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  <front>
    <journal-meta>
      <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-loc>S&#227;o Paulo, SP, Brazil</publisher-loc>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v3">FxGZDs8xp33tYMfGwT77tkQ</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2013000600006</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(13)10000600006</article-id>
      <article-id pub-id-type="doi">10.5935/abc.20130092</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Artigos Originais</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Avalia&#231;&#227;o n&#227;o invasiva das press&#245;es de enchimento e remodela&#231;&#227;o do ventr&#237;culo esquerdo ap&#243;s infarto do mioc&#225;rdio</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Barberato</surname>
            <given-names>Silvio Henrique</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Souza</surname>
            <given-names>Admar Moraes de</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Costantini</surname>
            <given-names>Costantino Ortiz</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Costantini</surname>
            <given-names>Costantino Roberto</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <addr-line>
          <named-content content-type="city">Curitiba</named-content>
          <named-content content-type="state"/>
        </addr-line>
        <institution content-type="orgname">Hospital Cardiol&#243;gico Costantini</institution>
        <country country="BR">Brazil</country>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>06</month>
        <year>2013</year>
      </pub-date>
      <volume>100</volume>
      <issue>6</issue>
      <fpage>531</fpage>
      <lpage>537</lpage>
      <history>
        <date date-type="received">
          <day>22</day>
          <month>10</month>
          <year>2012</year>
        </date>
        <date date-type="accepted">
          <day>05</day>
          <month>02</month>
          <year>2013</year>
        </date>
        <date date-type="rev-recd">
          <day>13</day>
          <month>01</month>
          <year>2013</year>
        </date>
      </history>
      <permissions>
        <license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/4.0/" xml:lang="en">
          <license-p>This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.</license-p>
        </license>
      </permissions>
      <abstract>
        <p>FUNDAMENTO: A dilata&#231;&#227;o do ventr&#237;culo esquerdo (VE) ap&#243;s infarto agudo do mioc&#225;rdio (IAM) &#233; um importante determinante do progn&#243;stico. A raz&#227;o entre a velocidade diast&#243;lica E do fluxo mitral e a velocidade diast&#243;lica e' do anel mitral (rela&#231;&#227;o E/e') &#233; o melhor &#237;ndice n&#227;o invasivo para detectar eleva&#231;&#227;o aguda da press&#227;o de enchimento do VE. A hip&#243;tese deste estudo &#233; que a E/e' possa predizer remodela&#231;&#227;o do VE ap&#243;s IAM tratado. OBJETIVO: Avaliar se a E/e' prediz remodela&#231;&#227;o ventricular ap&#243;s IAM, em compara&#231;&#227;o aos dados cl&#237;nicos, laboratoriais e ecocardiogr&#225;ficos tradicionais. M&#201;TODO: Ecocardiogramas foram realizados em pacientes consecutivos com primeiro IAM, ap&#243;s angioplastia transluminal coronariana (ATC) seguida de recanaliza&#231;&#227;o efetiva, 48 horas e 60 dias ap&#243;s o evento. A E/e' foi calculada pela m&#233;dia de quatro s&#237;tios do anel mitral. Remodela&#231;&#227;o do VE foi definida como aumento &#8805; 15% do volume sist&#243;lico final ao m&#233;todo de Simpson. An&#225;lises estat&#237;sticas inclu&#237;ram teste t de Student, curvas receptor-operador (ROC) e regress&#227;o log&#237;stica multivariada, com p significante &lt; 0,05. RESULTADOS: Estudados 55 pacientes, com idade 58 &#177; 11 anos, 43 homens, observou-se E/e' maior (13 &#177; 4 versus 8,5 &#177; 2; p &lt; 0,001) no grupo com remodela&#231;&#227;o (n = 13) em rela&#231;&#227;o ao grupo sem remodela&#231;&#227;o (n = 42). A curva ROC indicou E/e' como preditor de remodela&#231;&#227;o (&#225;rea sob a curva = 0,81, p = 0,001). An&#225;lises de regress&#227;o contendo vari&#225;veis cl&#237;nicas, laboratoriais e Doppler-ecocardiogr&#225;ficas confirmaram E/e' como preditor independente da remodela&#231;&#227;o (odds ratio 1,42; p = 0,01). CONCLUS&#195;O: A rela&#231;&#227;o E/e' &#233; um preditor &#250;til de remodela&#231;&#227;o do VE ap&#243;s IAM, indicando pacientes com maior risco cardiovascular.</p>
      </abstract>
      <kwd-group xml:lang="pt" kwd-group-type="author-generated">
        <kwd>Remodela&#231;&#227;o Ventricular</kwd>
        <kwd>Infarto do Mioc&#225;rdio</kwd>
        <kwd>Ecocardiografia</kwd>
        <kwd>Volume Sist&#243;lico</kwd>
