).</p>
            <p>Systolic fiber shortening/thinning in the longitudinal and circumferential direction produces negative strain values, whereas systolic thickening results in positive strain values. Many authors express only the absolute value (modulus value), and we will do the same herein.</p>
          </sec>
          <sec>
            <title>1.2.3. Timing Mechanical Events</title>
            <p>Some fundamental definitions for clinical practice are provided below:<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B7">7</xref></sup></p>
            <list list-type="simple">
              <list-item>
                <p><bold>&#8226;End-systole:</bold> The point of aortic valve closure. Potential substitutes: peak global strain or the volume curve. The software should show which criterion is used to determine end-systole.</p>
              </list-item>
              <list-item>
                <p><bold>&#8226;End-diastole</bold>: The point at which the QRS complex peaks. Event timing should be performed using Doppler imaging in reference to the electrocardiogram.</p>
              </list-item>
            </list>
          </sec>
          <sec>
            <title>1.2.4. Peak Measurements Extracted from Strain Curves (<xref ref-type="fig" rid="f03001">Figure 1.2</xref>)</title>
            <list list-type="simple">
              <list-item>
                <p><bold>&#8226;End-systolic strain:</bold> The point of the strain curve at end-systole, as defined above (aortic valve closure). This is the standard parameter for describing myocardial deformation.</p>
              </list-item>
              <list-item>
                <p><bold>&#8226;Peak systolic strain:</bold> The point at which the peak of the strain curve occurs during systole.</p>
              </list-item>
              <list-item>
                <p><bold>&#8226;Positive peak systolic strain:</bold> the highest positive value of local myocardial stretching at some point during systole.</p>
              </list-item>
              <list-item>
                <p><bold>&#8226;Peak strain:</bold> the highest point of the strain curve during the entire heart cycle. Although this point is usually reached before aortic valve closure, when it occurs afterwards, it is described as post-systolic strain<sup><xref ref-type="bibr" rid="B8">8</xref></sup> or post-systolic shortening. Post-systolic strain is the deformation of segments after aortic valve closure that does not contribute to ventricular ejection.</p>
              </list-item>
            </list>
            <p>
              <fig id="f03001">
                <label>Figure 1.2</label>
                <caption>
                  <title>&#8211; Peak measurements derived from strain curves A) Peak systolic strain, peak strain, and end-systolic (ES) strain coincide upon aortic valve closure (AVC). B) Peak systolic strain and peak strain coincide, although both occur immediately before AVC (red bar), resulting in slight dissociation between these and ES strain. C) Peak and end-systolic strain coincide (both with lower absolute values), although peak strain occurs after AVC (post-systolic shortening phenomenon).</title>
                </caption>
                <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf03-en.tif"/></fig>
            </p>
          </sec>
        </sec>
      </sec>
      <sec>
        <title>1.3. Factors Affecting Strain Estimation</title>
        <sec>
          <title>1.3.1 Image Quality</title>
          <p>Image quality is a critical factor in any software that estimates myocardial strain. Several authors have reported the sensitivity of strain and strain rate estimation proportional to the quality of the image and the tracking algorithm.<sup><xref ref-type="bibr" rid="B9">9</xref>-<xref ref-type="bibr" rid="B11">11</xref></sup></p>
        </sec>
        <sec>
          <title>1.3.2. Cardiovascular Imaging Modality</title>
          <p>Different cardiovascular imaging modalities provide different strain values. Tee et al.<sup><xref ref-type="bibr" rid="B12">12</xref></sup> reported differences between transthoracic echocardiography, computed tomography, and cardiac magnetic resonance imaging (MRI).</p>
        </sec>
        <sec>
          <title>1.3.3. Software Manufacturer and Version</title>
          <p>Two studies by the European Association of Cardiovascular Imaging and the American Society of Echocardiography tested the variability of global longitudinal strain (GLS) measurements among different equipment types and software, finding significant divergences.<sup><xref ref-type="bibr" rid="B13">13</xref>-<xref ref-type="bibr" rid="B14">14</xref></sup> However, such differences are smaller than the ejection fraction (EF) variability reported in the literature.<sup><xref ref-type="bibr" rid="B9">9</xref>-<xref ref-type="bibr" rid="B10">10</xref>,<xref ref-type="bibr" rid="B15">15</xref></sup> In addition to variability among manufacturers, measures can vary in different programs by the same manufacturer, with significant changes in GLS having been reported.<sup><xref ref-type="bibr" rid="B11">11</xref>,<xref ref-type="bibr" rid="B15">15</xref></sup></p>
          <p>Thus, serial echocardiographic studies should ideally be performed using the same device and software and under similar hemodynamic conditions, especially when GLS variation in can restrict therapy options, such as when assessing chemotherapy-induced cardiotoxicity.<sup><xref ref-type="bibr" rid="B4">4</xref></sup></p>
        </sec>
        <sec>
          <title>1.3.4. Hemodynamic Conditions</title>
          <p>LV deformation varies considerably according to the ventricle&#8217;s preload and afterload conditions.</p>
        </sec>
      </sec>
      <sec>
        <title>1.4. Global Longitudinal Strain</title>
        <p>The evidence is more robust for GLS than for any other cardiac strain parameter, and it is the most relevant type for clinical practice.<sup><xref ref-type="bibr" rid="B9">9</xref></sup> It reflects relative LS (%) in the LV myocardium, which occurs from the isovolumetric contraction until the end of the ejection period.<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B5">5</xref>,<xref ref-type="bibr" rid="B15">15</xref></sup></p>
        <p>Mathematically, the contraction at any instant is computed using the algorithm: <inline-formula><mml:math><mml:mrow><mml:mi>G</mml:mi><mml:mi>L</mml:mi><mml:mi>S</mml:mi></mml:mrow><mml:mo>(</mml:mo><mml:mrow><mml:mi>t</mml:mi></mml:mrow><mml:mo>)</mml:mo><mml:mo>=</mml:mo><mml:mn>100</mml:mn><mml:mo>[</mml:mo><mml:mrow><mml:mtext> </mml:mtext><mml:mi>L</mml:mi></mml:mrow><mml:mo>(</mml:mo><mml:mrow><mml:mi>t</mml:mi></mml:mrow><mml:mo>)</mml:mo><mml:mo>&#8722;</mml:mo><mml:mrow><mml:mi>L</mml:mi></mml:mrow><mml:mo>(</mml:mo><mml:mrow><mml:mi>E</mml:mi><mml:mi>D</mml:mi></mml:mrow><mml:mo>)</mml:mo><mml:mrow><mml:mo>/</mml:mo></mml:mrow><mml:mrow><mml:mi>L</mml:mi></mml:mrow><mml:mo>(</mml:mo><mml:mrow><mml:mi>E</mml:mi><mml:mi>D</mml:mi></mml:mrow><mml:mo>)</mml:mo><mml:mo>]</mml:mo></mml:math></inline-formula>, in which L(t) is the longitudinal length at time t, with L(ED) being the end-diastolic length.<sup><xref ref-type="bibr" rid="B1">1</xref></sup></p>
        <p>Programs vary significantly regarding L(ED) length: the entire line of the region of interest x the mean of a given number of points in a region of interest x the mean value in each segment of the same frame. The normal GLS value is approximately 20%,<sup><xref ref-type="bibr" rid="B9">9</xref></sup> although there is evidence that normality varies according to sex and age.<sup><xref ref-type="bibr" rid="B7">7</xref></sup></p>
        <p>To analyze LVGLS by speckle tracking, a series of image acquisition precautions are necessary:</p>
        <list list-type="simple">
          <list-item>
            <p>1) The patient must be monitored electrocardiographically.</p>
          </list-item>
          <list-item>
            <p>2) If possible, an attempt should be made to achieve expiratory apnea, avoiding translational movements of the heart with respiratory incursions.</p>
          </list-item>
          <list-item>
            <p>3) Balance should be sought between the echocardiographic method&#8217;s spatial and temporal resolution (focus, depth, and width adjustments) to optimize the cardiac chamber of interest vs frame rate. The latter should be kept between 40-80 frames per second in patients with a normal heart rate. The higher the heart rate, the higher the required RR values.</p>
          </list-item>
          <list-item>
            <p>4) Avoid foreshortening in LV images.</p>
          </list-item>
          <list-item>
            <p>5) Four-, 3-, and 2-chamber apical acoustic windows must be acquired, preferably with a minimum of 3 beats, excluding extrasystoles.</p>
          </list-item>
        </list>
        <p><xref ref-type="table" rid="t2001">Table 1.1</xref> and <xref ref-type="fig" rid="f04001">Figure 1.3</xref> summarize the GLS measurement procedure.</p>
        <p>
          <table-wrap id="t2001">
            <label>Table 1.1</label>
            <caption>
              <title>&#8211; Step-by-step measurement of global longitudinal strain for most manufacturers4</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="100%">
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left" style="font-weight:normal">
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Good quality cardiac electrocardiographic monitoring</p>
                      </list-item>
                    </list>
                  </th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Obtain 3-, 4-, and 2-chamber acoustic windows with a frame rate between 40-80 frames per second.</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Mark aortic valve closure.</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Mark topographic definitions to determine the region of interest in the 3-, 4- and 2-chamber windows.</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Accept or discard the myocardial segments tracked in each window and make adjustments if necessary.</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Evaluate the curves and interpret the results of the polar map.</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Properly record the hemodynamic conditions under which GLS was measured.</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
              </tbody>
            </table>
          </table-wrap>
        </p>
        <p>
          <fig id="f04001">
            <label>Figure 1.3</label>
            <caption>
              <title>&#8211; Step by step to obtain the global longitudinal strain. Initially, images are acquired in 3, 4 and 2 chambers, with good quality EKG. Images must be acquired at an adequate frame rate (40-80 frames per second) (A: blue ovoid). Aortic valve closure (AVC) is marked using pulsed or continuous Doppler tracking (B). Three points (2 at the base and 1 at the apex) are then marked on the 3 acquired images, determining whether the software adequately tracked the 2D images (C and D). Finally, the curves (E), bull&#8217;s eye map (F), and global longitudinal strain values are obtained. Adapted from Tressino et al.<italic>4</italic></title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf04-en.tif"/></fig>
        </p>
      </sec>
      <sec>
        <title>2. General Recommendations for Using Strain: Clinical Applicability, Comparison with Ejection Fraction, and Adequate Description for Echocardiography Reports</title>
        <sec>
          <title>2.1. Prognostic Value, Parametric Patterns, and Subclinical Detection of Heart Disease Through Myocardial Strain</title>
          <p>Myocardial strain analysis is a robust and versatile tool that offers additional information with less variability than normal prognosis parameters, in addition to parametric cardiomyopathy patterns, and subclinical lesion detection.</p>
          <p>Recent studies have shown the increasing value of LVGLS in relation to left ventricular ejection fraction (LVEF).<sup><xref ref-type="bibr" rid="B10">10</xref></sup> The inter- and intraobserver variability of strain analysis is 4.9-8.6%, which is much lower than LVEF, probably because it is less influenced by ventricular preload and afterload.<sup><xref ref-type="bibr" rid="B13">13</xref>,<xref ref-type="bibr" rid="B16">16</xref></sup> LVGLS is superior to LVEF in patients with heart failure (HF) and in those with reduced and preserved EF (HFrEF and HFpEF, respectively).<sup><xref ref-type="bibr" rid="B17">17</xref>,<xref ref-type="bibr" rid="B18">18</xref></sup> In addition to LV analysis, worsening right ventricular (RV) strain provides additive prognostic value in patients with HFpEF.<sup><xref ref-type="bibr" rid="B19">19</xref></sup></p>
          <p>The morphological findings of cardiomyopathies usually overlap, which is a major diagnostic challenge in daily clinical practice. Increased ventricular mass and thickness is common, being associated with diastolic dysfunction (DD) and preserved LVEF in earlier stages. Parametric analysis of LVGLS with polar mapping can reveal some diagnoses in echocardiogram examination that are undetectable through normal parameters, having been described as a fingerprint for some. One example is the apical sparing pattern in amyloidosis, which will be described below in a specific chapter.<sup><xref ref-type="bibr" rid="B20">20</xref></sup> Such phenotypic characterization has been met with enthusiasm since it facilitates diagnosis of rare pathologies. However, if strain data are not combined with the patient&#8217;s clinical history and morphological and hemodynamic aspects, diagnostic error can result. See examples of apical sparing in <xref ref-type="fig" rid="f05001">Figure 2.1</xref>.</p>
          <p>
            <fig id="f05001">
              <label>Figure 2.1</label>
              <caption>
                <title>&#8211; Global longitudinal strain with apical sparing patterns in different heart diseases. 1: Anthracycline cardiotoxicity; 2: Non-compacted myocardium; 3: Hypothyroidism; 4: Transthyretin amyloidosis.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf05-en.tif"/></fig>
          </p>
          <p>Strain&#8217;s utility as a diagnostic and prognostic tool was consolidated through application in cardio-oncology. This is currently the only area of clinical practice in which it guides conduct (ie, variation from baseline values during chemotherapy). When a relative reduction &gt; 15% occurs, cardiotoxicity with subclinical myocardial injury is considered to have occurred.<sup><xref ref-type="bibr" rid="B21">21</xref></sup> In 2019, a group of societies developed criteria for the proper use of different imaging modalities to evaluate cardiac structures in non-valvular heart disease. Of their 81 recommendations, only 4 dealt with the adequate use of strain: 3 in cardio-oncology and 1 in hypertrophic cardiomyopathy (HCM).<sup><xref ref-type="bibr" rid="B22">22</xref></sup> Although well-designed studies have not validated strain for other applications, it is widely used in large cardio-oncology centers and was reinforced in a recent update of the Brazilian Cardio-oncology Guidelines.<sup><xref ref-type="bibr" rid="B23">23</xref></sup></p>
        </sec>
        <sec>
          <title>2.2. Which is Better, Strain or Ejection Fraction?</title>
          <p>LVEF is one of the main echocardiographic parameters for assessing ventricular function in daily practice, since the data are easy to interpret and are widely accessible through basic ultrasound equipment. This parameter has been extensively validated for heart disease, having being used as a patient inclusion criterion in large therapeutic-intervention studies, as well as a parameter for evaluating and monitoring the results.<sup><xref ref-type="bibr" rid="B24">24</xref></sup> The prognostic value of LVEF has been well established in chronic HF,<sup><xref ref-type="bibr" rid="B25">25</xref></sup> and the European Society of Cardiology&#8217;s current recommendation is for HF to be classified according to the following LVEF values: <bold>1)</bold> HFpEF: EF &#8805; 50%; <bold>2)</bold> HF with a moderately reduced EF (40-49%); and <bold>3)</bold> HFrEF: EF &lt; 40%).<sup><xref ref-type="bibr" rid="B26">26</xref></sup></p>
          <p>LVEF is an important quantitative parameter for defining specific strategies in HF, eg, it is used to indicate cardiac resynchronization therapy in patients with refractory HF (LVEF &#8804; 35%) or to detect cardiotoxicity in cancer patients who are using anthracyclines (&#8805; 10% drop in LVEF compared to baseline and values below the lower limit of normality).<sup><xref ref-type="bibr" rid="B27">27</xref></sup> However, its accuracy is limited when estimated with the 2D Simpson method due to high interobserver variability, which can reach up to 13%.<sup><xref ref-type="bibr" rid="B28">28</xref></sup> Unlike the 2D Simpson method, 3D echocardiography is not based on geometric assumptions and directly measures cavity volumes and LVEF. Its results are quite comparable to those obtained by cardiac MRI. Since it involves automatic algorithms and a lower susceptibility to variation in the acquisition windows (orientation of the apical slices), 3D echocardiography has less intra- and interobserver variability than the 2D method (0.4 [SD, 4.5%]),<sup><xref ref-type="bibr" rid="B29">29</xref></sup> making it a good alternative for monitoring patients who have ventricular dysfunction or are at risk of myocardial damage.</p>
          <p>Myocardial deformation assessment techniques, such as strain, consider the 3 directions of myocardial fiber contraction: longitudinal, radial, and circumferential. LVEF is primarily determined by the radial and circumferential components, which result in thickening of the myocardial walls and reduction of the ventricular cavity in systole. However, LVEF (ie, the &#8220;ejective&#8221; function) is not the only determinant of ventricular performance: it also depends on adequate LV end-diastolic volume for normal systolic volume. This is why patients with cardiomyopathies involving phenotypic expression of concentric parietal hypertrophy (eg, infiltrative or hypertrophic) can have normal LVEF and low cardiac output. These patients clinically present as HFpEF and, despite normal LVEF, generally have a worse prognosis than patients with normal LVEF and preserved cardiac output due to changes in contractile function detectable only by GLS.<sup><xref ref-type="bibr" rid="B30">30</xref></sup></p>
          <p>In fact, longitudinal deformation is the earliest myocardial contractility component to change in most cardiomyopathies and may signal the process at an initial and subclinical stage (prior to reduced LVEF), when therapeutic or cardioprotective measures could have better results. GLS may even be altered in genetic diseases that are not phenotypically expressed, such as Friedreich&#8217;s ataxia, which presents with normal mass and LVEF, and might even predict reduced LVEF and its prognosis.<sup><xref ref-type="bibr" rid="B31">31</xref></sup></p>
          <p>The prognostic value of GLS has been demonstrated in patients with HF, facilitating the prognostic effect of LVEF, especially in patients with EF &gt; 35%.<sup><xref ref-type="bibr" rid="B32">32</xref></sup> For this reason, Potter et al. suggested a new classification of ventricular function, complimenting LVEF with LVGLS to facilitate clinical decision-making and prognostic evaluation, especially in patients with LVEF &gt; 53% (HFpEF).<sup><xref ref-type="bibr" rid="B10">10</xref></sup></p>
        </sec>
        <sec>
          <title>2.3. General Recommendations for Reporting Strain Results and Normality Values</title>
          <p>To simplify description in echocardiography reports, the type of strain (which defines the contraction or relaxation movements) should be indicated, as well as its absolute values (mainly in sequential comparative studies) to prevent mistaken interpretations of worsening strain. The patient&#8217;s vital signs (blood pressure and heart rate) should also be included, due to preload and afterload changes that influence the overall strain value, in addition to the brand of ultrasound equipment and software version, due to varying normality parameters between the manufacturers.<sup><xref ref-type="bibr" rid="B33">33</xref>,<xref ref-type="bibr" rid="B34">34</xref></sup><xref ref-type="table" rid="t3001">Table 2.1</xref> lists essential information to be included in a complete strain report.<sup><xref ref-type="bibr" rid="B9">9</xref></sup></p>
          <p>
            <table-wrap id="t3001">
              <label>Table 2.1</label>
              <caption>
                <title>&#8211; Essential elements for describing strain in echocardiography reports</title>
              </caption>
              <table frame="hsides" rules="groups">
                <colgroup width="50%">
                  <col/>
                  <col/>
                </colgroup>
                <thead>
                  <tr>
                    <th align="left">Relevant Strain Information</th>
                    <th align="left">Description</th>
                  </tr>
                </thead>
                <tbody>
                  <tr>
                    <td>Vital signs</td>
                    <td>Blood pressure and heart rate <sup>16</sup></td>
                  </tr>
                  <tr>
                    <td>
                      <italic>Strain type</italic>
                    </td>
                    <td>Longitudinal, circumferential, and radial</td>
                  </tr>
                  <tr>
                    <td>
                      <italic>Absolute strain value</italic>
                    </td>
                    <td>For describing chamber function</td>
                  </tr>
                  <tr>
                    <td>Cardiac chamber</td>
                    <td>LV, RV, or LA</td>
                  </tr>
                  <tr>
                    <td>Polar map pattern (<xref ref-type="fig" rid="f06001">Figure 2.2</xref>)</td>
                    <td>Any typical patterns, such as amyloidosis or hypertrophic cardiomyopathy <sup>40</sup></td>
                  </tr>
                  <tr>
                    <td>Variation (%) in sequential exams</td>
                    <td>Proven use in cardio-oncology. &#8710;%= baseline strain examination (current/baseline)<sup>21</sup></td>
                  </tr>
                  <tr>
                    <td>Equipment and software version</td>
                    <td>Normal strain values vary according to equipment brand and version<sup>37</sup></td>
                  </tr>
                </tbody>
              </table>
              <table-wrap-foot>
                <attrib>
                  <italic>&#8710;%: percentage (delta) change; LA: left atrium; LV: left ventricle; RV: right ventricle.</italic>
                </attrib>
              </table-wrap-foot>
            </table-wrap>
          </p>
          <p>
            <fig id="f06001">
              <label>Figure 2.2</label>
              <caption>
                <title>&#8211; Strain pattern in polar mapping: A: Typical amyloidosis pattern (apical sparing); B: Typical hypertrophic cardiomyopathy pattern with apical predominance (lower strain predominates in the apex, where hypertrophy was more pronounced in 2D assessment).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf06-en.tif"/></fig>
          </p>
          <p>Normal strain reference values<sup><xref ref-type="bibr" rid="B9">9</xref>,<xref ref-type="bibr" rid="B35">35</xref>-<xref ref-type="bibr" rid="B39">39</xref></sup> must be included in the report. <xref ref-type="table" rid="t4001">Table 2.2</xref> describes simplified average normality values for different strain types, as well as the degree of use in clinical practice. Unlike LVEF, strain normality values have not yet been consistently assimilated in clinical cardiology and, thus, they must be included in the report as a reference.</p>
          <p>
            <table-wrap id="t4001">
              <label>Table 2.2</label>
              <caption>
                <title>&#8211; General normality values for different strain and cardiac chamber modalities and applicaiton in clinical practice</title>
              </caption>
              <table frame="hsides" rules="groups">
                <colgroup width="33%">
                  <col/>
                  <col/>
                  <col/>
                </colgroup>
                <thead>
                  <tr>
                    <th align="left">Chamber/strain type</th>
                    <th>Normality value (absolute value)</th>
                    <th>Application in clinical practice</th>
                  </tr>
                </thead>
                <tbody>
                  <tr>
                    <td>
                      <list list-type="simple">
                        <list-item>
                          <p>
                            <bold>LV</bold>
                          </p>
                        </list-item>
                        <list-item>
                          <p>Longitudinal (negative)</p>
                        </list-item>
                        <list-item>
                          <p>Radial (positive)</p>
                        </list-item>
                        <list-item>
                          <p>Circumferential (negative)</p>
                        </list-item>
                      </list>
                    </td>
                    <td>
                      <list list-type="simple">
                        <list-item>
                          <p>18%<sup>35,39</sup></p>
                        </list-item>
                        <list-item>
                          <p>20%<sup>35</sup></p>
                        </list-item>
                        <list-item>
                          <p>40%<sup>35</sup></p>
                        </list-item>
                        <list-item>
                          <p>20%</p>
                        </list-item>
                      </list>
                    </td>
                    <td align="center">
                      <list list-type="simple">
                        <list-item>
                          <p>++++</p>
                        </list-item>
                        <list-item>
                          <p>+</p>
                        </list-item>
                        <list-item>
                          <p>+</p>
                        </list-item>
                      </list>
                    </td>
                  </tr>
                  <tr>
                    <td>
                      <list list-type="simple">
                        <list-item>
                          <p>
                            <bold>RV</bold>
                          </p>
                        </list-item>
                        <list-item>
                          <p>Longitudinal free wall (negative)</p>
                        </list-item>
                      </list>
                    </td>
                    <td>
                      <list list-type="simple">
                        <list-item>
                          <p>20%<sup>35,36</sup></p>
                        </list-item>
                      </list>
                    </td>
                    <td align="center">
                      <list list-type="simple">
                        <list-item>
                          <p>+++</p>
                        </list-item>
                      </list>
                    </td>
                  </tr>
                  <tr>
                    <td>
                      <list list-type="simple">
                        <list-item>
                          <p><bold>LA</bold> (varies with age, positive)</p>
                        </list-item>
                        <list-item>
                          <p>Reservoir (most common)</p>
                        </list-item>
                        <list-item>
                          <p>Conduit</p>
                        </list-item>
                        <list-item>
                          <p>Pump</p>
                        </list-item>
                      </list>
                    </td>
                    <td>
                      <list list-type="simple">
                        <list-item>
                          <p>39%<sup>38,39</sup></p>
                        </list-item>
                        <list-item>
                          <p>23%<sup>38</sup></p>
                        </list-item>
                        <list-item>
                          <p>17%<sup>38,41</sup></p>
                        </list-item>
                      </list>
                    </td>
                    <td align="center">
                      <list list-type="simple">
                        <list-item>
                          <p>+++</p>
                        </list-item>
                        <list-item>
                          <p>+</p>
                        </list-item>
                        <list-item>
                          <p>+</p>
                        </list-item>
                      </list>
                    </td>
                  </tr>
                </tbody>
              </table>
              <table-wrap-foot>
                <attrib>
                  <italic>LA: left atrium; LV: left ventricle; RV: right ventricle. ++++ Commonly used; +++ Used; ++ Limited use in clinical practice; + Limited use in clinical practice and not included in echocardiography equipment software.</italic>
                </attrib>
              </table-wrap-foot>
            </table-wrap>
          </p>
        </sec>
        <sec>
          <title>2.4. Conclusion</title>
          <p>Although current evidence for incorporating strain into daily clinical practice is robust, there are still several challenges to doing so in Brazil, such as unequal access to echocardiogram services with analysis software and a lack of national population data. We used values extrapolated from a population with a very different sociodemographic profile, with application adapted for the Brazilian population. The Brazilian Cardiology Society&#8217;s Department of Cardiovascular Imaging is promoting a multicentric work (already in progress), when echocardiographic data from healthy Brazilians is being analyzed. Strain adds to normal echocardiogram values, increasing prognostic robustness, enabling the diagnosis of cardiomyopathies (especially those presenting with increased myocardial thickness) and subclinical myocardial injury.</p>
        </sec>
      </sec>
      <sec>
        <title>3. Strain in Cardio-oncology</title>
        <p>Cancer treatment-related cardiac dysfunction is an important cause of morbidity and mortality.<sup><xref ref-type="bibr" rid="B42">42</xref>,<xref ref-type="bibr" rid="B43">43</xref></sup> This complication can interrupt treatment and compromise healing and/or adequate cancer control.<sup><xref ref-type="bibr" rid="B44">44</xref>,<xref ref-type="bibr" rid="B45">45</xref></sup>HF due to the cardiotoxicity of chemotherapy drugs often has a worse prognosis than many neoplasms, with a 2-year mortality of up to 60%.<sup><xref ref-type="bibr" rid="B42">42</xref></sup> Early identification of cardiotoxicity and cardioprotective intervention could affect prognosis in such cases.<sup><xref ref-type="bibr" rid="B46">46</xref>,<xref ref-type="bibr" rid="B47">47</xref></sup> However, normal diagnostic methods, such as the 2D LVEF, have low sensitivity.<sup><xref ref-type="bibr" rid="B48">48</xref>,<xref ref-type="bibr" rid="B49">49</xref></sup> Thus, earlier markers, such as strain analysis, could be of great importance.</p>
        <p>Diagnostic imaging methods play a fundamental role in such circumstances, and echocardiography has been the most common tool due to its anatomical correspondence, non-invasive nature, easy access, low cost, and lack of ionizing radiation.<sup><xref ref-type="bibr" rid="B27">27</xref></sup> Two-dimensional LVEF, the most common parameter for diagnosing cardiotoxicity, is calculated using Simpson&#8217;s method.<sup><xref ref-type="bibr" rid="B21">21</xref></sup> However, 3D echocardiography, when available, is the technique of choice for monitoring LVEF in cancer patients. Its main advantages include greater accuracy in recognizing LVEF values below the lower limit of normality and greater reproducibility than the 2D technique, with accuracy similar to cardiac MRI. However, its low availability, high cost, and learning curve prevent more widespread use.<sup><xref ref-type="bibr" rid="B27">27</xref>,<xref ref-type="bibr" rid="B50">50</xref></sup></p>
        <p>Cancer treatment-related ventricular dysfunction is defined as a &gt; 10% absolute drop in LVEF to &lt; 50%, with or without HF symptoms. This echocardiographic examination should be repeated within 2-3 weeks to assess the effects of preload and afterload on LVEF.</p>
        <p>Despite being an important and established prognostic factor, LVEF has low sensitivity for diagnosing cardiotoxicity. LVEF is dependent on certain factors, such as cardiac preload, image quality, and examiner experience. It can underestimate real cardiac damage, since compensatory hemodynamic mechanisms allow adequate LV systolic performance despite myocyte dysfunction.<sup><xref ref-type="bibr" rid="B48">48</xref></sup> Thus, reduced LVEF often occurs at a very late stage, when therapeutic intervention does not lead to functional recovery in most cases.<sup><xref ref-type="bibr" rid="B46">46</xref>,<xref ref-type="bibr" rid="B48">48</xref>,<xref ref-type="bibr" rid="B49">49</xref></sup></p>
        <p>When cardiotoxicity is detected and treated early, patients have a greater chance of recovering ventricular function,<sup><xref ref-type="bibr" rid="B46">46</xref>,<xref ref-type="bibr" rid="B51">51</xref></sup> and myocardial strain analysis can play an important role in this. Determining strain through 2D speckle-tracking has emerged as a sensitive and reproducible means of analyzing systolic function and LV contractility; this method has been validated in both in vitro and in vivo models<italic>.</italic><sup><xref ref-type="bibr" rid="B52">52</xref>,<xref ref-type="bibr" rid="B53">53</xref></sup> A growing number of publications have shown that myocardial strain analysis through 2D speckle-tracking is useful for early and subclinical detection of chemotherapy-induced cardiotoxicity, especially regarding relative decreases in GLS.<sup><xref ref-type="bibr" rid="B23">23</xref>,<xref ref-type="bibr" rid="B54">54</xref>-<xref ref-type="bibr" rid="B57">57</xref></sup></p>
        <p>GLS analysis is recommended for patients who undergo potentially cardiotoxic chemotherapy treatment. A &#8805; 12% decrease in GLS in relation to baseline suggests a subclinical diagnosis of cardiotoxicity.<sup><xref ref-type="bibr" rid="B21">21</xref>,<xref ref-type="bibr" rid="B27">27</xref></sup>Without baseline (pre-chemotherapy) values for comparison, expert opinion suggests an absolute strain value of &lt; 17% as a marker of subclinical cardiotoxicity, provided there is no other underlying myocardial disease. GLS reductions &lt; 8% from baseline are considered non-significant. <xref ref-type="fig" rid="f07001">Figure 3.1</xref> presents an example of subclinical cardiotoxicity suggested by relative GLS reduction.</p>
        <p>
          <fig id="f07001">
            <label>Figure 3.1</label>
            <caption>
              <title>&#8211; Example of subclinical cardiotoxicity in a patient with breast cancer. Analysis of LVEF through Simpson&#8217;s method and GLS with bull&#8217;s eye mapping. A and B: pre-chemotherapy evaluation; B and C: evaluation after a cumulative dose of 240 mg/m2 of doxorubicin. Although there was no significant reduction in LVEF, there was a 22% relative decrease in GLS. LVEF: left ventricular ejection fraction; GLS: global longitudinal strain.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf07-en.tif"/></fig>
        </p>
        <p><xref ref-type="fig" rid="f08001">Figure 3.2</xref> presents an algorithm for echocardiographic follow-up in cancer patients based on LVEF and GLS. <xref ref-type="fig" rid="f09001">Figures 3.3</xref> and <xref ref-type="fig" rid="f10001">3.4</xref> present echocardiographic monitoring data in patients treated with anthracyclines and trastuzumab, respectively.</p>
        <p>
          <fig id="f08001">
            <label>Figure 3.2</label>
            <caption>
              <title>&#8211; Algorithm for evaluating cancer patients during chemotherapy treatment, based on LVEF and GLS. ACE: angiotensin-converting enzyme; CV: cardiovascular; CT: chemotherapy Echo: echocardiography; GLS: global longitudinal strain; HF: heart failure; LVEF: left ventricular ejection fraction.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf08-en.tif"/></fig>
        </p>
        <p>
          <fig id="f09001">
            <label>Figure 3.3</label>
            <caption>
              <title>&#8211; Echocardiographic monitoring during anthracycline therapy. Echo: echocardiography; GLS: global longitudinal strain; LVEF: left ventricular ejection fraction.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf09-en.tif"/></fig>
        </p>
        <p>
          <fig id="f10001">
            <label>Figure 3.4</label>
            <caption>
              <title>&#8211; Echocardiographic monitoring during trastuzumab therapy. Echo: echocardiography. GLS: global longitudinal strain; LVEF: left ventricular ejection fraction.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf10-en.tif"/></fig>
        </p>
        <p>SUCCOUR was the first prospective multicenter trial to show the prognostic impact of GLS-based cardioprotection compared to LVEF (3D echocardiography)-based cardioprotection. In patients receiving anthracycline-based chemotherapy (ie, at high risk of cardiotoxicity), cardioprotective intervention (ACE inhibitors and beta-blockers) based on a &#8805; 12% reduction in GLS relative to baseline resulted in smaller LVEF reductions and a lower incidence of cancer treatment-related cardiac dysfunction over 1 year of follow-up.<sup><xref ref-type="bibr" rid="B58">58</xref></sup></p>
        <p>Compared to 2D speckle tracking, calculating strain through 3D tracking has shown technical advantages regarding accuracy, reproducibility, and applicability in different contexts.<sup><xref ref-type="bibr" rid="B59">59</xref>-<xref ref-type="bibr" rid="B62">62</xref></sup> Recently, small studies have demonstrated the impact of 3D speckle-tracking on early recognition of chemotherapy-related mechanical changes.<sup><xref ref-type="bibr" rid="B63">63</xref>-<xref ref-type="bibr" rid="B66">66</xref></sup> However, larger studies with longer follow-up are needed to assess this technique&#8217;s prognostic value.</p>
        <p>Nevertheless, GLS analysis has certain limitations, among which we highlight measurement variability among equipment manufacturers. Thus, measurements must always be performed on the same devices. Like LVEF, GLS is influenced by preload and afterload effects, ventricular geometry, tissue changes (eg, infarction and myocarditis) and conduction disorders. Finally, certain clinical and oncological information is essential and must be clear in the echocardiography report for accurate interpretation, as shown in the <xref ref-type="table" rid="t5001">Table 3.1</xref>.</p>
        <p>
          <table-wrap id="t5001">
            <label>Table 3.1</label>
            <caption>
              <title>&#8211; Relevant Clinical and Oncological Information in Echocardiography Reports</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="100%">
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left" style="font-weight:normal">Time between chemotherapy drug infusion and echocardiography (pre- or post-)</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>Heart rate</p>
                      </list-item>
                      <list-item>
                        <p>Blood pressure</p>
                      </list-item>
                      <list-item>
                        <p>Volume status (description of the diameter and variation of the inferior vena cava)</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Comparison with baseline, especially left ventricular ejection fraction and GLS: if there is a relative decrease, report the percentage)</td>
                </tr>
                <tr>
                  <td>Equipment/software used for GLS analysis</td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>GLS: global longitudinval strain.</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
      </sec>
      <sec>
        <title>4. Strain in Diastolic Dysfunction</title>
        <sec>
          <title>4.1. Introduction</title>
          <p>DD is considered an early marker of myocardial damage and, even when asymptomatic, it has high mortality rates. As DD increases, LV filling pressures and HFpEF increase.<sup><xref ref-type="bibr" rid="B67">67</xref>,<xref ref-type="bibr" rid="B68">68</xref></sup> The latter accounts for more than 50% of HF hospitalizations, with mortality rates comparable to those of HFrEF.<sup><xref ref-type="bibr" rid="B69">69</xref></sup> Unlike HFpEF, preclinical DD may be reversible. However, its pathophysiology is complex and, despite involving several parameters, the currently recommended algorithm is not very sensitive for subclinical stages.<sup><xref ref-type="bibr" rid="B70">70</xref>,<xref ref-type="bibr" rid="B71">71</xref></sup></p>
          <p>Indeterminate cases are also frequent since these parameters do not always change simultaneously or linearly.<sup><xref ref-type="bibr" rid="B70">70</xref></sup> Non-diastolic factors can also contribute to HFpEF, leading to varied phenotypic expression depending on the predominant pathophysiological mechanism.<sup><xref ref-type="bibr" rid="B72">72</xref></sup> Tools that assess LV and left atrial (LA) mechanics by measuring strain can overcome these diagnostic challenges.<sup><xref ref-type="bibr" rid="B73">73</xref>,<xref ref-type="bibr" rid="B74">74</xref></sup> The role of RV mechanics in this context is still under investigation.<sup><xref ref-type="bibr" rid="B75">75</xref></sup></p>
        </sec>
        <sec>
          <title>4.2. Left Ventricle Strain</title>
          <p>Several studies have shown that myocardial strain parameters evaluated through speckle tracking, especially LVGLS, have a better correlation with LV relaxation and more accurately predict filling pressures and exercise intolerance than those derived from tissue Doppler.<sup><xref ref-type="bibr" rid="B76">76</xref>-<xref ref-type="bibr" rid="B78">78</xref></sup> Reduced LVGLS helps detect DD at earlier stages and also predicts cardiovascular events in HFpEF.<sup><xref ref-type="bibr" rid="B17">17</xref>,<xref ref-type="bibr" rid="B79">79</xref>-<xref ref-type="bibr" rid="B82">82</xref></sup> In light of this evidence, reduced LVGLS (&lt;16%) has already been included as a diagnostic criterion in a new algorithm in recent HFpEF guidelines.<sup><xref ref-type="bibr" rid="B83">83</xref></sup></p>
        </sec>
        <sec>
          <title>4.3. Left Atrial Strain</title>
          <p>LA strain allows for a more detailed analysis of LA function and its various components (reservoir, conduit, and pump function).<sup><xref ref-type="bibr" rid="B70">70</xref></sup> Changes in LA strain express ventriculoatrial coupling and result from chronic exposure to elevated LV pressure, and reductions in LA compliance and relaxation,<sup><xref ref-type="bibr" rid="B41">41</xref>,<xref ref-type="bibr" rid="B84">84</xref>,<xref ref-type="bibr" rid="B85">85</xref></sup> which may precede morphological remodeling.<sup><xref ref-type="bibr" rid="B86">86</xref>-<xref ref-type="bibr" rid="B88">88</xref></sup> Although reductions in all LA strain components has been described,<sup><xref ref-type="bibr" rid="B86">86</xref>,<xref ref-type="bibr" rid="B89">89</xref>,<xref ref-type="bibr" rid="B90">90</xref></sup> the reservoir LA strain is the most robust parameter, changing linearly with DD progression.<sup><xref ref-type="bibr" rid="B91">91</xref>-<xref ref-type="bibr" rid="B93">93</xref></sup> Morris et al, among other authors, demonstrated that reduced reservoir LA strain (&lt; 23%) increased DD detection and correlated with filling pressures and clinical outcomes.<sup><xref ref-type="bibr" rid="B93">93</xref>-<xref ref-type="bibr" rid="B99">99</xref></sup></p>
          <p>Due to the growing evidence, LVGLS and LA reservoir strain could be integrated into the current DD algorithm, as proposed in the <xref ref-type="fig" rid="f01001">Central Figure</xref>. This strategy may help reclassify indeterminate cases and increase accuracy in identifying earlier stages of DD, especially in individuals with cardiovascular risk factors or unexplained dyspnea.<sup><xref ref-type="bibr" rid="B97">97</xref></sup></p>
          <p>Standardization of strain methodology has helped minimize variability between manufacturers, which is still a limitation.<sup><xref ref-type="bibr" rid="B7">7</xref>,<xref ref-type="bibr" rid="B92">92</xref>,<xref ref-type="bibr" rid="B100">100</xref>,<xref ref-type="bibr" rid="B101">101</xref></sup> New prospective multicenter studies are expected to determine whether modifying these indices with treatment can improve DD and HFpEF prognosis.</p>
        </sec>
        <sec>
          <title>4.4. Conclusion</title>
          <p>LVGLS and LA reservoir strain are subclinical disease markers that can be incorporated into current recommendations to refine the diagnosis, staging, and prognosis of DD. Considering the complex nature of such assessments, using artificial intelligence to validate and implement algorithms would be beneficial.</p>
        </sec>
      </sec>
      <sec>
        <title>5. Strain in Cardiomyopathies</title>
        <sec>
          <title>5.1. Introduction</title>
          <p>Generally speaking, cardiomyopathies are disorders of the heart muscle. Strictly speaking, they are not associated with certain conditions known to be aggressive to the myocardium, such as coronary artery disease, arterial hypertension, valvular heart disease, and congenital heart disease. They can be divided into the following groups: dilated, hypertrophic, restrictive, arrhythmogenic cardiomyopathy, and &#8220;unclassified&#8221;.<sup><xref ref-type="bibr" rid="B102">102</xref></sup></p>
        </sec>
        <sec>
          <title>5.2. Dilated Cardiomyopathy</title>
          <p>Dilated cardiomyopathy is a disease that, by definition, affects myocardial tissue and leads to a progressive reduction in systolic function and dilation of the LV cavity. Clinically, individuals may present signs and symptoms of HF, requiring treatment, hospitalization, and finally, heart transplantation.<sup><xref ref-type="bibr" rid="B102">102</xref>-<xref ref-type="bibr" rid="B107">107</xref></sup></p>
          <p>Echocardiography, part of the first-line diagnostic arsenal, plays an extremely important role in diagnosis and prognosis. Its main objectives are to determine the volume of the cardiac chambers and assess LV systolic performance. This usually involves estimating the EF, which should be done according to Simpson&#8217;s method. Strain assessment is an additional echocardiographic tool that can enrich this process. It allows detection of subtle, subclinical abnormalities in the early stages of disease.</p>
          <p>Abduch et al. found excellent correlation between volumetric parameters obtained by 3D echocardiography and strain assessment in patients with dilated cardiomyopathy.<sup><xref ref-type="bibr" rid="B108">108</xref></sup> Since the clinical course of dilated cardiomyopathy leads to more pronounced phases of LV systolic impairment, there will be greater reductions in strain and strain rate in the longitudinal, radial, and circumferential components <xref ref-type="fig" rid="f11001">Figure 5.1</xref>.<sup><xref ref-type="bibr" rid="B109">109</xref></sup> LV torsion also follows this downward trend with disease progression. Additionally, in very advanced stages, the rotations may also be inverted, ie, basal segments rotating counterclockwise and apical segments rotating clockwise.<sup><xref ref-type="bibr" rid="B110">110</xref>-<xref ref-type="bibr" rid="B112">112</xref></sup></p>
          <p>
            <fig id="f11001">
              <label>Figure 5.1</label>
              <caption>
                <title>&#8211; A) Example of normal left ventricle global longitudinal strain. Note the negative deflections of the curves, which are relatively homogeneous in the 3 views. In the lower right is the parametric bull&#8217;s eye mapping, with all fields in more intense red, indicating good global strain; B) Example of strain in an individual with dilated cardiomyopathy due to Chagas disease. Note the reduced amplitude of the curves, which are also very heterogeneous. The septal and inferior wall strain curves have a positive deflection, ie, indicating distension or dyskinesia, which in the bull&#8217;s eye map appears blue (yellow arrows), in addition to pink areas, which indicate low strain values (GLS = -5.6%).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf11-en.tif"/></fig>
          </p>
          <p>GLS is an independent predictor of all-cause mortality in patients with HFrEF, especially men without AF.<sup><xref ref-type="bibr" rid="B113">113</xref></sup> In patients with recovered LVEF, abnormal GLS predicts the likelihood of decreased LVEF during follow-up, whereas normal GLS predicts the likelihood of stable LVEF during recovery.<sup><xref ref-type="bibr" rid="B114">114</xref></sup></p>
        </sec>
        <sec>
          <title>5.3. Arrhythmogenic Cardiomyopathy</title>
          <p>Arrhythmogenic cardiomyopathy is histologically characterized by fibrofatty infiltration in the myocardial tissue. Although this infiltration generally occurs in the entrance, exit, and apex of the RV (the &#8220;dysplasia triangle&#8221;), the LV can also be affected concomitantly or even exclusively.<sup><xref ref-type="bibr" rid="B115">115</xref>-<xref ref-type="bibr" rid="B117">117</xref></sup></p>
          <p>Macroscopically, the ventricular wall tends to thin and forms microaneurysms, progressing to systolic impairment and cavity dilation. The gold standard diagnostic method is cardiac MRI, although echocardiography is the initial examination. RV free wall strain assessment can help determine systolic impairment in this cavity.</p>
          <p>In 2007 Prakasa et al. were the first to analyze strain in RV dysplasia/cardiomyopathy, finding a consistent difference in strain values between diseased (10% [SD 6%]) and healthy individuals (28% [SD 11%], P = 0.001).<sup><xref ref-type="bibr" rid="B118">118</xref></sup></p>
          <p>RV free wall LS is associated with the rate of structural progression in patients with arrhythmogenic cardiomyopathy. It can be a useful marker for determining which patients require closer follow-up and treatment. Patients with RV strain &lt; 20% have a higher risk of structural progression (odds ratio: 18.4; 95% CI, 2.7-125.8; P = 0.003).<sup><xref ref-type="bibr" rid="B119">119</xref></sup></p>
          <p>Patients with arrhythmogenic cardiomyopathy have reduced right atrial (RA) strain in all diastole phases, even when the RA volume is normal. RA strain, obtained during the reservoir and pump phases, is associated with a greater risk of cardiovascular events.<sup><xref ref-type="bibr" rid="B120">120</xref></sup></p>
        </sec>
        <sec>
          <title>5.4. Hypertrophic Cardiomyopathy</title>
          <p>HCM, an autosomal dominant disease, is the most common heart disease of genetic etiology. It is characterized by increased ventricular myocardial thickness of different morphologies (concentric, apical, or septal, hypertrophy of the LV free wall and RV) and is related to increased morbidity and mortality in affected patients.<sup><xref ref-type="bibr" rid="B121">121</xref>-<xref ref-type="bibr" rid="B123">123</xref></sup></p>
          <p>Echocardiography is the most common imaging method for morphological and hemodynamic diagnosis. About 25% of these patients have an LV outflow tract gradient &gt; 30 mm Hg at rest, which can be quantified by continuous Doppler.<sup><xref ref-type="bibr" rid="B124">124</xref></sup> The gradient, which may be dynamic in these patients, can be better evaluated echocardiographically either using the Valsalva maneuver or through physical or pharmacological stress with dobutamine.<sup><xref ref-type="bibr" rid="B125">125</xref></sup> A high intraventricular gradient in HCM may be a determinant of decreased myocardial deformity and torsion mechanisms, as well as LA strain.<sup><xref ref-type="bibr" rid="B126">126</xref></sup></p>
          <p>Myocardial strain measured through speckle-tracking helps clarify regional and global cardiac mechanics in HCM and can detect early changes in systolic function, fibrosis, and a greater risk of arrhythmia, even in patients with normal systolic function.<sup><xref ref-type="bibr" rid="B126">126</xref>-<xref ref-type="bibr" rid="B130">130</xref></sup> Polar mapping helps differentiate phenocopies that lead to increased thickness and reduced longitudinal myocardial strain at the site of hypertrophy<sup><xref ref-type="bibr" rid="B20">20</xref>,<xref ref-type="bibr" rid="B131">131</xref>,<xref ref-type="bibr" rid="B132">132</xref></sup> (<xref ref-type="fig" rid="f12001">Figure 5.2</xref>).</p>
          <p>
            <fig id="f12001">
              <label>Figure 5.2</label>
              <caption>
                <title>&#8211; A) Two-dimensional image demonstrating non-obstructive asymmetric septal hypertrophy, with an interventricular septum measuring 23 mm and a posterior wall measuring 11 mm; B) normal global longitudinal strain (GLS) of the LV (20%), with parametric bull&#8217;s eye mapping segments with good myocardial strain are darker red, while pink indicates lower strain values in the septal segments (8%); C) 4-chamber view, with lower myocardial strain in the middle and basal inferoseptal segments; D) note the reduced amplitude of the curves representing septal segments, also shown in pink in the bull&#8217;s eye map, representing lower strain values (8%).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf12-en.tif"/></fig>
          </p>
          <p>Hiemstra et al. found that indexed LA volume and LVGLS were independent prognostic factors for adverse outcomes, such as sudden death and heart transplantation, as well as independent GLS values &gt; 10%.<sup><xref ref-type="bibr" rid="B133">133</xref></sup> Although RV global longitudinal strain (RVGLS) may be altered in HCM patients due to structural heart disease, its prognostic significance is unknown.<sup><xref ref-type="bibr" rid="B133">133</xref>,<xref ref-type="bibr" rid="B134">134</xref></sup></p>
        </sec>
        <sec>
          <title>5.5. Endomyocardial Fibrosis</title>
          <p>Endomyocardial fibrosis is the most common restrictive cardiomyopathy in tropical climates, affecting approximately 10 million people worldwide. It is characterized by subendocardial fibrosis of the apices and inflow tracts of one or both ventricles. Its etiology, which is still unknown, may be related to hypereosinophilia, parasitic infestations, or protein malnutrition, especially in populations of low socioeconomic status.</p>
          <p>Echocardiography will show ventricles of normal or reduced size with &#8220;mushroom&#8221; or &#8220;V&#8221; ventricular morphology due to fibrosis, which may be associated with apical endocardial thrombosis, hyperkinesis of the basal portion of the LV (Merlon sign), greatly increased atrial volume, often preserved ventricular systolic function, and DD.<sup><xref ref-type="bibr" rid="B135">135</xref>-<xref ref-type="bibr" rid="B137">137</xref></sup></p>
          <p>Although few studies have assessed endomyocardial fibrosis using 3D echocardiography with speckle-tracking, they have found reduced GLS, especially with more severe apical involvement.<sup><xref ref-type="bibr" rid="B137">137</xref>,<xref ref-type="bibr" rid="B138">138</xref></sup></p>
        </sec>
        <sec>
          <title>5.6. Noncompacted Myocardium</title>
          <p>Noncompacted myocardial tissue is characterized by prominent trabeculae and deep intertrabecular recesses due to incomplete compaction during embryonic life. This can lead to a clinical picture of HF, arrhythmias, and thromboembolic events. Existing in sporadic and familial forms, the latter are related to sarcomere protein mutations. Myocardial strain indices allow a proper regional analysis of ventricular function in patients with noncompacted myocardium and help differentiate it from other forms of HCM.</p>
          <p>An Indian study compared the myocardial strain in 12 patients with noncompacted myocardium, 18 patients with HCM, and 18 healthy controls. Both patient groups had reduced LS, although it was lower in the apical region in the noncompacted myocardium group than the HCM group (12.18 [SD, 6.25] vs 18.37 [SD, 3.67]; p &lt; 0.05), suggesting that this region was more involved in myocardial noncompaction. Furthermore, an apical-basal gradient in LS was observed in noncompacted myocardium but not HCM.<sup><xref ref-type="bibr" rid="B139">139</xref></sup> DD was found in both patient groups. Another study found greater LS in a LV non-contraction group than a non-specific dilated cardiomyopathies group, reporting that the base-apex mid-wall gradient of strain is a useful index for differentiating these diseases (sensitivity: 88.4 %; specificity: 66.7%).<sup><xref ref-type="bibr" rid="B140">140</xref></sup></p>
          <p>In normal hearts, the base rotates clockwise during systole, while the apex rotates counterclockwise, with torsion being the apical minus basal rotation. A study found that 50% of patients with noncompacted myocardium have rigid body rotation, with clockwise rotation of the apex and base, although others have found prevalences of 53.3% and 83%.<sup><xref ref-type="bibr" rid="B141">141</xref>,<xref ref-type="bibr" rid="B142">142</xref></sup> A study of 28 children with noncompacted myocardium found that 39% had rigid body rotation. This group had lower LS, but not LVEF than those without rigid body rotation, which may have prognostic value.<sup><xref ref-type="bibr" rid="B143">143</xref></sup> These authors also suggested that rigid body rotation may be related to dysfunction of the compacted subepicardial apical layer and unrelated to trabeculae distribution. Another study of 101 children with noncompacted myocardium found that the adverse outcome group had lower longitudinal, radial, and circumferential strain, which suggests that this disease affects the heart globally rather than just the non-compacted region.<sup><xref ref-type="bibr" rid="B144">144</xref></sup></p>
        </sec>
      </sec>
      <sec>
        <title>6. Strain in Valvular Heart Disease</title>
        <p>Due to its combined analysis of changes in anatomy and valve function, transthoracic Doppler echocardiography is the first-line method for diagnosing valvular heart disease and classifying its severity.<sup><xref ref-type="bibr" rid="B145">145</xref></sup> This method helps define the best intervention type and time point for treating valvular heart diseases.</p>
        <p>Classically, treatment is based on symptoms and complicating factors,<sup><xref ref-type="bibr" rid="B145">145</xref></sup>with LV dysfunction considered the most important complicating factor.<sup><xref ref-type="bibr" rid="B145">145</xref></sup>LV function is usually determined through echocardiographic LVEF measurement.<sup><xref ref-type="bibr" rid="B146">146</xref></sup></p>
        <p>However, there is evidence that LV strain can identify ventricular dysfunction before EF decreases. Perhaps mitral regurgitation can best represent this paradox, since in this condition the high preload and low afterload mean that EF does not adequately represent LV systolic function. For this reason, the definition of LV dysfunction in this condition is quite conservative in clinical guidelines.<sup><xref ref-type="bibr" rid="B145">145</xref>,<xref ref-type="bibr" rid="B147">147</xref>-<xref ref-type="bibr" rid="B149">149</xref></sup> However, some studies have indicated that even with these parameters, clinical outcomes after surgical correction of mitral regurgitation may not be satisfactory, especially regarding EF reduction and the presence of HF.<sup><xref ref-type="bibr" rid="B150">150</xref>-<xref ref-type="bibr" rid="B151">151</xref></sup> Thus, studies have shown that even in patients with an EF &gt; 60% and an LV end-systolic diameter &lt; 40 mm, reduced GLS (&#8804; 19%) is associated with a postoperative EF &lt; 50%.<sup><xref ref-type="bibr" rid="B152">152</xref>-<xref ref-type="bibr" rid="B154">154</xref></sup> GLS &lt; 18.1%, has also been associated with higher mortality and more cardiovascular events in a prospectively followed cohort of mitral regurgitation patients who underwent corrective surgery.<sup><xref ref-type="bibr" rid="B155">155</xref></sup></p>
        <p>In aortic insufficiency, valvular heart disease severity has been correlated with decreased LV strain.<sup><xref ref-type="bibr" rid="B156">156</xref></sup> Furthermore, in patients with asymptomatic severe chronic aortic insufficiency and preserved EF, GLS &lt; 19% was associated with higher mortality over time, which was corrected through valve replacement.<sup><xref ref-type="bibr" rid="B157">157</xref></sup> In the same group, postoperatively, GLS &lt; 19% or a &gt; 5% drop in GLS was correlated with higher mortality.<sup><xref ref-type="bibr" rid="B158">158</xref></sup></p>
        <p>In severe aortic stenosis, EF &lt; 50% and/or symptoms have been the standard factors for indicating treatment.<sup><xref ref-type="bibr" rid="B145">145</xref>,<xref ref-type="bibr" rid="B147">147</xref>-<xref ref-type="bibr" rid="B149">149</xref></sup> However, waiting for the LVEF to drop &lt; 50% before indicating aortic surgery can lead to unsatisfactory clinical outcomes.<sup><xref ref-type="bibr" rid="B159">159</xref></sup> Thus, a robust parameter for detecting subclinical myocardial dysfunction, such as GLS, would be a valuable tool in risk stratification (<xref ref-type="fig" rid="f13001">Figure 6.1</xref>). While LVEF cannot be used to distinguish between degrees of aortic stenosis, GLS decreases linearly with disease progression,<sup><xref ref-type="bibr" rid="B160">160</xref></sup> leading to a higher risk of adverse clinical outcomes, even in asymptomatic patients.<sup><xref ref-type="bibr" rid="B161">161</xref></sup></p>
        <p>
          <fig id="f13001">
            <label>Figure 6.1</label>
            <caption>
              <title>&#8211; Two patients with classic severe high-flow aortic valve stenosis with normal left ventricular ejection fraction (LVEF) but very different global longitudinal strain (GLS) values. (A) Mean aortic transvalve gradient = 61 mm Hg, with normal EF and GLS. (B) Mean aortic transvalve gradient = 88 mm Hg, with normal EF and reduced GLS.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf13-en.tif"/></fig>
        </p>
        <p>Several studies have examined the prognostic value of GLS for predicting mortality and cardiovascular events in asymptomatic individuals with aortic stenosis and preserved LVEF to determine which ones should receive early valve intervention.<sup><xref ref-type="bibr" rid="B162">162</xref>-<xref ref-type="bibr" rid="B164">164</xref></sup> In a meta-analysis of these studies, GLS &lt; 14.7% was the cut-off for higher mortality risk (sensitivity 60% and specificity 70%; area under the curve [AUC] = 0.68).<sup><xref ref-type="bibr" rid="B165">165</xref></sup> GLS &lt; 14.7% was found in approximately one-third of the patients with moderate-to-severe aortic stenosis and preserved LVEF, resulting in a 2.6 times higher mortality risk. Of note, the relationship between GLS and mortality was significant in patients with LVEF 50%-59% as well as in those with LVEF &#8805; 60%. In contrast, GLS &gt; 18% was associated with an excellent clinical outcome (97% [SD, 1%]; 2-year survival). Therefore, together with other clinical and echocardiographic data, reduced GLS, despite preserved LVEF, must be considered a strong prognostic predictor in clinical decision making about asymptomatic severe aortic stenosis.</p>
      </sec>
      <sec>
        <title>7. Strain in Ischemic Heart Disease</title>
        <sec>
          <title>7.1. Introduction</title>
          <p>Echocardiography is an excellent tool in emergency departments for diagnosing acute coronary syndrome and its complications, providing information about the patient&#8217;s short- and long-term prognosis. Its role is well defined in risk stratification for stable coronary artery disease and in myocardial viability assessment.</p>
          <p>Two-dimensional echocardiography with strain assessment through 2D speckle tracking can add information without greatly extending the examination time. It accurately assesses subendocardial ischemia through LS in acute and chronic events.</p>
          <p>This chapter will review all indications for longitudinal, circumferential, and radial strain in ischemic heart diseases, as well as other data involved in calculating strain, such as mechanical dispersion. <xref ref-type="table" rid="t6001">Table 7.1</xref> shows the main indications for strain assessment in ischemic heart disease.</p>
          <p>
            <table-wrap id="t6001">
              <label>Table 7.1</label>
              <caption>
                <title>&#8211; Main applications of strain assessment in ischemic heart disease</title>
              </caption>
              <table frame="hsides" rules="groups">
                <colgroup width="100%">
                  <col/>
                </colgroup>
                <thead>
                  <tr>
                    <th align="left">Strain indications in ischemic heart disease</th>
                  </tr>
                </thead>
                <tbody>
                  <tr>
                    <td>Assessing segmental and global change</td>
                  </tr>
                  <tr>
                    <td>Differentiating subendocardial and transmural infarcts (longitudinal, radial, and circumferential change)</td>
                  </tr>
                  <tr>
                    <td>Determining the culprit artery according to &#8220;bulls eye&#8221; mapping</td>
                  </tr>
                  <tr>
                    <td>Assessing improvement in global and segmental strain after myocardial revascularization</td>
                  </tr>
                  <tr>
                    <td>Improving detection of coronary artery disease</td>
                  </tr>
                  <tr>
                    <td>Predicting outcomes and remodeling after acute mysocardial infarction</td>
                  </tr>
                  <tr>
                    <td>Predicting outcomes, such as hospitalization for heart failure and all-cause mortality</td>
                  </tr>
                  <tr>
                    <td>Identifying patients at risk of arrhythmia</td>
                  </tr>
                </tbody>
              </table>
            </table-wrap>
          </p>
        </sec>
        <sec>
          <title>7.2. Strain in Acute Coronary Syndrome</title>
          <p>Two-dimensional strain assessment has good sensitivity for detecting myocardial ischemia. It is considered more reproducible than LVEF and its accuracy has been confirmed in cardiac MRI.<sup><xref ref-type="bibr" rid="B52">52</xref>,<xref ref-type="bibr" rid="B166">166</xref></sup> Subendocardial fiber is more sensitive to the initial stages of ischemia, with the longitudinal component predominating in this type.<sup><xref ref-type="bibr" rid="B167">167</xref></sup> GLS is reduced in acute myocardial infarction (AMI) and correlates with the extent of the infarction, EF, adverse events, and response to reperfusion strategies.<sup><xref ref-type="bibr" rid="B168">168</xref>-<xref ref-type="bibr" rid="B172">172</xref></sup></p>
          <p>Patients with small infarcts have reduced global and radial strain, while circumferential and twist strain remain preserved. However, circumferential strain is compromised in transmural infarction.<sup><xref ref-type="bibr" rid="B173">173</xref></sup></p>
          <p>Identifying the extent of transmural infarction is important, since it is associated with poor prognosis and adverse events. Subendocardial and non-transmural infarcts are associated with recovery after revascularization (<xref ref-type="fig" rid="f14001">Figure 7.1</xref>).<sup><xref ref-type="bibr" rid="B174">174</xref></sup></p>
          <p>
            <fig id="f14001">
              <label>Figure 7.1</label>
              <caption>
                <title>&#8211; Two-dimensional bull&#8217;s eye mapping showing strain in the apical region of the left ventricle; the reduced segmental values are compatible with injury in the anterior descending artery.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf14-en.tif"/></fig>
          </p>
          <p>A strain value of 15% correlates with segmental changes (76% sensitivity and 95% specificity).<sup><xref ref-type="bibr" rid="B168">168</xref></sup>At a cutoff of 16.5%, radial strain differentiates transmural from non-transmural infarctions (70% sensitivity and 71.2% specificity), while circumferential strain &lt; 11% differentiates transmural from non-transmural infarctions (70% sensitivity and 71.2% specificity),<sup><xref ref-type="bibr" rid="B175">175</xref></sup> and 4.5% regional LS distinguishes transmural from non-transmural infarctions (81.2% sensitivity and 81.6% specificity).<sup><xref ref-type="bibr" rid="B176">176</xref>,<xref ref-type="bibr" rid="B177">177</xref></sup></p>
          <p>Another important diagnostic benefit of GLS is that it can help determine the culprit artery in non-ST-elevation acute coronary syndromes. In a cohort of 58 patients, 33 with significant coronary artery disease (lesion &gt; 50% determined through coronary angiography) who underwent strain analysis prior to the procedure, a cut-off of 19.7% could detect acute coronary disease (sensitivity 81%, specificity 88%, AUC = 0.92). A cut-off of 21% could exclude significant coronary stenosis in 100% of the patients. Regional LS was calculated as the mean systolic peak strain of each segment in the region of the studied vessel. If a cut-off of 21% were applied to the sample, 16 patients would have been spared from coronary angiography.<sup><xref ref-type="bibr" rid="B178">178</xref>,<xref ref-type="bibr" rid="B179">179</xref></sup></p>
          <p>Strain analysis can help detect acute coronary occlusion in patients without ST elevation who may benefit from early reperfusion therapy. One study evaluated 150 patients who underwent an echocardiographic examination prior to referral for coronary angiography, finding that 33 had an acute coronary occlusion. Although strain &lt; 14% identified acute coronary occlusion with 85% sensitivity and 70% specificity, more robust studies are needed to validate the technique.<sup><xref ref-type="bibr" rid="B180">180</xref></sup></p>
          <p>Strain analysis has emerged as a new technique for detecting subclinical segmental and global changes. Alongside enzymatic tests, electrocardiography, and risk scores, it enhances the prognostic evaluation of patients with acute coronary disease. This quick examination can be performed at bedside prior to coronary angiography, especially by trained echocardiographers. The above-mentioned studies on non-ST-elevation acute coronary syndromes indicate the technique for assessing segmental alterations and global ventricular function, differentiating small and transmural infarctions, determining the likely culprit artery, and for evaluating percutaneous revascularization outcomes. It can also be used to assess myocardial viability after an AMI.<sup><xref ref-type="bibr" rid="B181">181</xref>,<xref ref-type="bibr" rid="B182">182</xref></sup></p>
        </sec>
        <sec>
          <title>7.3. Strain in Chronic Coronary Syndromes</title>
          <p>The subendocardial region, in which the fibers are oriented longitudinally, is the most susceptible area to ischemia. Thus, assessing LS with 2D speckle-tracking could be a better method of detecting ischemia in this region than conventional echocardiography.<sup><xref ref-type="bibr" rid="B183">183</xref></sup></p>
          <p>Interaction between normal and abnormal myocardium generates typical regional myocardial strain patterns, indicating that myocardial contraction and myocardial strain are not interchangeable parameters.<sup><xref ref-type="bibr" rid="B16">16</xref>,<xref ref-type="bibr" rid="B184">184</xref></sup></p>
          <p>Since it assesses longitudinal LV function, GLS may be much more sensitive than LVEF for early detection of myocardial ischemia, although its specificity is not better than changes in wall mobility.<sup><xref ref-type="bibr" rid="B185">185</xref>,<xref ref-type="bibr" rid="B186">186</xref></sup></p>
          <p>The variability of regional strain measurements in speckle tracking is relatively high, which makes these assessments less suitable for routine use. However, GLS measurements have proven reproducible and robust, probably due to being largely automated.<sup><xref ref-type="bibr" rid="B187">187</xref></sup> The other change is regional heterogeneity of myocardial activation, which affects the temporal sequence of myocardial contraction and relaxation.</p>
          <p>In ischemia, not only is the amplitude of contraction reduced, but the beginning and duration of fiber contraction change, which leads to characteristic shortening or thickening of the myocardium after aortic valve closure.<sup><xref ref-type="bibr" rid="B187">187</xref></sup> This &#8220;post-systolic shortening&#8221; is characteristic of ischemia, although it can also occur in any type of regional dysfunction (scarring, dyssynchrony, etc.).<sup><xref ref-type="bibr" rid="B187">187</xref>,<xref ref-type="bibr" rid="B188">188</xref></sup> Post-systolic shortening can be understood as a signal to delay relaxation so that the ischemic region can shorten while the LV pressure reduces and the surrounding tissue relaxes.<sup><xref ref-type="bibr" rid="B16">16</xref></sup> In healthy hearts, less post-systolic shortening with normal systolic function is a frequent finding (30%-40% of myocardial segments) and can be found mainly at the apex and base of the inferior, septal, and anteroseptal walls.<sup><xref ref-type="bibr" rid="B16">16</xref>,<xref ref-type="bibr" rid="B189">189</xref></sup> In the context of ischemic cardiomyopathy, temporal evaluation of the GLS curve pattern is important, since ischemic segments can often have preserved peak systolic values but are temporally delayed in relation to non-ischemic segments.</p>
          <p>It should be pointed out that regional LS measurements do not necessarily align visually with contraction changes, which involve radial thickening and endocardial movement into the cavity.<sup><xref ref-type="bibr" rid="B16">16</xref></sup></p>
          <p>GLS can help detect coronary artery disease in patients with stable angina (stenosis &#8805; 70%), having reduced values in the presence of coronary artery disease (17.1 [SD 2.5%] vs 18.8 [SD 2.6%]; p &lt; 0.001), especially when associated with exercise testing. It can also determine which artery has likely been affected.<sup><xref ref-type="bibr" rid="B183">183</xref></sup> LS and (especially) strain rate can detect segmental changes in the late post-myocardial infarction period with higher sensitivity and accuracy.<sup><xref ref-type="bibr" rid="B189">189</xref></sup></p>
          <p>In stratifying post-AMI patients, GLS &lt; 15% prior to hospital discharge was an independent predictor of LV dilation in 3-6 months of follow-up, in addition to indicating the size of the infarct area.<sup><xref ref-type="bibr" rid="B190">190</xref></sup>In the same context, GLS &lt; 14% was an independent predictor of cardiovascular death and hospitalization due to HF.<sup><xref ref-type="bibr" rid="B191">191</xref></sup> In stable chronic patients, GLS &lt; 11.5% was a predictor of all-cause mortality and the combined outcome (all-cause mortality and hospitalization for HF).<sup><xref ref-type="bibr" rid="B192">192</xref></sup></p>
          <p>Heterogenous regional myocardial contraction can also be assessed by mechanical dispersion, which is the standard deviation of the time to maximum myocardial shortening across all LV segments. This index has a predictive value for ventricular tachyarrhythmia in post-infarction patients. Mechanical dispersion was higher in patients with recurrent arrhythmias after AMI than in those without them (85 [SD, 29] ms vs 56 [SD, 13] ms, p &lt; 0.001).<sup><xref ref-type="bibr" rid="B193">193</xref></sup></p>
        </sec>
        <sec>
          <title>7.4. Right Ventricular Strain in Ischemic Heart Disease</title>
          <p>RV function is compromised in approximately one-third of inferior wall infarctions, and its involvement has been described as an important predictor of hospital mortality and major complications. Assessing RV function is challenging due to its structural complexity. RV free wall strain has been shown to predict proximal right coronary artery occlusion in patients with inferior wall AMIs (RV free wall strain &lt; 14.5%, AUC = 0.81; p &lt; 0.001) .<sup><xref ref-type="bibr" rid="B194">194</xref></sup></p>
          <p>In the stable phase of chronic ischemic disease, RV free wall strain is altered in patients with right coronary stenosis (lesions &gt; 50%) and can be used to detect subclinical dysfunction.<sup><xref ref-type="bibr" rid="B19">19</xref><xref ref-type="bibr" rid="B5">5</xref></sup></p>
        </sec>
      </sec>
      <sec>
        <title>8. Strain Assessment in Systemic Diseases (Amyloidosis and Fabry Disease)</title>
        <sec>
          <title>8.1. Strain Assessment in Cardiac Amyloidosis</title>
          <p>Amyloidosis is a systemic disease caused by extracellular deposition of insoluble amyloid fibrils in tissue. Cardiac involvement is an important prognostic factor and has a great impact on quality of life, occurring more commonly in light chain amyloidosis and transthyretin amyloidosis.<sup><xref ref-type="bibr" rid="B196">196</xref></sup></p>
          <p>Echocardiography is a first-line method for diagnosis and prognostic evaluation of cardiac amyloidosis (CA) and other infiltrative heart diseases. Most classic echocardiography findings and more specific signs of CA only occur at very advanced stages.<sup><xref ref-type="bibr" rid="B30">30</xref></sup> Clinical conditions such as HFpEF and ventricular hypertrophy may be warning signs for CA.<sup><xref ref-type="bibr" rid="B197">197</xref></sup></p>
          <sec>
            <title>8.1.1. Myocardial Strain Assessment in the Diagnosis of Cardiac Amyloidosis</title>
            <p>The consistent LVGLS changes in patients with CA are directly related to the degree of amyloid infiltration, which is quantified in MRI through the degree of delayed gadolinium enhancement and extracellular volume calculated in T1 imaging.<sup><xref ref-type="bibr" rid="B30">30</xref></sup> A relative apical sparing pattern of LS has been described in the literature, characterized by a basal-apical gradient (&#8220;cherry-on-top&#8221; pattern) (<xref ref-type="fig" rid="f15001">Figure 8.1</xref>).</p>
            <p>
              <fig id="f15001">
                <label>Figure 8.1</label>
                <caption>
                  <title>&#8211; Longitudinal 2D strain of the left ventricle in a patient with cardiac transthyretin amyloidosis, showing relative apical preservation (apical sparing pattern), with lower strain in the middle and basal segments and higher strain in the apical segments.</title>
                </caption>
                <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf15-en.tif"/></fig>
            </p>
            <p>Phelan et al., originally calculated relative apical sparing with the following equation: mean apical LS/(mean LS of the middle segments + mean LS of the basal segments). Values &gt; 1.0 had good accuracy in diagnosing CA and differentiating it from ventricular hypertrophy due to aortic stenosis and HCM (AUC: 0.94).<sup><xref ref-type="bibr" rid="B20">20</xref></sup></p>
            <p>This regional LS pattern, with its basal-apical gradient, is indistinct in immunoglobulin light chain amyloidosis and transthyretin amyloidosis. It should be pointed out that the classic apical sparing pattern, although generally characteristic of CA, may be absent, as reported by Ternacle et al., who found that 52% of CA patients had &#8220;non-diagnostic&#8221; relative apical sparing (&lt; 1.0).<sup><xref ref-type="bibr" rid="B198">198</xref></sup> In some cases, this could be explained by a low degree of amyloid infiltration in the myocardium in very early stages of the disease. LS &gt; 2.1 in the basal and apical regions of the septum associated with a mitral inflow deceleration time &lt; 200 ms also accurately differentiated CA from other diseases involving LV hypertrophy and a parietal phenotype, such as Fabry disease, Friedreich&#8217;s ataxia, and LV hypertrophy related to systemic arterial hypertension.<sup><xref ref-type="bibr" rid="B199">199</xref></sup></p>
            <p>An LVEF/GLS ratio &gt; 4.1 accurately differentiated CA from HCM, performing better than relative apical sparing or LS in the basal and apical regions of the septum, regardless of CA type.<sup><xref ref-type="bibr" rid="B200">200</xref></sup> RV myocardial strain is generally reduced in CA patients, and it may help differentiate CA from other causes of parietal hypertrophy (<xref ref-type="fig" rid="f16001">Figure 8.2</xref>). A relative apical sparing pattern has also been found, similar to what has described in the LV.<sup><xref ref-type="bibr" rid="B201">201</xref></sup> Bellavia et al. demonstrated that RV changes can occur early in patients with immunoglobulin light chain amyloidosis, even in cases where LV parietal thickness is still normal.<sup><xref ref-type="bibr" rid="B202">202</xref></sup></p>
            <p>
              <fig id="f16001">
                <label>Figure 8.2</label>
                <caption>
                  <title>&#8211; Longitudinal 2D strain assessment in the right ventricle of a patient with cardiac transthyretin amyloidosis, showing a lower absolute global value (RVGLS = 9.9%) and an absolute reduction in mean free wall strain (FWS) (11.4%), with lower values in middle and basal segments and higher values in apical segments. TAPSE: tricuspid annular plane systolic excursion.</title>
                </caption>
                <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf16-en.tif"/></fig>
            </p>
            <p>In CA, like other infiltrative cardiomyopathies, other myocardial strain components may be significantly compromised, such as circumferential strain,<sup><xref ref-type="bibr" rid="B203">203</xref></sup> radial strain,<sup><xref ref-type="bibr" rid="B204">204</xref></sup> and twist (<xref ref-type="fig" rid="f17001">Figure 8.3</xref>). In early-stage systemic amyloidosis with no evidence of CA, twist and untwist may be increased in compensation,<sup><xref ref-type="bibr" rid="B205">205</xref></sup> with these parameters progressively deteriorating during the clinical course of the disease.<sup><xref ref-type="bibr" rid="B206">206</xref></sup> In advanced cases, the cardiac base and apex may rotate in the same direction, creating a pattern called &#8220;rigid body rotation&#8221;, in which the important contribution of cardiac torsion to ventricular mechanics is completely lost.</p>
            <p>
              <fig id="f17001">
                <label>Figure 8.3</label>
                <caption>
                  <title>&#8211; Transthyretin amyloidosis. Significantly lower absolute left ventricular (LV) radial strain values in all basal segments in 2D assessment (A). There is also a change in circumferential strain, resulting in significantly reduced &#8220;twist&#8221; (4&#186;) and LV torsion (B).</title>
                </caption>
                <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf17-en.tif"/></fig>
            </p>
            <p>LA strain often undergoes significant change in CA, due partially to LV DD but also to direct amyloid fibril infiltration in the atrial wall (<xref ref-type="fig" rid="f18001">Figure 8.4</xref>). In a recent study by Aimo et al., only peak atrial LS (in addition to classic echocardiographic variables and cardiac biomarkers) was independently associated with CA diagnosis.<sup><xref ref-type="bibr" rid="B207">207</xref></sup> It was also found that advanced atrial infiltration could cause severe dysfunction and loss of mechanical efficiency, leading to atrial electromechanical dissociation.<sup><xref ref-type="bibr" rid="B208">208</xref></sup> In a large cohort, Bandera et al. found atrial electromechanical dissociation (determined by LS analysis) in 22.1% of the patients in sinus rhythm, which was a determining factor for poor prognosis compared to patients in sinus rhythm with preserved atrial mechanical function.<sup><xref ref-type="bibr" rid="B209">209</xref></sup> In a Mayo Clinic series of 156 CA patients, intracardiac thrombi were detected by transesophageal echocardiography in 27%,<sup><xref ref-type="bibr" rid="B210">210</xref></sup> which has been reproduced in other studies, with thrombi occurring even in patients in sinus rhythm (<xref ref-type="fig" rid="f19001">Figure 8.5</xref>).<sup><xref ref-type="bibr" rid="B211">211</xref>,<xref ref-type="bibr" rid="B212">212</xref></sup></p>
            <p>
              <fig id="f18001">
                <label>Figure 8.4</label>
                <caption>
                  <title>&#8211; Immunoglobulin light chain amyloidosis. Two-dimensional left atrial (LA) strain, with 4-chamber and 2-chamber apical windows, showing an important reduction in LA strain (reservoir strain = 4%).</title>
                </caption>
                <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf18-en.tif"/></fig>
            </p>
            <p>
              <fig id="f19001">
                <label>Figure 8.5</label>
                <caption>
                  <title>&#8211; Transthyretin amyloidosis. The 2D apical window shows: (A) a large mobile mass inside the right atrium in a patient with sinus rhythm; (B) a 3D-rendered transesophageal echocardiography image showing a large mass (thrombus) adhered to the right atrial appendage. IAS: interatrial septum; SVC: superior vena cava; TV: tricuspid valve.</title>
                </caption>
                <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf19-en.tif"/></fig>
            </p>
            <p>Three-dimensional strain assessment can help demonstrate changes in all components of myocardial strain in patients with CA. Vitarelli et al. found that LV peak basal rotation and RV and LV basal LS could accurately distinguish CA from other ventricular hypertrophies.<sup><xref ref-type="bibr" rid="B213">213</xref></sup> In 3D echocardiography LS, Baccouche et al.<sup><xref ref-type="bibr" rid="B214">214</xref></sup> found the same apical sparing pattern, with a characteristic basal-apical gradient.</p>
            <p>Myocardial work (MW) has also been assessed in patients with CA. Clemmensen et al. found that patients with CA had a lower left ventricular myocardial work (LVMW) index than the control group, with more pronounced changes in basal segments and when undergoing stress echocardiography. The LVMW index from rest to peak exercise increased 1974 mm Hg% in controls (95% CI, 1699-2250 mm Hg%; P &lt; 0.0001) but only 496 mm Hg% in CA patients (95% CI, 156-835 mm Hg%; P &lt; 0. 01).<sup><xref ref-type="bibr" rid="B215">215</xref></sup></p>
            <p>The use of strain to assess clinical course and monitor response to specific CA treatments is very promising. Giblin et al. retrospectively evaluated 45 patients with cardiac transthyretin amyloidosis at 1 year of follow-up, comparing LS and MW values between groups of patients treated or not with Tafamidis.<sup><xref ref-type="bibr" rid="B216">216</xref></sup> In untreated patients, they found greater deterioration in GLS (p = 0.02), LVMW index, and MW efficiency (p = 0.04), with no significant differences between groups in circumferential strain, radial strain, or twist.</p>
            <p>Myocardial deformation parameters have also been extensively studied as prognostic indices in CA due to their ability to provide quantitative data, as well as to their high sensitivity and reproducibility. At a mean follow-up of 11 months Ternacle et al. found that mean apical LS (cut-off: -14.5%), elevated N-terminal pro&#8211;B-type natriuretic peptide, and New York Heart Association functional class III or IV were independent predictors of major cardiovascular events.<sup><xref ref-type="bibr" rid="B198">198</xref></sup> In another study, relative apical sparing index was independently associated with a composite outcome of death or heart transplantation within 5 years (hazard ratio [HR] 2.45; p = 0.003), maintaining its predictive value even in the multivariate analysis (p = 0.018).<sup><xref ref-type="bibr" rid="B217">217</xref></sup></p>
            <p>A large study by Buss et al. of 206 patients with systemic light chain amyloidosis found that Doppler-based LS and GLS were strongly associated with N-terminal pro&#8211;B-type natriuretic peptide levels and survival (best cut-off: -11.78%); in the multivariate analysis, only DD and GLS remained as independent predictors of survival.<sup><xref ref-type="bibr" rid="B218">218</xref></sup></p>
            <p>A recent study by Liu et al. included 40 patients with multiple myeloma with preserved EF before beginning bortezomib treatment, measuring baseline GLS and MW parameters. Global MW efficiency was significantly associated with adverse cardiac events after 6 months of chemotherapy (AUC = 0.896; 95% CI: 0.758-0.970; p &lt; 0.05).<sup><xref ref-type="bibr" rid="B219">219</xref></sup> RVLS has also been associated with CA prognosis. In a study of 136 patients with CA, Huntjens et al. found that strain values in all cavities were significantly associated with survival in median follow-up of 5 years.<sup><xref ref-type="bibr" rid="B220">220</xref></sup> Peak LALS and mean RV free wall strain continued to be independently associated with prognosis in the multivariate analysis. As an independent variable, peak LALS had the most robust association with survival (p &lt; 0.001), while the greatest prognostic value was obtained by combining LALS, GLS, and mean RV free wall strain (p &lt; 0.001).</p>
          </sec>
        </sec>
      </sec>
      <sec>
        <title>8.2. Fabry Disease</title>
        <p>Fabry disease (or Anderson-Fabry disease) is the most common glycogen storage disease, affecting 1 in 50,000 individuals.<sup><xref ref-type="bibr" rid="B221">221</xref></sup> Being an X-linked recessive disease, it is more common in men; women are carriers without alpha-galactose activity. The condition leads to a progressive accumulation of globotriaosylceramide in the kidneys, heart, and nerves. Clinically, patients present with skin changes (angiokeratomas), peripheral neuropathy, renal failure, and HF due to restrictive cardiomyopathy with increased myocardial thickness. Although these clinical manifestations can occur in childhood, they are more common after the third decade of life.<sup><xref ref-type="bibr" rid="B222">222</xref></sup></p>
        <p>Morphological analysis shows characteristically increased LV thickness, which may progress to a reduced compliance and HFpEF due to restrictive cardiomyopathy. Other interesting findings that may be considered red flags are papillary muscle hypertrophy, double contour sign, and dynamic obstruction of the LV outflow tract.<sup><xref ref-type="bibr" rid="B223">223</xref></sup> This similar phenotype to HCM is described in 6% of men<sup><xref ref-type="bibr" rid="B224">224</xref></sup> and 12% of women diagnosed in later age.<sup><xref ref-type="bibr" rid="B225">225</xref></sup> On the other hand, bull&#8217;s eye parametric analysis of LVLS plays an important role in differentiating cardiomyopathies that involve increased myocardial thickness, especially in asymmetric LV hypertrophy with an etiological possibility of HCM, amyloidosis (mainly transthyretin), Fabry disease, or hypertensive heart disease in older patients.</p>
        <p>HCM typically involves lower segmental values and greater thickness, while amyloid cardiomyopathy produces an apical sparing pattern and has a greater effect on the middle and basal regions of the LV. On the other hand, hypertensive heart disease can present with slightly reduced GLS. Curiously, Fabry disease involves a unique pattern in which, despite an asymmetrical increase in ventricular thickness, the basal portion of the inferolateral wall is most affected by LS (<xref ref-type="fig" rid="f20001">Figure 8.6</xref>); a progressive decreasing pattern occurs in untreated disease. There is a good correlation between LVLS assessment and delayed-enhanced cardiac MRI in different stages of the disease.<sup><xref ref-type="bibr" rid="B222">222</xref></sup> In addition, a study compared Fabry disease patients without myocardial alterations to a healthy control group, finding significantly lower myocardial values for LV, RV, LA in the Fabry group than the control group (18.1 [SD, 4.0], 21.4 [SD, 4.9], and 29.7 [SD, 9.9] vs 21.6 [SD, 2.2], 25.2 [SD, 4.0], and 44.8 [SD, 11.1%], respectively, P &lt; 0.001). Interestingly, in addition to these differences, strain changes correlated well with symptom severity.<sup><xref ref-type="bibr" rid="B226">226</xref></sup></p>
        <p>
          <fig id="f20001">
            <label>Figure 8.6</label>
            <caption>
              <title>&#8211; Global longitudinal strain in a patient with Fabry disease: bull&#8217;s eye map shows the lowest values in the in the basal portions of the left ventricle inferolateral wall. AVC: aortic valve closure.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf20-en.tif"/></fig>
        </p>
        <p>Treatment is currently available for Fabry disease, and morphological changes in the heart, such as reduced thickness, can appear after 1 year of treatment.<sup><xref ref-type="bibr" rid="B227">227</xref>,<xref ref-type="bibr" rid="B228">228</xref></sup> Thus, improved LVLS is expected to occur earlier, even before ventricular mass reduction. However, therapeutic response and GLS patterns throughout treatment should still be investigated.</p>
        <p>Myocardial strain assessment is an important tool for diagnosing ventricular hypertrophies of unknown etiology, mainly within a coherent clinical context and a good echocardiographic window, including follow-up of family members without access to genetic assessment or therapeutic response (<xref ref-type="fig" rid="f20001">Figure 8.6</xref>).,</p>
      </sec>
      <sec>
        <title>9. Strain in Hypertension</title>
        <sec>
          <title>9.1. Introduction</title>
          <p>This section discusses the main advantages and disadvantages of strain assessment in hypertension, with and without criteria for hypertensive cardiomyopathy (ie, LV hypertrophy), and its current clinical value.</p>
        </sec>
        <sec>
          <title>9.2. Hypertension without Left Ventricular Hypertrophy Criteria</title>
          <p>During its clinical course, hypertension causes changes in myocardial contractility, which appear as reduced LS in response to afterload and high wall systolic stress. These changes have proven prognostic significance. Reduced GLS reflects subclinical myocardial dysfunction even before the onset of LV hypertrophy or EF reduction (detected through traditional measurement methods); strain is the only measurement to change in stage I hypertension.<sup><xref ref-type="bibr" rid="B229">229</xref>-<xref ref-type="bibr" rid="B239">239</xref></sup>GLS reduction initially occurs in the basal region of the interventricular septum, extending to the basal and middle regions of other walls, which is likely because of overload in the interventricular septum due to systolic wall stress in the early stages of hypertension (<xref ref-type="fig" rid="f21001">Figure 9.1</xref>).<sup><xref ref-type="bibr" rid="B240">240</xref>,<xref ref-type="bibr" rid="B241">241</xref></sup> The longitudinal fibers of the subendocardial layer are affected early in this phase, along with the mesocardium, but not the epicardium, as suggested in some studies.<sup><xref ref-type="bibr" rid="B242">242</xref></sup></p>
          <p>
            <fig id="f21001">
              <label>Figure 9.1</label>
              <caption>
                <title>&#8211; Examples of global longitudinal strain polar mapping with peak systolic strain curves obtained in 4, 2 and 3 chambers. (A) healthy non-hypertensive patient with preserved GLS; (B) hypertensive patient without LV hypertrophy whose GLS is at the lower limit of normality (note altered myocardial strain in the basal septum); (C) hypertensive patient with LV hypertrophy and reduced GLS (note greater change in myocardial strain in basal and middle segments than apical segments).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf21-en.tif"/></fig>
          </p>
          <p>Another study found that LS change in the epicardial layer was the only variable that could predict cardiovascular events, indicating that it may correspond to the most severe and chronic type of damage.<sup><xref ref-type="bibr" rid="B243">243</xref></sup> However, the majority of currently available devices cannot analyze myocardial layers separately. On the other hand, radial and circumferential strain, which are based on overall myocardial thickness, tend to remain unchanged or even increase in a probable attempt to mechanically compensate for lower GLS,<sup><xref ref-type="bibr" rid="B60">60</xref>,<xref ref-type="bibr" rid="B236">236</xref></sup> with a change in circumferential component indicating more severe myocardial dysfunction.<sup><xref ref-type="bibr" rid="B244">244</xref></sup></p>
          <p>The main explanations for reduced GLS are an increase in the synthesis of collagen, culminating in fibrosis, which is a strong marker of myocardial dysfunction. Reduced GLS correlates not only with plasma markers of fibrosis, such as elevated tissue metalloproteinase inhibitor, but with fibrosis detected through delayed gadolinium-enhanced MRI in hypertensive patients.<sup><xref ref-type="bibr" rid="B231">231</xref>,<xref ref-type="bibr" rid="B234">234</xref>,<xref ref-type="bibr" rid="B238">238</xref>,<xref ref-type="bibr" rid="B239">239</xref></sup> Decreased GLS has also been observed in patients with masked and white-coat hypertension,<sup><xref ref-type="bibr" rid="B245">245</xref>,<xref ref-type="bibr" rid="B246">246</xref></sup> being correlated with conventional echocardiographic markers of DD,<sup><xref ref-type="bibr" rid="B240">240</xref></sup> as well as greater long-term deterioration in individuals who discontinue antihypertensive treatment.<sup><xref ref-type="bibr" rid="B247">247</xref></sup></p>
        </sec>
        <sec>
          <title>9.3. Hypertension with Left Ventricular Hypertrophy Criteria</title>
          <p>The myocardial consequences of chronic hypertension include myocyte hypertrophy, myocardial fibrosis, and medial thickening of the intramyocardial coronary arteries.<sup><xref ref-type="bibr" rid="B248">248</xref></sup> Consequently, hypertension and changes in myocardial remodeling are risk factors for major cardiac events, such as HF and premature death. Thus, the purpose of strain analysis in these cases is to detect subtle changes in systolic function, even before conventionally determined EF is compromised, thus facilitating the selection of HFpEF cases for treatment.</p>
          <p>LV remodeling may affect various types of strain. In concentric hypertrophy, for example, GLS values can progressively decrease according to geometric type, from concentric remodeling to eccentric hypertrophy with LV dilation.<sup><xref ref-type="bibr" rid="B249">249</xref>-<xref ref-type="bibr" rid="B251">251</xref></sup> Although most studies find preserved global circumferential strain and global radial strain values,<sup><xref ref-type="bibr" rid="B252">252</xref></sup> some series have found them to be reduced<sup><xref ref-type="bibr" rid="B249">249</xref></sup> and that they tend to remain normal in the epicardial layers in individuals with hypertension and LV hypertrophy.<sup><xref ref-type="bibr" rid="B250">250</xref></sup> Torsion and twisting behavior can also vary, with normal or reduced values according to the ventricular geometry.<sup><xref ref-type="bibr" rid="B249">249</xref>,<xref ref-type="bibr" rid="B253">253</xref></sup> In 3D analysis of hypertensive patients, GLS tends to deteriorate according to the degree of hypertrophy and LV cavity diameter.<sup><xref ref-type="bibr" rid="B62">62</xref>,<xref ref-type="bibr" rid="B250">250</xref></sup></p>
          <p>In addition to the correlation between reduced GLS and different patterns of LV hypertrophy, strain assessment can clarify the cause of hypertrophy, since it is more often reduced in HCM than LV hypertrophy due to hypertension.<sup><xref ref-type="bibr" rid="B254">254</xref></sup></p>
        </sec>
        <sec>
          <title>9.4. Clinical Treatment</title>
          <p>GLS decreases concomitantly with functional class<sup><xref ref-type="bibr" rid="B241">241</xref></sup> and increases with long-term treatment, as found in 3-year follow-up after antihypertensive treatment<sup><xref ref-type="bibr" rid="B255">255</xref></sup> and described in case reports of emergency antihypertensive treatment.<sup><xref ref-type="bibr" rid="B256">256</xref></sup> Reduced GLS is also correlated with abnormal blood pressure in patients undergoing treatment, even after adjusting for other clinical variables, such as age, diabetes, and LV mass index.<sup><xref ref-type="bibr" rid="B257">257</xref></sup></p>
        </sec>
        <sec>
          <title>9.5. Conclusion</title>
          <p>There is enough evidence to recommend strain assessment for patients with hypertension, regardless of LV hypertrophy, both to identify subclinical structural alterations and to identify the best treatment for HFpEF conditions. On the other hand, more robust studies are needed to guide systematic assessment in this population</p>
        </sec>
      </sec>
      <sec>
        <title>10. Strain in Athletes</title>
        <p>Regular intense physical activity results in a series of profound adaptive electrical, structural, and functional changes, usually referred to as athlete&#8217;s heart.<sup><xref ref-type="bibr" rid="B258">258</xref></sup> Analysis of this condition is important for a better understanding of the mechanisms of cardiac adaptation and how to improve training to optimize performance. Analysis can also differentiate pathologies with similar morphological characteristics to those induced by training.</p>
        <p>High-performance athletes with large LV volumes are considered to be on the healthy physiological spectrum of athlete&#8217;s heart. Some studies have reported slightly lower GLS in resting athletes than sedentary people, while others report the opposite.<sup><xref ref-type="bibr" rid="B259">259</xref>,<xref ref-type="bibr" rid="B260">260</xref></sup> However, most studies have found no significant difference between these groups.<sup><xref ref-type="bibr" rid="B261">261</xref></sup> This variation may be related to the effects of different factors such as preload and afterload, myocardial mass, and sinus bradycardia. Thus, reduced GLS values in athletes with normal or supranormal LV diastolic function may help distinguish between cardiac pathologies and secondary adaptations to exercise. Absolute values &#8805; 18% are still considered within normal limits. Much greater reductions in these indexes are found in patients with HCM and systemic arterial hypertension.<sup><xref ref-type="bibr" rid="B262">262</xref></sup>However, global circumferential strain and radial strain were found to differ significantly between athletes and controls.<sup><xref ref-type="bibr" rid="B261">261</xref></sup> Bull&#8217;s-eye mapping can help differentiate athlete&#8217;s heart from other diseases involving hypertrophy.<sup><xref ref-type="bibr" rid="B263">263</xref></sup></p>
        <p>When athletes are categorized according to exercise type and intensity (static vs dynamic), differences arise predominantly in mechanical aspects of the LV. A recent study showed that cardiac torsion was greater in low dynamic/high static (weightlifting, martial arts) athletes and in low static/high dynamic (marathon, soccer) athletes than controls. In contrast, torsion was lower in high dynamic/moderate static (swimming, water polo) athletes than controls, which could be explained by changes in apical, but not basal, rotation. Peak untwisting was higher in low dynamic/high static athletes and lower in high dynamic/high static athletes.<sup><xref ref-type="bibr" rid="B261">261</xref></sup> Studies using speckle tacking to quantify myocardial strain have shown that competitive endurance athletes have normal or increased strain values.<sup><xref ref-type="bibr" rid="B264">264</xref>-<xref ref-type="bibr" rid="B268">268</xref></sup></p>
        <p>In the RV, tissue Doppler and speckle tracking myocardial strain indices may be slightly lower in the basal and middle segments of the RV free wall (notably in endurance athletes) than controls.<sup><xref ref-type="bibr" rid="B269">269</xref></sup> It is still unclear whether this reduction is an adaptive response to exercise or a subclinical change due to myocardial injury.<sup><xref ref-type="bibr" rid="B270">270</xref></sup> Some authors assume that it can be explained by curvature changes between the apex and base of the RV, resulting in a strain difference between segments.</p>
        <p>Speckle tracking studies of atrial function in athletes are still in their infancy and show conflicting results. One study found that LA contraction assessed by GLS significantly decreased after training.<sup><xref ref-type="bibr" rid="B271">271</xref></sup> Another study found no differences in atrial strain between athletes and sedentary controls.<sup><xref ref-type="bibr" rid="B272">272</xref></sup></p>
        <p>Strain measurement is also important in diastolic function assessment. Dynamic exercise leads to more effective ventricular relaxation and biventricular dilation, while static exercise may be related to increased myocardial thickness and LV concentric hypertrophy, which could lead to some degree of diastolic impairment.<sup><xref ref-type="bibr" rid="B273">273</xref></sup> In addition, illicit performance-enhancing drugs can lead to deterioration of ventricular, systolic, and/or diastolic function, and speckle tracking echocardiography can detect these alterations early.<sup><xref ref-type="bibr" rid="B274">274</xref></sup></p>
        <p>Thus, when evaluating ventricular function in professional and/or amateur athletes, all available tools in the echocardiography arsenal are to be used. Strain analysis can detect incipient changes in systolic function, long before contractility changes or EF reductions can be detected in 2D assessment.</p>
        <p>When evaluating athletes, speckle tracking echocardiography has shown great promise as a complement to routine 2D echocardiography. Unlike sedentary individuals, absolute GLS values &gt; 16% in this population can be considered normal; lower values should raise suspicion of pathology, especially when combined with signs such as significant ventricular hypertrophy or dilation.<sup><xref ref-type="bibr" rid="B275">275</xref></sup></p>
      </sec>
      <sec>
        <title>11. Strain in Stress Echocardiography</title>
        <p><xref ref-type="table" rid="t7001">Table 11.1</xref> shows the main applications of strain in stress echocardiography.</p>
        <p>
          <table-wrap id="t7001">
            <label>Table 11.1</label>
            <caption>
              <title>&#8211; Strain applications in stress echocardiography</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="50%">
                <col/>
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left">Clinical scenario</th>
                  <th align="left">Concept</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>Ischemia detection<sup>189,276-280</sup></td>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Regional LS detects endocardial ischemia.</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;CS can help differentiate transmural and non-transmural infarctions.</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;Increased time to peak LS can help detect ischemia.</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;Post-systolic shortening (sensitive but not specific for detecting ischemia).</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;Systolic RLS (lower dependence on load and heart rate than strain).</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;Diastolic strain parameters.</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Feasibility assessment<sup>281-285</sup></td>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;LS and RLS increase the accuracy of viability detection in MI patients treated with TCA and low doses of dobutamine.</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;LS is the best predictor of functional improvement after CABG.</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;Lack of response to dobutamine accurately predicts lack of improvement after CABG.</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;Differentiation between stunned and hibernating myocardium (lower LS and RLS and post-systolic shortening).</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Aortic stenosis<sup>286,287</sup></td>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;GLS in the evaluation of low-flow/low-gradient aortic stenosis.</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;Patients with GLS &gt; 10% after dobutamine use have longer survival.</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;Stress GLS is more accurate than resting GLS.</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Hypertensive cardiomyopathy<sup>288</sup></td>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;LS and RS deficits are more evident during stress than rest in the initial phases, allowing prevention measures.</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Diabetic cardiomyopathy<sup>289,290</sup></td>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Lower RLS in middle and basal segments during DSE.</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;Early decreased myocardial velocities in asymptomatic patients with insulin resistance during DSE.</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Cardiomyopathies<sup>132,291-293</sup></td>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Lower systolic functional reserve detected in LS and RS after stress.</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;No improvement in diastolic function parameters.</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;Increased time-to-peak in HCM with important dyssynchrony.</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;Low RVLS values in arrhythmogenic dysplasia do not significantly improve with stress.</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Athlete&#8217;s heart<sup>294,295</sup></td>
                  <td>
                    <list list-type="simple">
                      <list-item>
                        <p>&#8226;Slightly lower LS values with preserved or supranormal myocardial reserve.</p>
                      </list-item>
                      <list-item>
                        <p>&#8226;Stress GLS helps differentiate athlete&#8217;s heart from cardiomyopathy.</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>CABG: coronary artery bypass grafting; CS: circumferential strain; DSE: dobutamine stress echocardiography; GLS: global longitudinal strain; HCM: hypertrophic cardiomyopathy; LS: longitudinal strain; MI: myocardial infarction; RLS: regional longitudinal strain; RS: radial strain; RV: right ventricle; TCA: transluminal coronary angioplasty.</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
        <p>A more complete review article on stress echocardiography will soon be published in this journal.</p>
      </sec>
      <sec>
        <title>12. Strain in Congenital Heart Disease</title>
        <p>Some studies have demonstrated the high prognostic value of speckle tracking strain assessment, reinforcing its usefulness for both congenital and acquired pathologies.<sup><xref ref-type="bibr" rid="B9">9</xref></sup>However, myocardial strain is subject to physiological variations due to age, sex, heart rate, preload, blood pressure, and body surface area, as well as the analysis software.<sup><xref ref-type="bibr" rid="B296">296</xref></sup> Continuous effort has been made to determine normal strain values for universal reference in pediatrics so that myocardial strain assessment of can be included in the clinical routine.<sup><xref ref-type="bibr" rid="B297">297</xref>-<xref ref-type="bibr" rid="B299">299</xref></sup></p>
        <p><xref ref-type="table" rid="t8001">Tables 12.1</xref><xref ref-type="table" rid="t9001"/>to <xref ref-type="table" rid="t19001">12.3</xref> present the myocardial strain values found in the literature for normal children and those with congenital heart diseases, while <xref ref-type="table" rid="t20001">Table 12.4</xref> shows the recommended cut-off values. A more complete review article on the subject is forthcoming in this journal.</p>
        <p>
          <table-wrap id="t8001">
            <label>Table 12.1</label>
            <caption>
              <title>&#8211; Normal left ventricular strain values according to age group298</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="14%">
                <col/>
                <col/>
                <col/>
                <col/>
                <col/>
                <col/>
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left">Age in years</th>
                  <th>Peak systolic GLS</th>
                  <th>Peak strain in apical 4-chamber view</th>
                  <th>Peak circumferential systolic global strain</th>
                  <th>Peak circumferential systolic strain at the papillary muscle level</th>
                  <th>Peak radial global systolic strain</th>
                  <th>Peak radial systolic strain at the papillary muscle level</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>0-1</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>18.7%</p>
                      </list-item>
                      <list-item>
                        <p>(20.8, 16.7)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>19.4%</p>
                      </list-item>
                      <list-item>
                        <p>(22.2, 16.6)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>_____</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>18.2%</p>
                      </list-item>
                      <list-item>
                        <p>(22.6, 13.7)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>_____</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>44.4%</p>
                      </list-item>
                      <list-item>
                        <p>(36.6, 52.1)</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>2-9</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>21.7%</p>
                      </list-item>
                      <list-item>
                        <p>(23.0, 20.5)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>21.0%</p>
                      </list-item>
                      <list-item>
                        <p>(21.8, 20.2)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>24.5%</p>
                      </list-item>
                      <list-item>
                        <p>(27.2, 21.7)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>20.3%</p>
                      </list-item>
                      <list-item>
                        <p>(21.4, 19.1)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>48.0%</p>
                      </list-item>
                      <list-item>
                        <p>(33.3, 62.8)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>50.8%</p>
                      </list-item>
                      <list-item>
                        <p>(47.4, 54.1)</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>10-13</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>20%</p>
                      </list-item>
                      <list-item>
                        <p>(20.8, 19.1)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>20.5%</p>
                      </list-item>
                      <list-item>
                        <p>(21.7, 19.2)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>21.9%</p>
                      </list-item>
                      <list-item>
                        <p>(26.5, 17.4)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>21.5%</p>
                      </list-item>
                      <list-item>
                        <p>(23.1, 19.8)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>43.7%</p>
                      </list-item>
                      <list-item>
                        <p>(33.0, 54.5)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>52.1%</p>
                      </list-item>
                      <list-item>
                        <p>(48.5, 55.8)</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>14-21</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>19.9</p>
                      </list-item>
                      <list-item>
                        <p>(20.6, 19.2)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>19.9%</p>
                      </list-item>
                      <list-item>
                        <p>(21.2, 18.6)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>16.4%</p>
                      </list-item>
                      <list-item>
                        <p>(23.3, 9.6)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>16.4%</p>
                      </list-item>
                      <list-item>
                        <p>(23.3, 9.6)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>44.0%</p>
                      </list-item>
                      <list-item>
                        <p>(41.6, 46.4)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>46.4%</p>
                      </list-item>
                      <list-item>
                        <p>(39.7, 53.1)</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Overall</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>20.2%</p>
                      </list-item>
                      <list-item>
                        <p>(20.8, 19.6)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>20.4%</p>
                      </list-item>
                      <list-item>
                        <p>(21.1, 19.8)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>22.3%</p>
                      </list-item>
                      <list-item>
                        <p>(19.9, 24.6)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>20.4%</p>
                      </list-item>
                      <list-item>
                        <p>(21.1, 19.8)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>45.2%</p>
                      </list-item>
                      <list-item>
                        <p>(38.8, 51.7)</p>
                      </list-item>
                    </list>
                  </td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>49.4%</p>
                      </list-item>
                      <list-item>
                        <p>(47.2, 51.6)</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>GLS: global longitudinal strain. Values expressed as mean and 95% CI.</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
        <p>
          <table-wrap id="t9001">
            <label>Table 12.2</label>
            <caption>
              <title>&#8211; Normal right ventricular strain values according to age group300</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="20%">
                <col/>
                <col/>
                <col/>
                <col/>
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left" style="font-weight:normal"> </th>
                  <th>31 days- 24 months</th>
                  <th>2-5 years</th>
                  <th>5-11 years</th>
                  <th>11-18 years</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>GLS RV %</td>
                  <td align="center">25.4 (3.9)</td>
                  <td align="center">25.9 (4.0)</td>
                  <td align="center">25.8 (4.7)</td>
                  <td align="center">25.4 (4.1)</td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>GLS: global longitudinal strain; RV: right ventricle. Values expressed as mean (SD)</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
        <p>
          <table-wrap id="t19001">
            <label>Table 12.3</label>
            <caption>
              <title>&#8211; Valores normais de strain atrial direito e esquerdo, segundo as faixas et&#225;ria<bold>301</bold></title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="20%">
                <col/>
                <col/>
                <col/>
                <col/>
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left">Measure</th>
                  <th>31 days- 24 months</th>
                  <th>2-5 years</th>
                  <th>5-11 years</th>
                  <th>11-18 years</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>
                    <bold>LA strain (R)%</bold>
                  </td>
                  <td align="center">52.8 (10.1)</td>
                  <td align="center">55.7 (10.7)</td>
                  <td align="center">58.1 (10)</td>
                  <td align="center">57.6 (10.5)</td>
                </tr>
                <tr>
                  <td>
                    <bold>LA strain (C)%</bold>
                  </td>
                  <td align="center">14.2 (6.6)</td>
                  <td align="center">12.7 (6.1)</td>
                  <td align="center">14.0 (6.7)</td>
                  <td align="center">15.1 (7.0)</td>
                </tr>
                <tr>
                  <td>
                    <bold>RA strain (R)%</bold>
                  </td>
                  <td align="center">47.1 (9.6)</td>
                  <td align="center">49.6 (10.2)</td>
                  <td align="center">51.6 (10.7)</td>
                  <td align="center">52.0 (10.6)</td>
                </tr>
                <tr>
                  <td>
                    <bold>RA strain (C)%</bold>
                  </td>
                  <td align="center">11.5 (6.0)</td>
                  <td align="center">11.9 (5.9)</td>
                  <td align="center">11.8 (6.3)</td>
                  <td align="center">12.8 (5.8)</td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>C: atrial contraction phase; LA: left atrium; R: reservoir phase; RA atrium. Values expressed as mean (SD)</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
        <p>
          <table-wrap id="t20001">
            <label>Table 12.4</label>
            <caption>
              <title>&#8211; A selection of studies evaluating the use of strain in idiopathic pulmonary hypertension and congenital heart disease</title>
            </caption>
            <table frame="hsides" rules="groups">
              <colgroup width="17%">
                <col/>
                <col/>
                <col/>
                <col/>
                <col/>
                <col/>
              </colgroup>
              <thead>
                <tr>
                  <th align="left" style="font-weight:normal"> </th>
                  <th>Authors</th>
                  <th>Parameter</th>
                  <th>Cut-off</th>
                  <th>Findings</th>
                  <th>Sn/Sp</th>
                </tr>
              </thead>
              <tbody>
                <tr>
                  <td>Idiopathic pulmonary hypertension</td>
                  <td align="center">Muntean et al.<sup>302</sup></td>
                  <td align="center">mid-segment FW RV strain</td>
                  <td align="center">18.5%</td>
                  <td align="center">Predictor of clinical worsening</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>Sn: 91.7%, Sp: 30.8%</p>
                      </list-item>
                      <list-item>
                        <p>AUC=0.88, SD 0.06</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Ebstein's anomaly</td>
                  <td align="center">K&#252;hn et al.<sup>303</sup></td>
                  <td align="center">RVGLS (6 segments)</td>
                  <td align="center">20.15%</td>
                  <td align="center">Diagnosis of RV dysfunction (EF &lt; 50% in MRI)</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>Sn: 77%</p>
                      </list-item>
                      <list-item>
                        <p>Sp: 46%</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Systemic RV (PO TGA Senning/Mustard)</td>
                  <td align="center">Lipczy&#324;ska et al.<sup>304</sup></td>
                  <td align="center">RVGLS (6 segments)</td>
                  <td align="center">14.2%</td>
                  <td align="center">Diagnosis of RV Dysfunction (EF&lt; 45% in MRI)</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>Sn: 83%, Sp: 90%</p>
                      </list-item>
                      <list-item>
                        <p>AUC= 0.882</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Systemic RV (CTGA)</td>
                  <td align="center">Kowalik et al.<sup>305</sup></td>
                  <td align="center">RVGLS (6 segments)</td>
                  <td> </td>
                  <td align="center">Diagnosis of RV dysfunction (EF &lt; 45% in MRI)</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>Sn: 77.3%</p>
                      </list-item>
                      <list-item>
                        <p>Sp: 72.7%</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>PO AOLCA</td>
                  <td align="center">Castaldi et al.<sup>306</sup></td>
                  <td align="center">LV peak segmental strain</td>
                  <td align="center">14.8%</td>
                  <td align="center">Predictor of fibrosis in MRI</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>Sn: 92.5%</p>
                      </list-item>
                      <list-item>
                        <p>Sp: 93.7%</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
                <tr>
                  <td>Univentricular physiology (PO Fontan)</td>
                  <td align="center">Park et al.<sup>307</sup></td>
                  <td align="center">Circumferential strain rate</td>
                  <td align="center">-1.0s<sup>-1</sup></td>
                  <td align="center">Predictor of hospital stay &gt;14 days after TCC anastomosis</td>
                  <td align="center">
                    <list list-type="simple">
                      <list-item>
                        <p>Sn: 72%</p>
                      </list-item>
                      <list-item>
                        <p>Sp: 60%</p>
                      </list-item>
                    </list>
                  </td>
                </tr>
              </tbody>
            </table>
            <table-wrap-foot>
              <attrib>
                <italic>AOLCA: anomalous origin of the left coronary artery; AUC: area under the curve; TCC: total cavopulmonary connection; CTGA: corrected transposition of the great arteries; EF: ejection fraction; FW: free wall; GLS: global longitudinal strain; MRI: magnetic resonance; PO: postoperative; RV: right ventricle; Sn: sensitivity; Sp: specificity.</italic>
              </attrib>
            </table-wrap-foot>
          </table-wrap>
        </p>
      </sec>
      <sec>
        <title>13. Right Ventricle Strain</title>
        <sec>
          <title>13.1. Introduction</title>
          <p>The RV plays an important role in the pathophysiology of cardiopulmonary disease. A large amount of evidence has shown that RV dysfunction is an important independent marker of morbidity and mortality in clinical conditions such as HF, valvular heart disease, pulmonary hypertension, pulmonary embolism, and ischemic heart disease, as well as in congenital heart disease in adults.<sup><xref ref-type="bibr" rid="B308">308</xref>-<xref ref-type="bibr" rid="B313">313</xref></sup></p>
          <p>Cardiac MRI is the gold standard non-invasive test for RV volume, EF, and structural assessment. However, its main limitations are its high cost, longer image acquisition time, and poor availability in most centers.<sup><xref ref-type="bibr" rid="B314">314</xref></sup> Two-dimensional echocardiography is the most common initial test for structural and functional evaluation of the RV due to its wide availability, low cost, non-invasiveness, and shorter image acquisition time. However, 2D RV assessment is challenging due to the complex structure of the cavity, its unfavorable position in the thoracic wall, and intense myocardial trabeculation, which prevents better visualization of the endocardium due to its thinner walls and high dependence on loading conditions in the most common systolic function indices.<sup><xref ref-type="bibr" rid="B315">315</xref></sup></p>
          <p>Several echocardiographic parameters are used to indicate RV systolic function in clinical practice. Recently, 2D speckle-tracking was introduced into clinical practice as an objective indicator of regional and global myocardial contractility, initially for LV and more recently for RV evaluation. Research has highlighted the advantages of this new methodology over conventional echocardiographic parameters.<sup><xref ref-type="bibr" rid="B316">316</xref></sup></p>
        </sec>
        <sec>
          <title>13.2. Anatomical and Functional Characteristics of the Right Ventricle</title>
          <p><xref ref-type="table" rid="t21001">Table 13.1</xref> shows the main characteristics that differentiate the ventricles.<sup><xref ref-type="bibr" rid="B317">317</xref>-<xref ref-type="bibr" rid="B319">319</xref></sup> LV and RV function are closely related (a phenomenon called systolic ventricular interaction) since they share obliquely arranged muscle fibers in the interventricular septum. These have a mechanical advantage over the transverse fibers of the RV free wall.<sup><xref ref-type="bibr" rid="B36">36</xref></sup> The continuity of these muscle fibers allows the RV free wall to be pulled during LV contraction, with an estimated 20%-40% of RV stroke volume and systolic pressure due to LV contraction.<sup><xref ref-type="bibr" rid="B318">318</xref>,<xref ref-type="bibr" rid="B319">319</xref></sup></p>
          <p>
            <table-wrap id="t21001">
              <label>Table 13.1</label>
              <caption>
                <title>&#8211; Anatomical and functional characteristics of the ventricles</title>
              </caption>
              <table frame="hsides" rules="groups">
                <colgroup width="33%">
                  <col/>
                  <col/>
                  <col/>
                </colgroup>
                <thead>
                  <tr>
                    <th align="left" style="font-weight:normal"> </th>
                    <th>Right ventricle</th>
                    <th>Left ventricle</th>
                  </tr>
                </thead>
                <tbody>
                  <tr>
                    <td>Structure</td>
                    <td align="center">Inlet, trabecular region, infundibulum.</td>
                    <td align="center">No infundibulum and limited trabeculation.</td>
                  </tr>
                  <tr>
                    <td>Form</td>
                    <td align="center">
                      <list list-type="simple">
                        <list-item>
                          <p>Multiple muscle bands</p>
                        </list-item>
                        <list-item>
                          <p>Triangular in the coronal plane</p>
                        </list-item>
                        <list-item>
                          <p>Crescent in the transverse plane</p>
                        </list-item>
                      </list>
                    </td>
                    <td align="center">Elliptical</td>
                  </tr>
                  <tr>
                    <td>Predominant myocardial fiber orientation</td>
                    <td align="center">
                      <list list-type="simple">
                        <list-item>
                          <p>Subepicardium: circumferential</p>
                        </list-item>
                        <list-item>
                          <p>Subendocardium: longitudinal</p>
                        </list-item>
                      </list>
                    </td>
                    <td align="center">
                      <list list-type="simple">
                        <list-item>
                          <p>Subepicardium: oblique</p>
                        </list-item>
                        <list-item>
                          <p>Mesocardium: circumferential</p>
                        </list-item>
                        <list-item>
                          <p>Subendocardium: longitudinal</p>
                        </list-item>
                      </list>
                    </td>
                  </tr>
                  <tr>
                    <td>Arrangement of fibers in the free wall</td>
                    <td align="center">Transverse predominance</td>
                    <td align="center">Olique predominance</td>
                  </tr>
                  <tr>
                    <td>Arrangement of fibers in the IVS</td>
                    <td align="center">Obliquely, extending to the outflow tract</td>
                    <td align="center">Obliquely</td>
                  </tr>
                  <tr>
                    <td>Contribution of IVS thickening in the transverse axis and shortening in the longitudinal axis in systole</td>
                    <td align="center">+++</td>
                    <td align="center">+++</td>
                  </tr>
                  <tr>
                    <td>Contraction pattern</td>
                    <td align="center">Mainly longitudinal from base to apex</td>
                    <td align="center">
                      <list list-type="simple">
                        <list-item>
                          <p>Subepicardium and Subendocardium: longitudinal shortening in opposite directions.</p>
                        </list-item>
                        <list-item>
                          <p>Mesocardium: circumferential direction</p>
                        </list-item>
                      </list>
                    </td>
                  </tr>
                  <tr>
                    <td>Mass (g/m<sup>2</sup>)</td>
                    <td align="center">26 (SD, 5)</td>
                    <td align="center">87 (SD,12)</td>
                  </tr>
                  <tr>
                    <td>Wall thickness (mm)</td>
                    <td align="center">2-5</td>
                    <td align="center">7-11</td>
                  </tr>
                </tbody>
              </table>
              <table-wrap-foot>
                <attrib>
                  <italic>IVS: Interventricular septum</italic>
                </attrib>
              </table-wrap-foot>
            </table-wrap>
          </p>
        </sec>
        <sec>
          <title>13.3. Right Ventricle and Echocardiographic Parameters in Systolic Function Assessment</title>
          <p>Several indices are routinely used to assess RV systolic function, such as fractional area change, tricuspid annular plane systolic excursion, tricuspid annular peak systolic velocity, and myocardial performance index. Each has its advantages and limitations, varying feasibility and reproducibility, and debatable diagnostic and prognostic efficacy.<sup><xref ref-type="bibr" rid="B35">35</xref>,<xref ref-type="bibr" rid="B36">36</xref></sup> At present, no single method is considered a good indicator of RV systolic function. However, due to the orientation of the predominant longitudinal muscle fibers from the tricuspid annulus to the apex, preference is given to indices that explore movement along the longitudinal axis when assessing regional or global RV longitudinal function.<sup><xref ref-type="bibr" rid="B92">92</xref></sup></p>
          <p>Two-dimensional speckle tracking echocardiography is an imaging modality that evaluates myocardial deformation, an intrinsic property of the myocardium, in the 3 directions (longitudinal, circumferential, and radial). The longitudinal direction is the most common due to its good reproducibility, relevant prognostic information, validation in an experimental study<sup><xref ref-type="bibr" rid="B75">75</xref></sup> and in clinical cardiac MRI studies of various cardiovascular diseases.<sup><xref ref-type="bibr" rid="B320">320</xref>-<xref ref-type="bibr" rid="B323">323</xref></sup> Thus, RV 2D speckle-tracking can be considered a good marker of systolic function, with prognostic value in several cardiovascular diseases.<sup><xref ref-type="bibr" rid="B75">75</xref>,<xref ref-type="bibr" rid="B324">324</xref>-<xref ref-type="bibr" rid="B330">330</xref></sup></p>
        </sec>
        <sec>
          <title>13.4. Acquisition and Limitations</title>
          <p>Determining RVGLS through 2D speckle tracking requires a modified apical 4-chamber window focused on the RV, with the transducer displaced more laterally and towards the right shoulder, which allows better visualization of the free wall and more reproducible measurements (<xref ref-type="fig" rid="f22001">Figure 13.1</xref>). It is important to optimize the orientation, depth, and gain to maximize the size of the RV, and to view its apex throughout the entire cardiac cycle.<sup><xref ref-type="bibr" rid="B36">36</xref></sup> During image acquisition, the transducer should not be positioned anteriorly or posteriorly (avoiding the aortic valve and coronary sinus, respectively), showing only the interatrial septum.<sup><xref ref-type="bibr" rid="B331">331</xref></sup> Once adequate visualization is obtained, the device should be set to record 3 cardiac cycles and acquire images at 50-80 frames per second. This rate can be obtained through indirect adjustments, such as image depth, resolution, and the ultrasound beam size, as well as by direct adjustment of the echocardiography device. Some software still requires the beginning and end of the RV ejection time to be defined, using pulsed Doppler echocardiography in the RV outflow tract.</p>
          <p>
            <fig id="f22001">
              <label>Figure 13.1</label>
              <caption>
                <title>&#8211; Imaging protocol for right ventricular (RV) strain measurement through speckle tracking echocardiography in an apical 4-chamber view: A) apical 4-chamber window (inappropriate acquisition method); B) apical 4-chamber window focused on the RV (adequate acquisition method). RVFWS: RV free wall strain; RVGLS: RV global longitudinal strain.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf22-en.tif"/></fig>
          </p>
          <p>The region of interest is defined by the endocardial border, which includes the RV free wall and interventricular septum. It should not include the pericardium and its width should not to be too narrow, since this could lead to erroneous results. The baseline reference points must be positioned correctly; suboptimal positioning, eg, on the atrial side of the tricuspid annulus, could result in reduced LS values.<sup><xref ref-type="bibr" rid="B332">332</xref></sup> The region of interest can be manually plotted or generated automatically; if generated automatically, the user must have permission to check and edit it manually as needed.<sup><xref ref-type="bibr" rid="B92">92</xref></sup> After a tracking quality check and final operator approval, the regional strain values are displayed. According to current recommendations, the highest value reached during systole (peak systolic strain) should be used, with Doppler tracking of the pulmonary valve used to determine the end-diastole and end-systole.<sup><xref ref-type="bibr" rid="B92">92</xref></sup> Whenever possible, appropriate software should be used, since the automatic detection algorithm of RV segments reduces the need for operator intervention, thus contributing to reproducible results.</p>
          <p>The RV free wall is divided into basal, middle, and apical segments. The interventricular septum is similarly segmented. RV free wall LS is the mean strain value of all 3 segments, while RVGLS is the mean strain value of the free wall segments and the interventricular septum. RV free wall LS is more common in practice and clinical research, since LV function can interfere with RVGLS through the interventricular septum, leading to lower absolute values.<sup><xref ref-type="bibr" rid="B333">333</xref></sup> RV free wall LS must be reported as a standard parameter, with RVGLS being optional.<sup><xref ref-type="bibr" rid="B92">92</xref></sup></p>
          <p>As limitations, in addition to inadequate acoustic windows, experimental studies and mathematical models have shown that the magnitude of myocardial strain is influenced by heart rate, in addition to preload and afterload. In preserved systolic function, studies have confirmed that strain can increase with higher preload and heart rate and can decrease when they are lower.<sup><xref ref-type="bibr" rid="B16">16</xref>,<xref ref-type="bibr" rid="B334">334</xref></sup></p>
        </sec>
        <sec>
          <title>13.5. Indications/Normal Values</title>
          <p>The association between RV systolic dysfunction and poor prognosis in several cardiovascular diseases has been well-established, and RVGLS is an independent prognostic marker in pulmonary hypertension, HF, ischemic heart disease, and other cardiomyopathies; according to cardiac MRI, it is better correlated with right ventricular ejection fraction in than traditional parameters.<sup><xref ref-type="bibr" rid="B35">35</xref>,<xref ref-type="bibr" rid="B320">320</xref>-<xref ref-type="bibr" rid="B23">23</xref>,<xref ref-type="bibr" rid="B334">334</xref>-<xref ref-type="bibr" rid="B336">336</xref></sup></p>
          <p>RVGLS is lower in patients with pulmonary hypertension, showing good correlation with invasive hemodynamic parameters of RV performance.<sup><xref ref-type="bibr" rid="B337">337</xref></sup> Furthermore, RVGLS has been found to be an independent predictor of all-cause mortality and pulmonary hypertension-related events. Aiming to assess the prognostic value of RVGLS in these patients, a recent meta-analysis found that a 19% relative reduction in RVGLS is associated with an increased risk of pulmonary hypertension-related events, while a 22% relative reduction is associated with a higher risk of all-cause mortality.<sup><xref ref-type="bibr" rid="B324">324</xref></sup><xref ref-type="fig" rid="f23001">Figure 13.2</xref> shows an example of RV strain in a patient with primary pulmonary hypertension.</p>
          <p>
            <fig id="f23001">
              <label>Figure 13.2</label>
              <caption>
                <title>&#8211; Example of right ventricular (RV) strain in a patient with primary pulmonary hypertension. TomTec software. RVFWS: RV free wall strain; RVGLS: RV global longitudinal strain.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf23-en.tif"/></fig>
          </p>
          <p>In patients with HF, RVGLS has high sensitivity and accuracy for diagnosing RV systolic dysfunction.<sup><xref ref-type="bibr" rid="B338">338</xref></sup> A recent study found that absolute values &lt; 14.8% are associated with adverse events, such as mortality, heart transplantation, and hospitalization, regardless of LVEF or LV DD.<sup><xref ref-type="bibr" rid="B19">19</xref></sup> In addition, RVGLS and RV free wall LS could detect subtle RV systolic function abnormalities in patients with HF and reduced LVEF, and to a lesser extent in those with HF and preserved LVEF.<sup><xref ref-type="bibr" rid="B329">329</xref></sup> In patients eligible for LV assist device implantation, RVGLS is useful for stratifying the risk of RV failure. With a sensitivity of 68% and a specificity of 76%, an absolute RVGLS value &lt; 9.6% can identify patients with post-procedure RV failure (ie, requiring an RV assist device or inotrope therapy &gt; 14 days).<sup><xref ref-type="bibr" rid="B339">339</xref></sup> In heart transplant patients, a combination of LVGLS and RV free wall LS measurements can help exclude acute cellular rejection and reduce the number of routine biopsies.<sup><xref ref-type="bibr" rid="B340">340</xref></sup><xref ref-type="fig" rid="f24001">Figures 13.3</xref> and <xref ref-type="fig" rid="f25001">13.4</xref> show examples of VR strain in a patient with a ventricular assist device and a heart transplant patient, respectively.</p>
          <p>
            <fig id="f24001">
              <label>Figure 13.3</label>
              <caption>
                <title>&#8211; Example of right ventricular strain in a patient using a ventricular assist device. GE EchoPAC software. AVC: aortic valve closure; GLS: global longitudinal strain.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf24-en.tif"/></fig>
          </p>
          <p>
            <fig id="f25001">
              <label>Figure 13.4</label>
              <caption>
                <title>&#8211; Example of right ventricular strain in a heart transplant patient. TomTec Software. RVFWS: right ventricular free wall strain; RV4CS: right ventricular global longitudinal strain.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf25-en.tif"/></fig>
          </p>
          <p>In acute myocardial infarction, cardiac MRI RVGLS has the best correlation with right ventricular ejection fraction.<sup><xref ref-type="bibr" rid="B341">341</xref></sup> It has been shown to be an independent predictor of death, reinfarction, and hospitalization due to HF, which confirms its fundamental role in assessing this population.<sup><xref ref-type="bibr" rid="B342">342</xref></sup> A separate section will discuss the assessment of patients with arrhythmogenic RV dysplasia.</p>
          <p>The role of RV systolic dysfunction has recently been investigated in other cardiomyopathies. In one study lower RVGLS values were found in an HCM group than in healthy controls,<sup><xref ref-type="bibr" rid="B343">343</xref></sup> while another reported that RVGLS can differentiate HCM and hypertrophy secondary to hypertension with high sensitivity and specificity.<sup><xref ref-type="bibr" rid="B344">344</xref></sup></p>
          <p>The valvular heart disease with the greatest effect on the RV is mitral stenosis, frequently changing its conventional assessment parameters. The pattern of change in RVGLS is segmental, with significantly lower values in the interventricular septum and RV basal free wall, and normal values in the middle and apical free wall.<sup><xref ref-type="bibr" rid="B345">345</xref>,<xref ref-type="bibr" rid="B346">346</xref></sup> Among patients with significant functional tricuspid regurgitation, RV free wall LS identified more individuals with RV dysfunction (84.9%) than fractional area change (48.5%) and tricuspid annular plane systolic excursion (71.7%). Furthermore, RV free wall LS was independently associated with all-cause mortality and had higher prognostic value when combined with traditional RV assessment parameters.<sup><xref ref-type="bibr" rid="B328">328</xref></sup></p>
          <p>Due to the lack of studies, there is no consensus about normal RV strain values. According to the most recent American Society of Echocardiography/European Association of Cardiovascular Imaging recommendations for echocardiographic cardiac chamber quantification in adults, RVGLS and RV free wall LS values below 20% are considered abnormal.<sup><xref ref-type="bibr" rid="B35">35</xref></sup> However, this requires caution since different equipment types use different software programs, particular reference values, and differences in mapping level (endocardial, epicardial, or the entire myocardial wall).</p>
          <p><xref ref-type="table" rid="t22001">Table 13.2</xref> summarizes the main recommendations for GLS in RV assessment.</p>
          <p>
            <table-wrap id="t22001">
              <label>Table 13.2</label>
              <caption>
                <title>&#8211; IIndications for global longitudinal strain in RV assessment</title>
              </caption>
              <table frame="hsides" rules="groups">
                <colgroup width="100%">
                  <col/>
                </colgroup>
                <thead>
                  <tr>
                    <th align="left" style="font-weight:normal">
                      <list list-type="simple">
                        <list-item>
                          <p>&#8226;Pulmonary hypertension (including patients with acute or chronic pulmonary embolism)</p>
                        </list-item>
                      </list>
                    </th>
                  </tr>
                </thead>
                <tbody>
                  <tr>
                    <td>
                      <list list-type="simple">
                        <list-item>
                          <p>&#8226;Heart failure with reduced or preserved ejection fraction</p>
                        </list-item>
                      </list>
                    </td>
                  </tr>
                  <tr>
                    <td>
                      <list list-type="simple">
                        <list-item>
                          <p>&#8226;Acute myocardial infarction</p>
                        </list-item>
                      </list>
                    </td>
                  </tr>
                  <tr>
                    <td>
                      <list list-type="simple">
                        <list-item>
                          <p>&#8226;Cardiomyopathies (ADRV, HCM, DCM)</p>
                        </list-item>
                      </list>
                    </td>
                  </tr>
                  <tr>
                    <td>
                      <list list-type="simple">
                        <list-item>
                          <p>&#8226;Valvular heart disease (mitral stenosis, functional tricuspid regurgitation)</p>
                        </list-item>
                      </list>
                    </td>
                  </tr>
                  <tr>
                    <td>
                      <list list-type="simple">
                        <list-item>
                          <p>&#8226;Candidates for ventricular assist device implantation</p>
                        </list-item>
                      </list>
                    </td>
                  </tr>
                  <tr>
                    <td>
                      <list list-type="simple">
                        <list-item>
                          <p>&#8226;Heart transplant</p>
                        </list-item>
                      </list>
                    </td>
                  </tr>
                </tbody>
              </table>
              <table-wrap-foot>
                <attrib>
                  <italic>ADRV: arrhythmogenic dysplasia of the right ventricle; DCM: dilated cardiomyopathy; HCM: hypertrophic cardiomyopathy.</italic>
                </attrib>
              </table-wrap-foot>
            </table-wrap>
          </p>
        </sec>
      </sec>
      <sec>
        <title>14. Left and Right Atrial Strain</title>
        <sec>
          <title>14.1. Left Atrial Strain Assessment Techniques</title>
          <p>Strain analysis involves the 3 components of LA function: reservoir, conduit, and contractile. Strain rate is also used, although less commonly, ie, the peak strain rate during the reservoir phase, the conduit phase, and atrial contraction.<sup><xref ref-type="bibr" rid="B92">92</xref>,<xref ref-type="bibr" rid="B347">347</xref></sup></p>
          <p>Four- and 2-chamber apical images are optimized for the LA and taken at a high frame rate, usually 40-80 frames per second. A specific cardiac cycle is selected and point-to-point tracking is performed manually from the endocardial border of the mitral annulus to the opposite mitral annulus, extrapolating the entrance of the pulmonary veins and the left atrial appendage. The software creates the region of interest, which is adjusted to 3 mm in width and must include the endocardial and epicardial borders. If the tracking quality fails in &#8805; 2 segments after manual adjustment, this incidence must be excluded from the analysis. Finally, the software calculates the GLS for each of the above-mentioned apical windows.</p>
          <p>LA strain analysis can involve 2 different reference points: the beginning of the P-wave in the electrocardiogram<sup><xref ref-type="bibr" rid="B2">2</xref></sup> or the R-wave peak of the QRS complex.<sup><xref ref-type="bibr" rid="B348">348</xref></sup> The first method allows easier recognition of LA strain components, requiring the sum of the absolute values of LA conduit strain and LA contractile strain to obtain LA reservoir strain. The second method directly provides the LA reservoir strain value, which has the best prognostic value, while the other components are obtained from the graph. The most recommended and common method is to use the R-wave as a reference, since it has the smallest volume in the LA, and LA reservoir strain is thus more easily obtained.<sup><xref ref-type="bibr" rid="B92">92</xref></sup></p>
        </sec>
        <sec>
          <title>14.2. Normality Values</title>
          <p>There is great heterogeneity in the literature regarding normality values for LA strain. A meta-analysis by Pathan et al. is the best evidence at the moment, which found the following mean values for LA reservoir strain, LA conduit strain, and LA contractile strain, respectively: 39.4% (95% CI: 38%&#8211;40.8%); 23% (95% CI: 20.7%&#8211;25.2%) and 17.4% (95% CI: 16.0%&#8211;19.0%).<sup><xref ref-type="bibr" rid="B37">37</xref></sup></p>
        </sec>
        <sec>
          <title>14.3. Clinical Applicability of Left Atrial Strain</title>
          <p>LA strain assessment has shown greater prognostic value than volumetric measurement alone in several clinical contexts<sup><xref ref-type="bibr" rid="B349">349</xref></sup> (<xref ref-type="fig" rid="f26001">Figure 14.1</xref>).</p>
          <p>
            <fig id="f26001">
              <label>Figure 14.1</label>
              <caption>
                <title>&#8211; Strain assessment of mechanisms involved in left atrial dysfunction.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf26-en.tif"/></fig>
          </p>
          <sec>
            <title>14.3.1. Left Atrial Strain and Diastolic Function in Heart Failure</title>
            <p>LA strain is decreased in HFrEF and has prognostic value for all-cause mortality or rehospitalization for HF,<sup><xref ref-type="bibr" rid="B350">350</xref></sup> good correlation with functional capacity<sup><xref ref-type="bibr" rid="B351">351</xref></sup> and LV filling pressures,<sup><xref ref-type="bibr" rid="B352">352</xref></sup> and is a good predictor of response to myocardial resynchronization therapy.<sup><xref ref-type="bibr" rid="B353">353</xref></sup> In HFpEF, LA strain plays an important role in diagnosis<sup><xref ref-type="bibr" rid="B354">354</xref></sup> and prognosis,<sup><xref ref-type="bibr" rid="B73">73</xref>,<xref ref-type="bibr" rid="B355">355</xref></sup> and can predict the risk of AF.<sup><xref ref-type="bibr" rid="B98">98</xref></sup></p>
            <p>In about 20% of HFpEF cases, LV diastolic function may have an indeterminate pattern.<sup><xref ref-type="bibr" rid="B93">93</xref></sup> LA strain can recategorize these patients,<sup><xref ref-type="bibr" rid="B90">90</xref></sup> since the 3 atrial function components have shown good accuracy in determining increased LA pressure.<sup><xref ref-type="bibr" rid="B89">89</xref></sup></p>
          </sec>
          <sec>
            <title>14.3.2. Atrial Fibrillation</title>
            <p>In AF, the LA reservoir and conduit functions decrease and contractile function is absent. LA strain can predict new AF in several pathologies, such as HFrEF,<sup><xref ref-type="bibr" rid="B356">356</xref></sup> mitral stenosis,<sup><xref ref-type="bibr" rid="B357">357</xref></sup> and Chagas disease <sup><xref ref-type="bibr" rid="B358">358</xref></sup>, as well as after pacemaker implantation,<sup><xref ref-type="bibr" rid="B359">359</xref></sup> in addition to predicting AF recurrence after cardioversion<sup><xref ref-type="bibr" rid="B360">360</xref></sup> or ablation.<sup><xref ref-type="bibr" rid="B361">361</xref>-<xref ref-type="bibr" rid="B363">363</xref></sup> AT function assessment through strain could become part of the decision-making process for AF ablation. LA reservoir strain is also associated with ischemic stroke independent of CHA<sub>2</sub>DS<sub>2</sub>-VASc score, age, or anticoagulant use.<sup><xref ref-type="bibr" rid="B364">364</xref></sup></p>
          </sec>
          <sec>
            <title>14.3.3. Valvular Heart Disease</title>
            <p>LA strain may signal greater severity and an unfavorable course in mitral and aortic valve disease.<sup><xref ref-type="bibr" rid="B365">365</xref>,<xref ref-type="bibr" rid="B366">366</xref></sup> In severe primary mitral regurgitation, LA reservoir strain can predict hospitalization for HF or all-cause mortality, regardless of whether surgical intervention is recommended.<sup><xref ref-type="bibr" rid="B367">367</xref>,<xref ref-type="bibr" rid="B368">368</xref></sup></p>
          </sec>
          <sec>
            <title>14.3.4. Coronary Artery Disease</title>
            <p>Coronary artery disease is associated with atrial dysfunction through 2 main mechanisms: LV DD and direct LA ischemia.<sup><xref ref-type="bibr" rid="B369">369</xref></sup> LA strain may have important prognostic value in acute coronary syndrome, correlating with greater severity <sup><xref ref-type="bibr" rid="B370">370</xref></sup> and unfavorable outcomes.<sup><xref ref-type="bibr" rid="B371">371</xref></sup></p>
          </sec>
        </sec>
      </sec>
      <sec>
        <title>14.4. Right Atrial Strain</title>
        <p>Although data on RA strain is lacking, a recent study of 101 healthy volunteers found the following values using the QRS complex as a reference: reservoir 37.6% (SD 6.9), conduit 26.0% (SD 7.1), and contraction 11.6% (SD 4.4).<sup><xref ref-type="bibr" rid="B37">37</xref></sup> Assessing RA function is a target of interest in congenital heart diseases,<sup><xref ref-type="bibr" rid="B301">301</xref>,<xref ref-type="bibr" rid="B373">373</xref></sup> tricuspid valve disease, and pulmonary hypertension.<sup><xref ref-type="bibr" rid="B374">374</xref></sup></p>
      </sec>
      <sec>
        <title>15. Assessing Left Ventricular Torsion</title>
        <sec>
          <title>15.1. Introduction</title>
          <p>LV function is determined through complex interactions between tissue anatomy, myocardial contractility, and hemodynamics. The muscle fibers of the LV myocardial wall are oriented in different directions. In the subendocardial region, they are almost parallel to the wall and move in a right-handed rotation (right-handed helix), which gradually changes in subepicardial fibers to 60&#8211;70&#186;, leading to a left-handed rotation (left-handed helix).<sup><xref ref-type="bibr" rid="B375">375</xref>,<xref ref-type="bibr" rid="B376">376</xref></sup></p>
          <p>Subepicardial fiber contraction causes the apex of the LV to rotate counterclockwise and its base to rotate clockwise. Conversely, subendocardial fiber contraction causes the apex and base of the LV to rotate in opposite directions. Given the greater rotation radius of the epicardial layer, the direction of the subepicardial fibers prevails in the general direction of rotation when both layers contract simultaneously. This results in global counterclockwise rotation near the apex and clockwise rotation near the base during ventricular ejection,<sup><xref ref-type="bibr" rid="B377">377</xref></sup> as shown in <xref ref-type="fig" rid="f27001">Figure 15.1</xref>.</p>
          <p>
            <fig id="f27001">
              <label>Figure 15.1</label>
              <caption>
                <title>&#8211; Rotation direction of subendocardial fibers: (A) subepicardial fibers (B) overall LV rotation with (C) simultaneous contraction of the fibers. Adapted from St&#246;hr et al.384</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf27-en.tif"/></fig>
          </p>
          <p>This twisting motion in the LV contributes to an even distribution of fiber shortening and stress along all walls, thus producing a relatively high EF (~60%) despite limited shortening (~20%).<sup><xref ref-type="bibr" rid="B378">378</xref></sup> The twisting and shearing of the subendocardial fibers during ventricular ejection results in the storage of potential energy, which is subsequently used to unwind the coiled fibers during diastole, thus untwisting the helices, which together produce diastolic suction.<sup><xref ref-type="bibr" rid="B379">379</xref>,<xref ref-type="bibr" rid="B380">380</xref></sup> Preload and afterload conditions and contractility alter the extent of ventricular torsion.<sup><xref ref-type="bibr" rid="B381">381</xref></sup> Increased preload or contractility increases LV torsion, while increased afterload has the opposite effect.</p>
          <p>Several imaging techniques can be used to quantify the mechanics of ventricular torsion: echocardiography (tissue Doppler, 2D and 3D speckle tracking, velocity vector imaging, cardiac MRI (tissue tagging), and sonomicrometry. Currently, there is no gold standard for assessing LV torsion mechanics, and the above-mentioned imaging modalities have good agreement.<sup><xref ref-type="bibr" rid="B382">382</xref></sup> Due to its safety, availability, and cost-effectiveness, echocardiography is the most commonly used imaging modality.</p>
        </sec>
        <sec>
          <title>15.2. Definitions and Nomenclature</title>
          <p>Twist, twist rate, untwist, and untwist rate are the common terms for describing the systolic rotation and reverse diastolic rotation of the base and apex of the LV as seen from the apex. These terms are defined in <xref ref-type="table" rid="t23001">Tables 15.1</xref> and <xref ref-type="table" rid="t24001">15.2</xref>.</p>
          <p>
            <table-wrap id="t23001">
              <label>Table 15.1</label>
              <caption>
                <title>&#8211; Definitions and parameters used to assess left ventricular twist during systole</title>
              </caption>
              <table frame="hsides" rules="groups">
                <colgroup width="50%">
                  <col/>
                  <col/>
                </colgroup>
                <thead>
                  <tr>
                    <th align="left">Parameter</th>
                    <th align="left">Definition</th>
                  </tr>
                </thead>
                <tbody>
                  <tr>
                    <td>Apical rotation (&#186;)</td>
                    <td>Peak counterclockwise systolic rotation of the apical LV region (measured in degrees)</td>
                  </tr>
                  <tr>
                    <td>Apical rotation rate (&#186;/s)</td>
                    <td>Peak counterclockwise apical rotation speed (measured in degrees/second)</td>
                  </tr>
                  <tr>
                    <td>Basal rotation (&#186;)</td>
                    <td>Peak clockwise systolic rotation of the basal region of the LV (measured in degrees)</td>
                  </tr>
                  <tr>
                    <td>Basal rotation rate (&#186;/s)</td>
                    <td>Peak basal clockwise rotation velocity (measured in degrees/second)</td>
                  </tr>
                  <tr>
                    <td>LV twist (&#186;)</td>
                    <td>Peak difference of LV apex and base systolic rotation (measured in degrees)</td>
                  </tr>
                  <tr>
                    <td>LV torsion (&#186;/cm)</td>
                    <td>Normalized twist: ratio of the twist angle and the distance between the base and apex in systole (measured in degrees/centimeter)</td>
                  </tr>
                  <tr>
                    <td>Twist rate (&#186;/s)</td>
                    <td>Peak LV twist speed (measured in degrees/second)</td>
                  </tr>
                </tbody>
              </table>
              <table-wrap-foot>
                <attrib>
                  <italic>(o): degrees; (o/s): degrees per second; (&#186;/cm): degrees per centimeter. LV = left ventricle.</italic>
                </attrib>
              </table-wrap-foot>
            </table-wrap>
          </p>
          <p>
            <table-wrap id="t24001">
              <label>Table 15.2</label>
              <caption>
                <title>&#8211; Definitions and parameters used to assess left ventricular twist mechanism in diastole</title>
              </caption>
              <table frame="hsides" rules="groups">
                <colgroup width="50%">
                  <col/>
                  <col/>
                </colgroup>
                <thead>
                  <tr>
                    <th align="left">Parameter</th>
                    <th align="left">Definition</th>
                  </tr>
                </thead>
                <tbody>
                  <tr>
                    <td>Apical reverse rotation (&#186;)</td>
                    <td>Peak clockwise diastolic rotation of the apical LV region (measured in degrees)</td>
                  </tr>
                  <tr>
                    <td>Apical reverse rotation rate (&#186;/s)</td>
                    <td>Peak velocity of clockwise apical reverse rotation (measured in degrees/second)</td>
                  </tr>
                  <tr>
                    <td>Basal reverse rotation (&#186;)</td>
                    <td>Peak diastolic counterclockwise rotation of the basal region of the LV (measured in degrees)</td>
                  </tr>
                  <tr>
                    <td>Basal reverse rotation rate (&#186;/s)</td>
                    <td>Peak basal rotation speed (measured in degrees/second)</td>
                  </tr>
                  <tr>
                    <td>Untwist (&#186;)</td>
                    <td>Difference in peak reverse diastolic rotation of the apex and base of the LV (measured in degrees)</td>
                  </tr>
                  <tr>
                    <td>Untwist Rate (&#186;/s)</td>
                    <td>Peak LV untwist speed (measured in degrees/second)</td>
                  </tr>
                </tbody>
              </table>
              <table-wrap-foot>
                <attrib>
                  <italic>(o): degrees; (o/s): degrees per second; LV = left ventricle.</italic>
                </attrib>
              </table-wrap-foot>
            </table-wrap>
          </p>
        </sec>
        <sec>
          <title>15.3. Step-by-step Assessment of Ventricular Torsion by Speckle Tracking Echocardiography</title>
          <p>To evaluate the rotation mechanism, parasternal short-axis images of the LV are obtained at the basal (mitral valve) and apical levels (below the papillary muscles) (<xref ref-type="fig" rid="f28001">Figure 15.2</xref>). It is important to obtain apical images in which RV does not appear or only part of the LV appears, typically 1 or 2 intercostal spaces below the usual position. Most evaluation errors occur due to inappropriate selection of basal and apical planes and region of interest adjustment.</p>
          <p>
            <fig id="f28001">
              <label>Figure 15.2</label>
              <caption>
                <title>&#8211; Image acquisition plan for basal and apical rotation measurement (Images courtesy of Dr. Marcio Lima).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf28-en.tif"/></fig>
          </p>
          <p>By convention, when rotation is clockwise, tracking begins below the baseline, and when rotation is counterclockwise, tracking begins above the baseline. (<xref ref-type="fig" rid="f29001">Figure 15.3</xref>). The normal global twist value is 9.7&#176; (SD, 4.1&#176;), although there are few reference values in the literature for torsion, which is estimated at 1.35&#176;/cm (SD 0.54&#176;/cm).<sup><xref ref-type="bibr" rid="B383">383</xref></sup></p>
          <p>
            <fig id="f29001">
              <label>Figure 15.3</label>
              <caption>
                <title>&#8211; Clockwise (below baseline) and counterclockwise (above baseline) rotation (Images courtesy of Dr. Marcio Lima).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf29-en.tif"/></fig>
          </p>
        </sec>
        <sec>
          <title>15.4. Clinical Applications</title>
          <p>LV torsion parameters have generally been used to assess changes in ventricular mechanics in pathologies with reduced LVEF (ischemic and dilated cardiomyopathy) or preserved LVEF (HFpEF, hypertension, HCM, aortic stenosis, aortic insufficiency, and mitral insufficiency), as well as to assess subclinical myocardial dysfunction due to chemotherapy.</p>
          <p>Twist and torsion measurements, although good parameters for global systolic function analysis, are limited in terms of reproducibility, which is mainly due to the lack of anatomical parameters for the apical section. The findings on ventricular twist and torsion changes are not specific, but they could contribute to a better understanding of the pathophysiology of different cardiomyopathies, helping differentiate them (<xref ref-type="table" rid="t25001">Table 15.3</xref>).</p>
          <p>
            <table-wrap id="t25001">
              <label>Table 15.3</label>
              <caption>
                <title>&#8211; Left ventriclar twist in different cardiovascular diseases</title>
              </caption>
              <table frame="hsides" rules="groups">
                <colgroup width="33%">
                  <col/>
                  <col/>
                  <col/>
                </colgroup>
                <thead>
                  <tr>
                    <th align="left">Cardiovascular disease</th>
                    <th>LV twist</th>
                    <th align="left">Findings</th>
                  </tr>
                </thead>
                <tbody>
                  <tr>
                    <td>Ischemic cardiomyopathy</td>
                    <td align="center">Decreased</td>
                    <td>Twist decreases depending on the location and extent of ischemia.</td>
                  </tr>
                  <tr>
                    <td>Dilated cardiomyopathy</td>
                    <td align="center">Decreased</td>
                    <td>Twist decreases proportionally to decreased ejection fraction</td>
                  </tr>
                  <tr>
                    <td>Hypertrophic cardiomyopathy</td>
                    <td align="center">Increased</td>
                    <td>Twist increases especially if the LV outflow tract is obstructed</td>
                  </tr>
                  <tr>
                    <td>Aortic stenosis</td>
                    <td align="center">Increased</td>
                    <td>Increased twist in cases of increased LV afterload.</td>
                  </tr>
                </tbody>
              </table>
            </table-wrap>
          </p>
        </sec>
      </sec>
      <sec>
        <title>16. Strain in Ventricular Dyssynchrony Analysis</title>
        <sec>
          <title>16.1. Introduction</title>
          <p>Due to its expressive reduction of morbidity and mortality, cardiac resynchronization therapy (CRT) is indicated in national and international guidelines. CRT is a class I recommendation for symptomatic dilated cardiomyopathy patients who are undergoing optimized clinical treatment and have a left bundle branch block (LBBB) pattern in electrocardiography, QRS duration &#8805; 150 ms, and LVEF &lt; 35% (evidence level A).<sup><xref ref-type="bibr" rid="B385">385</xref></sup></p>
          <p>Due to a lack of data about echocardiographic synchrony assessment, these guidelines consider LBBB &#8805; 150 ms as a marker of dyssynchrony. However, echocardiography is also limited as a dyssynchrony marker. Thus, at present, echocardiographic dyssynchrony assessment for CRT selection must be performed in an individualized and judicious manner by an adequately trained examiner and interpreted together with the patient&#8217;s clinical data. It is also important to remember that not only can echocardiography assess cardiac synchrony but it can help select the best site for LV electrode implantation, as well as determine response and reverse remodeling. More recent findings indicate that it can identify ventricular arrhythmia risk.<sup><xref ref-type="bibr" rid="B385">385</xref></sup></p>
        </sec>
        <sec>
          <title>16.2. Dyssynchrony Assessment when Selecting Patients for Cardiac Resynchronization Therapy</title>
          <p>Assessing mechanical dyssynchrony and efficiency through strain alone is insufficient to indicate CRT. However, even with a precise recommendation, the chance of success (ie, improvement in clinical, functional, and/or imaging variables) is approximately 60%&#8211;70%. The CRT response rate can be estimated and even improved through echocardiography. In this context, myocardial strain measurement stands out.</p>
          <p>Initial analysis of dyssynchrony through radial strain describes the time difference between maximum radial strain of the middle anteroseptal and inferolateral segments. Values &gt; 130 ms indicate patients with a higher response rate,<sup><xref ref-type="bibr" rid="B386">386</xref></sup> as shown in <xref ref-type="fig" rid="f30001">Figure 16.1</xref>.</p>
          <p>
            <fig id="f30001">
              <label>Figure 16.1</label>
              <caption>
                <title>&#8211; Radial strain image showing curves for the middle segments of the anteroseptal and inferolateral walls. The interval &gt; 130 ms correlates with a higher CRT response rate, in this case 340 ms.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf30-en.tif"/></fig>
          </p>
          <p>In addition to radial dyssynchrony, independent predictors of long-term prognosis include an inhomogeneous pattern of septal rebound stretch in speckle-tracking and LV reverse remodeling with a higher value in LBBB and apical rocking detected by visual analysis. This pattern reflects incoordinated contraction, which results in reduced myocardial performance. Recent studies have indicated that septal rebound stretch assessment can improve patient selection for CRT, especially patients without defined LBBB.<sup><xref ref-type="bibr" rid="B387">387</xref></sup> The pattern consists of 3 three aspects of LS in the inferoseptal and anterolateral (frequently basal) segments: 1) peak opposition of the septal curves (negative) and lateral curves (positive); 2) peak negative septal strain in up to 70% of the ejection time; 3) peak negative strain in the lateral wall after aortic valve closure,<sup><xref ref-type="bibr" rid="B388">388</xref></sup> as shown in <xref ref-type="fig" rid="f31001">Figure 16.2</xref>.</p>
          <p>
            <fig id="f31001">
              <label>Figure 16.2</label>
              <caption>
                <title>&#8211; Longitudinal strain image with inferoseptal (yellow) and anterolateral (red) basal segment curves with typical left bundle branch block pattern: 1) initial opposition of the peak of the septal (negative) and lateral (positive) curves; 2) negative septal strain peak in &#8804; 70% of the ejection time, with shortening interrupted during systole, ie, prior to aortic valve closure (AVC) resulting in systolic stretching; 3) negative strain peak in the lateral wall after AVC.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf31-en.tif"/></fig>
          </p>
          <p>Global LVMW efficiency analysis has recently shown promise in CRT. Global LVMW efficiency can be quantified non-invasively through myocardial strain curves and blood pressure measurements. Lower global LVMW efficiency values have been independently associated with better long-term prognosis.<sup><xref ref-type="bibr" rid="B389">389</xref></sup><xref ref-type="fig" rid="f32001">Figure 16.3</xref> shows changes in strain, MW, and myocardial efficiency in a patient who underwent successful CRT.</p>
          <p>
            <fig id="f32001">
              <label>Figure 16.3</label>
              <caption>
                <title>&#8211; Pre- and post-procedure polar maps of (A) longitudinal strain, (B) myocardial work, and (C) myocardial efficiency in a patient who underwent successful resynchronization therapy.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf32-en.tif"/></fig>
          </p>
        </sec>
        <sec>
          <title>16.3. Myocardial Viability Assessment</title>
          <p>Another application of myocardial strain in the CRT context is the correlation between myocardial fibrosis and reduced strain values. Reduced global radial strain values correlate with a greater degree of fibrosis (detected in cardiac MRI), thus identifying patients with a lower chance of ventricular function recovery. Reduced LS in patients with ischemic heart disease can also be used for this purpose.</p>
        </sec>
        <sec>
          <title>16.4. Electrode Implantation Site</title>
          <p>Equally important as total LV fibrosis, compromised values at the LV electrode implantation site have been associated with lower CRT response. Studies have shown that positioning the LV electrode in the segment with the greatest delay in mechanical contraction results in higher CRT success rates. Speckle tracking can identify the segment that should be stimulated. In the TARGET study, LV electrode placement guided by 2D speckle-tracking resulted in better clinical response and lower rates of mortality and hospitalization for HF.<sup><xref ref-type="bibr" rid="B390">390</xref>,<xref ref-type="bibr" rid="B391">391</xref></sup></p>
        </sec>
        <sec>
          <title>16.5. Prognostic Assessment after CRT</title>
          <p>Post-CRT dyssynchrony analysis through LS is a strong predictor of ventricular arrhythmias. Speckle-tracking findings of persistent or increased mechanical scattering 6 months after CRT are associated with worse prognosis. Furthermore, CRT response (reverse remodeling) depends on improvement in both longitudinal and circumferential function after CRT.<sup><xref ref-type="bibr" rid="B392">392</xref></sup></p>
        </sec>
        <sec>
          <title>16.6. Adjustment of Resynchronization Parameters</title>
          <p>About 30% of patients who undergo CRT are considered non-responders due to a lack of clinical and/or functional improvement, including a lack of reverse remodeling (evidenced by lower ventricular dimensions and higher EF).<sup><xref ref-type="bibr" rid="B393">393</xref></sup> In these patients, adjustments to the atrioventricular, interventricular, and left intraventricular intervals may improve CRT response. Some studies have shown that speckle-tracking can guide adjustment of CRT parameters, leading to significant improvement in functional class and EF in non-responders.<sup><xref ref-type="bibr" rid="B394">394</xref></sup></p>
        </sec>
      </sec>
      <sec>
        <title>17. Myocardial Work</title>
        <sec>
          <title>17.1. Introduction</title>
          <p>Having recently emerged as an echocardiographic tool to increase information about ventricular function, MW adds the effects of LV afterload to LS measurement. After the experimental work of Suga et al. in 1979,<sup><xref ref-type="bibr" rid="B395">395</xref></sup> which demonstrated that the area under the pressure-volume curve, invasively acquired with an intraventricular conductance catheter, reflected regional MW and oxygen consumption per beat, interest has grown in non-invasive imaging methods to make such analysis feasible.<sup><xref ref-type="bibr" rid="B396">396</xref>,<xref ref-type="bibr" rid="B397">397</xref></sup></p>
          <p>In 2012, Russell et al.<sup><xref ref-type="bibr" rid="B398">398</xref></sup> validated a non-invasive method of analyzing the LV pressure-strain loop, integrating systolic blood pressure at the time of speckle tracking LS assessment, which after interpretation by the software, calculates pressure-strain loops globally and per segment (<xref ref-type="fig" rid="f33001">Figure 17.1</xref>). The AUC represents MW, which is highly correlated with direct intraventricular measurements. MW also reflects regional myocardial oxygen metabolism comparably to positron emission tomography with 18F- fluorodeoxyglucose.<sup><xref ref-type="bibr" rid="B399">399</xref>-<xref ref-type="bibr" rid="B401">401</xref></sup></p>
          <p>
            <fig id="f33001">
              <label>Figure 17.1</label>
              <caption>
                <title>&#8211; Left ventricular pressure-strain loop. Red: global pressure-strain loop. Green: pressure-strain loop for the basal segment of the inferolateral wall. AVC: aortic valve closure; AVO: aortic valve opening; IVCT: isovolumetric contraction time; IVRT: isovolumetric relaxation time LVP: left ventricular pressure estimated by systolic blood pressure; MVC: mitral valve closure; MVO: mitral valve opening.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf33-en.tif"/></fig>
          </p>
          <p>Modest increases in blood pressure can reduce GLS by up to 9%, which could be misinterpreted as reduced contractility, when in fact MW remains preserved, reflecting only increased afterload. Thus, MW is considered an advance in the understanding of ventricular mechanics.<sup><xref ref-type="bibr" rid="B398">398</xref>,<xref ref-type="bibr" rid="B402">402</xref></sup> The main differences between MW and the LV strain are shown in <xref ref-type="table" rid="t26001">Table 17.1</xref>.</p>
          <p>
            <table-wrap id="t26001">
              <label>Table 17.1</label>
              <caption>
                <title>&#8211; Main differences between myocardial work and left ventricular strain</title>
              </caption>
              <table frame="hsides" rules="groups">
                <colgroup width="33%">
                  <col/>
                  <col/>
                  <col/>
                </colgroup>
                <thead>
                  <tr>
                    <th align="left" style="font-weight:normal"> </th>
                    <th>Strain</th>
                    <th>Myocardial work</th>
                  </tr>
                </thead>
                <tbody>
                  <tr>
                    <td>AFI use</td>
                    <td align="center">yes</td>
                    <td align="center">yes</td>
                  </tr>
                  <tr>
                    <td>Measure</td>
                    <td align="center">AVO-AVC</td>
                    <td align="center">IVCT + ET + IVRT</td>
                  </tr>
                  <tr>
                    <td>Integrated with blood pressure</td>
                    <td align="center">no</td>
                    <td align="center">yes</td>
                  </tr>
                  <tr>
                    <td>Value</td>
                    <td align="center">%</td>
                    <td align="center">mmHg%</td>
                  </tr>
                  <tr>
                    <td>Incorporates postload</td>
                    <td align="center">no</td>
                    <td align="center">yes</td>
                  </tr>
                  <tr>
                    <td>Measures efficiency</td>
                    <td align="center">no</td>
                    <td align="center">yes</td>
                  </tr>
                  <tr>
                    <td>Estimates myocardial oxygen consumption</td>
                    <td align="center">no</td>
                    <td align="center">yes</td>
                  </tr>
                </tbody>
              </table>
              <table-wrap-foot>
                <attrib>
                  <italic>AFI: automated functional imaging AVO: Aortic valve opening; AVC: AV closure; IVCT: isovolumetric contraction time; ET: ejection time; IVRT: isovolumetric relaxation time.</italic>
                </attrib>
              </table-wrap-foot>
            </table-wrap>
          </p>
        </sec>
        <sec>
          <title>17.2. Calculating Myocardial Work</title>
          <p>To obtain accurate and reproducible results, appropriate MW calculation techniques must be used for image acquisition, as well as post-processing and parameter analysis. This technology is currently only available in workstations or devices embedded with GE software (GE Healthcare, Horten, Norway). Analyses can be performed directly on the device or post-processed in workstations using previously acquired images.</p>
          <p>The image acquisition protocol for calculating MW follows the same technical prerequisites for GLS analysis, which will be discussed in a subsequent chapter. After 2D strain is assessed using images acquired in the 3 apical projections through automated functional imaging, MW can be evaluated by the software (<xref ref-type="fig" rid="f34001">Figure 17.2</xref>). Blood pressure values measured non-invasively at the time of the examination must be manually entered into the patient identification form during the examination or later into the MW calculation form itself (<xref ref-type="fig" rid="f35001">Figure 17.3</xref>). These non-invasive blood pressure measurements will be automatically input into the pressure-strain loop.</p>
          <p>
            <fig id="f34001">
              <label>Figure 17.2</label>
              <caption>
                <title>&#8211; After assessing 2D LV longitudinal strain with the automated functional imaging method and processing the 3 apical windows, the software offers to calculate myocardial work (yellow arrow).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf34-en.tif"/></fig>
          </p>
          <p>
            <fig id="f35001">
              <label>Figure 17.3</label>
              <caption>
                <title>&#8211; Initial screen of myocardial work calculation. In this step, non-invasively measured blood pressure values can be inserted (bottom arrow), and cardiac events, such as the opening and closing of the mitral and aortic valves can be reassessed or marked (top arrow).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf35-en.tif"/></fig>
          </p>
          <p>For temporal indexing of the values, the events of the cardiac cycle must be marked, identifying the opening and closing of the mitral and aortic valves. This can be performed through spectral Doppler or 2D analysis of mitral and aortic flow through an apical 3-chamber projection, which shows the opening and closing of both valves (<xref ref-type="fig" rid="f36001">Figure 17.4</xref>). These points can also be marked on the MW calculation screen, modifying apical 3-chamber image frame-by-frame, selecting the exact moment of each event (<xref ref-type="fig" rid="f37001">Figure 17.5</xref>). After checking the images and markings, the software performs the calculations and displays a polar (bulls-eye) map beside GLS and peak strain values for each segment. A polar map with the MW index for each segment appears on the right side, with global MW index and MW efficiency values below it. When the &#8220;work efficiency&#8221; key is selected, the software shows the global MW efficiency values for each segment on the polar map (<xref ref-type="fig" rid="f38001">Figure 17.6</xref>). Selecting the &#8220;advanced&#8221; key generates curves and graphs of the LV pressure-strain loops throughout the cardiac cycle, in addition to a bar graph showing the proportions of constructive and wasted MW (<xref ref-type="fig" rid="f39001">Figure 17.7</xref>).</p>
          <p>
            <fig id="f36001">
              <label>Figure 17.4</label>
              <caption>
                <title>&#8211; Marking cardiac events through spectral Doppler: A) marking mitral valve opening (MVO) and mitral valve closing (MVC) according to mitral inflow; B) marking aortic valve opening (AVO) and aortic valve closing (AVC) through LV outflow.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf36-en.tif"/></fig>
          </p>
          <p>
            <fig id="f37001">
              <label>Figure 17.5</label>
              <caption>
                <title>&#8211; Cardiac events can also be marked on the myocardial work calculation screen, modifying apical 3-chamber images frame by frame and selecting the exact moment of each event in the right sidebar menu (arrows).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf37-en.tif"/></fig>
          </p>
          <p>
            <fig id="f38001">
              <label>Figure 17.6</label>
              <caption>
                <title>&#8211; After approval of the obtained data, appropriately marking events and pressure filling, the software displays the global and segmental longitudinal strain values on the left (white arrows) and polar maps with myocardial work index values (A: yellow arrow) and myocardial work efficiency (B: blue arrow).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf38-en.tif"/></fig>
          </p>
          <p>
            <fig id="f39001">
              <label>Figure 17.7</label>
              <caption>
                <title>&#8211; Selecting the &#8220;advanced&#8221; key shows analyses by curves and graphs, showing the LV pressure-strain loops throughout the cardiac cycle (yellow arrow), in addition to a bar chart showing the proportions of constructive and wasted MW (blue arrow).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf39-en.tif"/></fig>
          </p>
          <p>The following parameters are provided by the software:</p>
          <list list-type="simple">
            <list-item>
              <p>1. Global MW index: total work in the area under the pressure-strain curve, calculated from the closing to the opening of the mitral valve. A bull&#8217;s eye map with segmental and global MW values is provided (Figure 17.6).</p>
            </list-item>
            <list-item>
              <p>2. Constructive MW: work that contributes to LV ejection during systole, obtained by shortening during systole plus myocyte elongation during isovolumetric relaxation (<xref ref-type="fig" rid="f39001">Figure 17.7</xref>).</p>
            </list-item>
            <list-item>
              <p>3. Wasted MW: work that does not contribute to LV ejection, obtained by myocyte elongation (rather than shortening) during systole plus shortening during the isovolumetric relaxation phase (post-systolic shortening) (<xref ref-type="fig" rid="f39001">Figure 17.7</xref>).</p>
            </list-item>
            <list-item>
              <p>4. MW efficiency (MW efficiency/global MW efficiency): the result of the following formula: <inline-formula><mml:math><mml:mtext> constructive MW/ </mml:mtext><mml:mtext> (constructive MW + wasted MW) </mml:mtext></mml:math></inline-formula>; efficiency is rated as 0-100% (<xref ref-type="fig" rid="f38001">Figure 17.6</xref>).</p>
            </list-item>
          </list>
        </sec>
        <sec>
          <title>17.3. Normality Values</title>
          <p>Due to the recent validation of MW and its variables for clinical use, multicenter trials with an adequate number of patients have not yet been conducted to produce definitive normality values.</p>
          <p>Manganaro et al. recently analyzed data from the NORRE study to establish normal reference limits for MW. This prospective European multicenter study included 226 patients from 22 echocardiography laboratories, providing reference values for most 2D and 3D echocardiographic data.<sup><xref ref-type="bibr" rid="B403">403</xref></sup> The mean or median (SD) and/or CI of MW variables were, respectively, 1896 (SD, 308) mm Hg% (CI: 1292-2505) for global MW index, 2232 (SD, 331) mm Hg% (CI: 1582-2881) for constructive MW, 79 mm Hg% (CI: 53-122) for wasted MW, and 96% (CI: 94-97), for global MW efficiency.<sup><xref ref-type="bibr" rid="B403">403</xref></sup></p>
          <p>Another study found higher global MW index and constructive MW values in women &gt; 40 years of age, with a strong correlation between a higher global MW index and constructive MW values and higher systolic blood pressure.<sup><xref ref-type="bibr" rid="B404">404</xref></sup></p>
        </sec>
        <sec>
          <title>17.4. Potential Clinical Use</title>
          <p>A major limitation to more widespread use of MW is that the software is only produced by GE Healthcare. In addition, MW is calculated using manual systolic pressure measurements in afterload. Care should be taken in clinical situations involving additional afterload or increased systolic blood pressure, such as aortic stenosis, obstructive HCM, and some congenital heart diseases. Despite its promise as new tool, current scientific knowledge about MW assessment is still in the research phase.</p>
          <p>Certain publications on MW in clinical practice are gaining notoriety, one of which involves patient selection for myocardial resynchronization. Although LBBB analysis can sometimes be difficult to interpret (<xref ref-type="fig" rid="f40001">Figure 17.8</xref>), visual and quantitative analysis of MW has made it easier to recognize cases of QRS widening without an associated mechanical dyssynchrony (<xref ref-type="fig" rid="f41001">Figure 17.9</xref>). In addition to visual analysis, the ability of constructive MW to identify CRT responders has been recognized as equivalent to contractile reserve.<sup><xref ref-type="bibr" rid="B405">405</xref></sup> Another interesting way to identify patients who benefit from CRT is through wasted septal work.<sup><xref ref-type="bibr" rid="B406">406</xref></sup> Thus, MW assessment in patients with LBBB can improve stratification through visual analysis, as well as quantify constructive and wasted work.</p>
          <p>
            <fig id="f40001">
              <label>Figure 17.8</label>
              <caption>
                <title>&#8211; Two cases with similar left bundle branch block morphologies.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf40-en.tif"/></fig>
          </p>
          <p>
            <fig id="f41001">
              <label>Figure 17.9</label>
              <caption>
                <title>&#8211; Case 1 has no changes in myocardial mechanics: myocardial work in the pressure-strain loop (green line) is similar to the global value (red line). In case 2, &#8220;true&#8221; left bundle branch block; in the same septal portion, the green line assumes a figure-8 shape.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf41-en.tif"/></fig>
          </p>
          <p>Another interesting field for MW assessment is obstructive coronary disease. MW can detect obstructive coronary disease at rest better than LVGLS, even in patients with preserved EF and no segmental contractility changes.<sup><xref ref-type="bibr" rid="B407">407</xref></sup> MW can also identify AMI patients at greater risk of complications and predict recovery,<sup><xref ref-type="bibr" rid="B408">408</xref></sup> as well as predict long-term complications in patients with ST-elevation MI.<sup><xref ref-type="bibr" rid="B409">409</xref></sup></p>
          <p>In addition to these clinical situations, MW has shown promise for dilated cardiomyopathy, HCM, amyloidosis, and other conditions. Certainly, with greater software availability and more evidence in the literature, MW will quickly be incorporated into clinical practice.</p>
        </sec>
      </sec>
      <sec>
        <title>18. Three-dimensional Strain Assessment: What can be Added</title>
        <sec>
          <title>18.1. Introduction</title>
          <p>Three-dimensional myocardial strain assessment through speckle tracking has numerous advantages over 2D assessment. Considering that the LV myocardium consists of 3 layers of fibers arranged in different directions (longitudinal, circumferential, and transverse), the speckles have a non-linear trajectory, escaping the image&#8217;s 2D plane during part of the cardiac cycle. Although multiple longitudinal and transverse images of the LV myocardium may be acquired in 2D assessment, the speckles are interpolated. Thus the method is not as accurate as 3D, which allows monitoring throughout the cardiac cycle in multiple dimensions, being unaffected by extraplanar myocardial torsion or apical shortening.<sup><xref ref-type="bibr" rid="B410">410</xref></sup></p>
          <p>In the RV, global analysis of myocardial chambers is only possible through 3D methodology, whereas only the septum and/or free wall can be assessed in 2D. Furthermore, 3D strain assessment is more reliable and physiological, since different components of myocardial strain are analyzed simultaneously through a single dataset or cardiac cycle. Thus, 3D strain is a quantitative, objective, comprehensive, and reproducible assessment of myocardial mechanical function. However, it strongly depends on a good acoustic window and a regular heart rhythm, which limit the routine and systematic incorporation of 3D strain.<sup><xref ref-type="bibr" rid="B411">411</xref></sup> Clinical application is also limited by differences in the algorithms for monitoring the speckles and cut-off points for myocardial strain, which are not standardized across software platforms.<sup><xref ref-type="bibr" rid="B412">412</xref>,<xref ref-type="bibr" rid="B413">413</xref></sup></p>
          <p>Since 3D strain measurements obtained through different equipment and software manufacturers are not interchangeable, the baseline and follow-up imaging, as well as the analyses, must be performed using the same equipment, and the results must be interpreted in light of the equipment&#8217;s specific normality values.<sup><xref ref-type="bibr" rid="B410">410</xref>,<xref ref-type="bibr" rid="B412">412</xref></sup> Normality reference values also vary between 2D and 3D methodologies, with only a modest correlation between LS values. Finally, further clinical research is needed to determine the accuracy and prognostic value of 3D strain assessment.</p>
        </sec>
        <sec>
          <title>18.2. Left Ventricular Strain</title>
          <p>Three-dimensional speckle-tracking is superior to 2D speckle tracking in that it is not limited to a single slice and that it allows analysis of vectorized data in 3 orthogonal planes. Two-dimensional strain assessment requires a very high temporal resolution (34-50 volumes per second) due to the short duration of the speckles (ie, a few milliseconds) in the slice, which does not occur in 3D. Additionally, the ideal in 3D speckle tracking is to acquire 6 beats at the highest line density and 44 volumes per second at a frequency of 2-4 MHz (which is more accurate than MRI). Acquisition of single volumes is not recommended, since higher temporal resolution decreases image and tracking quality by reducing line density.<sup><xref ref-type="bibr" rid="B414">414</xref></sup></p>
          <p>The general feasibility of 3D speckle-tracking is approximately 85% due to the following limitations: unfavorable acoustic windows, cardiac arrhythmias (preventing acquisition of multiple beats), incomplete visualization of the apical segments of the LV and RV, speckle-tracking problems in follow-up (distance from the transducer), and determining normal values and clinical prognosis.</p>
        </sec>
        <sec>
          <title>18.3. Right Ventricular Strain</title>
          <p>The analysis of RV contraction is especially important to understand the mechanism of this chamber in the face of congenital and acquired diseases. However, unlike the LV, estimating the RV is more difficult due to the complex shape that the RV presents and due to its thin wall. Despite this, MRI images and speckle tracking by echocardiography have been promising in right ventricular analysis. However, the values obtained by ST3D for the RV are still not well established.<sup><xref ref-type="bibr" rid="B415">415</xref></sup> Technical problems persist for the 3D strain analysis when the objective is to analyze the right chambers, since the software was created for the analysis of the LV and still is adapted for the RV on most machines. Although the 3D strain allows global analysis of the entire right myocardium, the three-dimensional technology for this chamber is still in progress, with no well-defined cutoff values for the 3D strain of the RV so far.</p>
          <sec>
            <title>18.3.1. Full-volume 3D Acquisition and Analysis</title>
            <p>Harmonic imaging ideally provides 4 triggered beats per capture. The depth must be adequate so that only the RV, its walls, and the tricuspid annulus fill the volume; the systolic peak strain is generally used for analysis.</p>
          </sec>
        </sec>
      </sec>
      <sec>
        <title>18.4. Left Atrial Strain</title>
        <p>In 3D strain assessment of the LA (as well as the ventricles), ultrasound can acquire volumetric data in real time and can measure all strain components. However, 3D tracking is a great challenge, and the temporal and spatial resolution of 3D is lower than 2D, which makes 3D analysis more complex and time consuming, since high image quality is required to determine 3D strain.</p>
        <p>Another point under discussion is inter- and intraobserver variability in cardiac mechanics.<sup><xref ref-type="bibr" rid="B414">414</xref></sup> The reservoir, conduit, and pumping phases can be well analyzed in 2D strain, and the mean cut-off values for 2D strain in each of these phases have been relatively well defined. However, reference values for 3D strain have not yet been determined. When strain analysis becomes relevant, the main applications of this method in the LV are: HFpEF,<sup><xref ref-type="bibr" rid="B7">7</xref></sup> intracavitary filling pressures,<sup><xref ref-type="bibr" rid="B95">95</xref></sup> atrial function among elite athletes,<sup><xref ref-type="bibr" rid="B416">416</xref></sup> and cardiomyopathies.<sup><xref ref-type="bibr" rid="B417">417</xref></sup> Nevertheless, 2D strain data have been better corroborated than 3D strain data; the incorporation of 3D strain in LA assessment will depend on future research.</p>
      </sec>
      <sec>
        <title>19. The Role of Cardiac Resonance and Tomography in Strain Assessment</title>
        <sec>
          <title>19.1. Introduction</title>
          <p>Due to its high spatial and temporal resolution and non-invasiveness, cardiac MRI has become an important method of assessing global and segmental function in both ventricles. Strain assessment, an established and reliable method for measuring and quantifying regional and global contractile dysfunction, can detect subclinical cardiac dysfunction and, thus, is useful for assessing myocardial function. Echocardiography is currently the most available and least expensive method for assessing strain, but analysis may be impaired in patients with a limited acoustic window.</p>
        </sec>
        <sec>
          <title>19.2. Strain Acquisition Methods by Cardiac Magnetic Resonance Imaging</title>
          <p>Myocardial tagging, consisting of a preparation phase in which magnetic tags (black lines) are orthogonally superimposed on the myocardium at the beginning of a cine sequence, is the most validated technique for assessing strain in cardiac MRI.<sup><xref ref-type="bibr" rid="B12">12</xref>,<xref ref-type="bibr" rid="B418">418</xref></sup> Alternatives to tagging that provide direct analysis of myocardial strain in cardiac MRI are cine strain encoding and cine displacement encoding with stimulated echoes<italic>.</italic><sup><xref ref-type="bibr" rid="B419">419</xref></sup> Feature tracking (FT), a recently developed method, can quantify myocardial strain in traditional cine cardiac MRI images without additional acquisitions or lengthy analysis.<sup><xref ref-type="bibr" rid="B420">420</xref>,<xref ref-type="bibr" rid="B421">421</xref></sup></p>
          <p>In all strain analysis techniques, the global circumferential and LS parameters have proven more reproducible and consistent than regional ones.<sup><xref ref-type="bibr" rid="B422">422</xref></sup> Further details about strain acquisition through cardiac MRI can be found in the references.<sup><xref ref-type="bibr" rid="B12">12</xref>,<xref ref-type="bibr" rid="B418">418</xref>-<xref ref-type="bibr" rid="B422">422</xref></sup></p>
        </sec>
        <sec>
          <title>19.3. Determining Right Ventricle Strain Through Cardiac Magnetic Resonance Imaging</title>
          <p>Myocardial strain measurement is an accurate and practical method for assessing RV function, since it is an earlier and more sensitive marker of contractile dysfunction than other methods, such as EF. Studies have demonstrated the potential of RV cardiac MRI strain to provide additional information and independent prognosis.<sup><xref ref-type="bibr" rid="B423">423</xref>-<xref ref-type="bibr" rid="B428">428</xref></sup> A number of studies have analyzed RV strain in healthy individuals and control groups without heart disease.<sup><xref ref-type="bibr" rid="B423">423</xref>,<xref ref-type="bibr" rid="B426">426</xref>,<xref ref-type="bibr" rid="B429">429</xref>,<xref ref-type="bibr" rid="B430">430</xref></sup></p>
          <p>The pathologies that most affect RV, such as congenital heart disease, pulmonary hypertension, and arrhythmogenic dysplasia, have the greatest applicability in RV strain analysis. One study used cardiac MRI FT in patients with corrected tetralogy of Fallot, finding lower strain values in these patients than controls, which were related to systolic function parameters (biventricular EF), as well as functional capacity in cardiopulmonary testing.<sup><xref ref-type="bibr" rid="B425">425</xref></sup></p>
          <p>Assessing global and segmental RV function is fundamental for multi-parametric diagnosis of arrhythmogenic dysplasia, and RV strain has proven an extremely useful tool in this regard.<sup><xref ref-type="bibr" rid="B428">428</xref>,<xref ref-type="bibr" rid="B431">431</xref></sup> Global and segmental RV strain are significantly lower in patients with arrhythmogenic dysplasia, regardless of RV dimensions and function, and impaired RV strain may represent an early marker of the disease.<sup><xref ref-type="bibr" rid="B428">428</xref></sup><xref ref-type="fig" rid="f42001">Figure 19.1</xref> presents examples of RV strain in a normal patient and a patient with pulmonary hypertension.</p>
          <p>
            <fig id="f42001">
              <label>Figure 19.1</label>
              <caption>
                <title>&#8211; Global longitudinal strain analysis through feature tracking in patients with (above) and without pulmonary hypertension (below). GLS was 4.26% and 26.46% in the patients with and without pulmonary hypertension, respectively.</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-120-12-e20230646-30646-gf42-en.tif"/></fig>
          </p>
        </sec>
        <sec>
          <title>19.4. Determining Left Ventricular Strain Through Cardiac Magnetic Resonance Imaging</title>
          <p>In healthy individuals, mean values for LV strain types (global circumferential strain, global radial strain, and GLS) have been determined over the past decade with cardiac MRI FT,<sup><xref ref-type="bibr" rid="B419">419</xref>-<xref ref-type="bibr" rid="B423">423</xref></sup> including a major meta-analysis.<sup><xref ref-type="bibr" rid="B424">424</xref></sup> The largest and most recent studies on global circumferential strain and global radial strain by cardiac MRI FT analyzed the mean of 3 short-axis slices. In most cases, LVGLS was calculated using a 4-chamber slice, while more recent publications assessed the mean of 3 longitudinal slices. GLS and global circumferential strain values varied within a narrow range while global radial strain values had wider confidence intervals; it is speculated that planar movement and large personal variability could partially explain this phenomenon, although the real cause still remains uncertain.<sup><xref ref-type="bibr" rid="B424">424</xref></sup></p>
          <p>There is a strong relationship between myocardial strain and delayed myocardial enhancement, especially global circumferential strain, in addition to GLS derived from cardiac MRI FT. There is also good correlation between echocardiography-derived techniques and cardiac MRI.<sup><xref ref-type="bibr" rid="B425">425</xref></sup></p>
          <p>In dilated cardiomyopathy, markedly lower GLS is strongly associated with worse survival, even in patients with very low EF, regardless of functional class and other cardiac MRI findings.<sup><xref ref-type="bibr" rid="B426">426</xref></sup> Cardiac MRI FT can identify HFpEF and DD subgroups through altered GLS.<sup><xref ref-type="bibr" rid="B427">427</xref></sup></p>
          <p>The diagnostic value of cardiac MRI GLS and echocardiography GLS are similar when differentiating between constrictive pericarditis and restrictive cardiomyopathy, having a high discriminatory value. GLS values are significantly lower in restrictive cardiomyopathy, while they are close to normal in pericarditis.<sup><xref ref-type="bibr" rid="B428">428</xref></sup> Longitudinal and circumferential strain are also altered in myocarditis.<sup><xref ref-type="bibr" rid="B429">429</xref></sup></p>
          <p>Studies on MRI strain and myocardial tagging have found a high capacity to determine amyloidosis carriers; this method could even be more sensitive than the post-contrast sequence itself.<sup><xref ref-type="bibr" rid="B430">430</xref></sup> The lost base-apex gradient of circumferential strain seems to be an early finding of Fabry disease, since longitudinal and circumferential strain did not vary significantly from healthy controls.<sup><xref ref-type="bibr" rid="B431">431</xref></sup></p>
          <p>According to cardiac MRI FT, patients with HCM have lower GLS, global radial strain, and global circumferential strain than healthy controls, with GLS and global radial strain being predictors of adverse events,<sup><xref ref-type="bibr" rid="B432">432</xref></sup> just as significantly higher GLS has been found in hypertension patients than HCM patients.<sup><xref ref-type="bibr" rid="B433">433</xref></sup></p>
          <p>Ischemic coronary disease diagnosis by cardiac MRI can be improved by adding FT analysis, allowing detection of small changes in circumferential strain after dobutamine stress; GLS may be useful for detecting infarctions and assessing viability.<sup><xref ref-type="bibr" rid="B434">434</xref></sup> The 3 types of strain are reduced in patients who have suffered acute myocardial infarction with ST-segment elevation, being independent predictors of adverse cardiovascular events.<sup><xref ref-type="bibr" rid="B435">435</xref></sup></p>
          <p>Patients with severe aortic stenosis have lower GLS and global circumferential strain than healthy controls, despite the symptoms.<sup><xref ref-type="bibr" rid="B436">436</xref></sup> In patients with bicuspid aortic valve and preserved EF, signs of DD have been observed through circumferential strain changes.<sup><xref ref-type="bibr" rid="B437">437</xref></sup> Chemotherapy-induced cardiotoxicity results in GLS and global circumferential strain abnormalities long before LVEF is reduced.<sup><xref ref-type="bibr" rid="B438">438</xref></sup></p>
          <p>A recent study reported that cardiac MRI FT-derived GLS has a stronger association with mortality than a combination of LVEF and myocardial delayed enhancement. This has been the largest study to date to assess prognosis through cardiac MRI FT-derived GLS. After adjusting for classic risk factors, including LVEF and myocardial delayed enhancement, a 1% worsening in GLS was associated with an 89% higher mortality risk in both ischemic and non-ischemic patients.<sup><xref ref-type="bibr" rid="B439">439</xref></sup></p>
        </sec>
        <sec>
          <title>19.5. Determining Left Atrial Strain Through Cardiac Magnetic Resonance Imaging</title>
          <p>LA function assessment has been increasingly recognized as a factor in a variety of cardiac pathologies. Change in LA function is normally associated with worse prognosis and precedes HF diagnosis. The LA functions as a reservoir for pulmonary vein drainage, serving as a conduit for flow to the LV due to a pressure difference due to mitral leaflets opening and contractile function, with atrial systole occurring at the end of LV diastole.<sup><xref ref-type="bibr" rid="B440">440</xref></sup></p>
          <p>Cardiac MRI FT-derived atrial strain analysis reliably quantifies LA longitudinal strain and strain rate. Using standard cine MRI images, it can differentiate between patients with altered LV relaxation and healthy patients, as shown in <xref ref-type="table" rid="t27001">Table 19.1</xref>.<sup><xref ref-type="bibr" rid="B441">441</xref></sup> In a MESA substudy, global peak longitudinal atrial strain and LA volume indexes were independent predictors of HF onset, even after adjusting for LV mass and N-terminal pro&#8211;B-type natriuretic peptide.<sup><xref ref-type="bibr" rid="B442">442</xref></sup> LA phasic function has been found to be an independent risk predictor for mortality or hospitalization for HF, even after adjusting for LA volume and ventricular remodeling.<sup><xref ref-type="bibr" rid="B443">443</xref></sup></p>
          <p>
            <table-wrap id="t27001">
              <label>Table 19.1</label>
              <caption>
                <title>&#8211; Left Atrial Strain</title>
              </caption>
              <table frame="hsides" rules="groups">
                <colgroup width="25%">
                  <col/>
                  <col/>
                  <col/>
                  <col/>
                </colgroup>
                <thead>
                  <tr>
                    <th align="left">Type</th>
                    <th>HFpEF</th>
                    <th>HCM</th>
                    <th>Normal</th>
                  </tr>
                </thead>
                <tbody>
                  <tr>
                    <td>Reservoir</td>
                    <td align="center">16.3 &#177; 5.8</td>
                    <td align="center">22.1 &#177; 5.5</td>
                    <td align="center">29.1 &#177; 5.3</td>
                  </tr>
                  <tr>
                    <td>Conduit</td>
                    <td align="center">11.9 &#177; 4.0</td>
                    <td align="center">10.4 &#177; 3.9</td>
                    <td align="center">21.3 &#177; 5.1</td>
                  </tr>
                  <tr>
                    <td>Pump</td>
                    <td align="center">4.5 &#177; 2.9</td>
                    <td align="center">11.7 &#177; 4.0</td>
                    <td align="center">7.8 &#177; 2.5</td>
                  </tr>
                </tbody>
              </table>
              <table-wrap-foot>
                <fn id="TFN1001">
                  <p>HCM: Hypertrophic cardiomyopathy; HFpEF: Heart failure with preserved ejection fraction.</p>
                </fn>
              </table-wrap-foot>
            </table-wrap>
          </p>
        </sec>
        <sec>
          <title>19.6. Determining Strain Through Cardiac Tomography</title>
          <p>Strain can be assessed through cardiac tomography FT using contrast and triggered acquisitions, functionally reconstructing the cardiac cycle. Although data are still scarce, this method has been tested in patients with significant aortic stenosis undergoing transcutaneous aortic prosthesis implantation. Similar GLS values were found between cardiac tomography FT and echocardiography,<sup><xref ref-type="bibr" rid="B444">444</xref>,<xref ref-type="bibr" rid="B445">445</xref></sup> including high intraobserver and intraclass reproducibility for cardiac tomography FT LVGLS, despite apparently underestimating the values.<sup><xref ref-type="bibr" rid="B444">444</xref></sup></p>
          <p>Another study explored the relationship between cardiac tomography FT-derived strain and ischemic heart disease in patients with significant lesions in the left anterior descending artery. Lower LS was observed in segments related to the anterior descending artery, despite normal diastolic and systolic volumes and EF.<sup><xref ref-type="bibr" rid="B446">446</xref></sup></p>
          <p>Currently, strain assessment through cardiac MRI and cardiac tomography is limited due to availability issues and the high cost of post-processing software. However, like strain assessed through echocardiography, its application has been well established, facilitating early diagnosis of dysfunction in various cardiomyopathies.</p>
        </sec>
      </sec>
    </body>
    <back>
      <fn-group>
        <fn fn-type="other">
          <p><bold>Development:</bold> Department of Cardiovascular Imaging of Brazilian Society of Cardiology (Departamento de Imagem Cardiovascular da Sociedade Brasileira de Cardiologia &#8211; DIC/SBC)</p>
          <p><bold>Note:</bold> These statements are for information purposes and should not replace the clinical judgment of a physician, who must ultimately determine the appropriate treatment for each patient.</p>
        </fn>
      </fn-group>
    </back>
  </sub-article>
</article>