      </kwd-group>
      <pub-date publication-format="electronic" date-type="pub">
        <day>07</day>
        <month>05</month>
        <year>2013</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <p>
      <bold>Avalia&#231;&#227;o n&#227;o invasiva das press&#245;es de enchimento e remodela&#231;&#227;o do ventr&#237;culo esquerdo ap&#243;s infarto do mioc&#225;rdio</bold>
    </p>
    <p>
      <bold>Silvio Henrique Barberato; Admar Moraes de Souza; Costantino Ortiz Costantini; Costantino Roberto Costantini</bold>
    </p>
    <p>Hospital Cardiol&#243;gico Costantini, Curitiba, PR - Brasil</p>
    <p>
      <xref ref-type="corresp" rid="corresp">Correspond&#234;ncia</xref>
    </p>
    <p>
      <bold>RESUMO</bold>
    </p>
    <p><bold>FUNDAMENTO:</bold> A dilata&#231;&#227;o do ventr&#237;culo esquerdo (VE) ap&#243;s infarto agudo do mioc&#225;rdio (IAM) &#233; um importante determinante do progn&#243;stico. A raz&#227;o entre a velocidade diast&#243;lica E do fluxo mitral e a velocidade diast&#243;lica e' do anel mitral (rela&#231;&#227;o E/e') &#233; o melhor &#237;ndice n&#227;o invasivo para detectar eleva&#231;&#227;o aguda da press&#227;o de enchimento do VE. A hip&#243;tese deste estudo &#233; que a E/e' possa predizer remodela&#231;&#227;o do VE ap&#243;s IAM tratado. </p>
    <p><bold>OBJETIVO:</bold> Avaliar se a E/e' prediz remodela&#231;&#227;o ventricular ap&#243;s IAM, em compara&#231;&#227;o aos dados cl&#237;nicos, laboratoriais e ecocardiogr&#225;ficos tradicionais. </p>
    <p><bold>M&#201;TODO:</bold> Ecocardiogramas foram realizados em pacientes consecutivos com primeiro IAM, ap&#243;s angioplastia transluminal coronariana (ATC) seguida de recanaliza&#231;&#227;o efetiva, 48 horas e 60 dias ap&#243;s o evento. A E/e' foi calculada pela m&#233;dia de quatro s&#237;tios do anel mitral. Remodela&#231;&#227;o do VE foi definida como aumento &#8805; 15% do volume sist&#243;lico final ao m&#233;todo de Simpson. An&#225;lises estat&#237;sticas inclu&#237;ram teste t de Student, curvas receptor-operador (ROC) e regress&#227;o log&#237;stica multivariada, com p significante &lt; 0,05. </p>
    <p><bold>RESULTADOS:</bold> Estudados 55 pacientes, com idade 58 &#177; 11 anos, 43 homens, observou-se E/e' maior (13 &#177; 4 versus 8,5 &#177; 2; p &lt; 0,001) no grupo com remodela&#231;&#227;o (n = 13) em rela&#231;&#227;o ao grupo sem remodela&#231;&#227;o (n = 42). A curva ROC indicou E/e' como preditor de remodela&#231;&#227;o (&#225;rea sob a curva = 0,81, p = 0,001). An&#225;lises de regress&#227;o contendo vari&#225;veis cl&#237;nicas, laboratoriais e Doppler-ecocardiogr&#225;ficas confirmaram E/e' como preditor independente da remodela&#231;&#227;o (odds ratio 1,42; p = 0,01). </p>
    <p><bold>CONCLUS&#195;O:</bold> A rela&#231;&#227;o E/e' &#233; um preditor &#250;til de remodela&#231;&#227;o do VE ap&#243;s IAM, indicando pacientes com maior risco cardiovascular. </p>
    <p><bold>Palavras-chave:</bold> Remodela&#231;&#227;o Ventricular, Infarto do Mioc&#225;rdio, Ecocardiografia / utiliza&#231;&#227;o, Volume Sist&#243;lico / fisiopatologia.</p>
    <p>
      <bold>Introdu&#231;&#227;o</bold>
    </p>
    <p>A dilata&#231;&#227;o do ventr&#237;culo esquerdo (VE), ap&#243;s infarto agudo do mioc&#225;rdio (IAM), pode ocorrer mesmo com angioplastia transluminal coronariana (ATC) de bom resultado. Estudos pr&#233;vios observaram expressiva dilata&#231;&#227;o do VE em aproximadamente um ter&#231;o dos pacientes, a despeito da pat&#234;ncia da art&#233;ria relacionada ao IAM<sup>1,2</sup>. O aumento da cavidade ventricular esquerda em resposta a agress&#227;o frequentemente vem acompanhada de altera&#231;&#245;es da geometria e queda do desempenho global da c&#226;mara, o que se convencionou chamar de remodela&#231;&#227;o (ou <italic>remodelamento</italic>). Tal dilata&#231;&#227;o do VE, ap&#243;s IAM, &#233; um importante determinante do progn&#243;stico, aumentando o risco de insufici&#234;ncia card&#237;aca e morte s&#250;bita<sup>3</sup>. Diversos &#237;ndices derivados do ecodopplercardiograma t&#234;m sido usados para predizer desfechos em pacientes ap&#243;s IAM. A presen&#231;a de fluxo mitral restritivo, caracterizado pelo encurtamento do tempo de desacelera&#231;&#227;o (TD) da onda E do fluxo mitral secund&#225;rio &#224; eleva&#231;&#227;o da press&#227;o diast&#243;lica final, associou-se com maior risco de dilata&#231;&#227;o do VE ap&#243;s IAM<sup>4,5</sup>. Press&#245;es de enchimento elevadas, como sugerido por TD &lt; 130-140 ms, usualmente indicam infartos de maior tamanho, com disfun&#231;&#227;o sist&#243;lica mais acentuada e especial predisposi&#231;&#227;o &#224; remodela&#231;&#227;o<sup>6</sup>.</p>
    <p>No entanto, as velocidades do fluxo mitral e o TD s&#227;o de valor limitado em indiv&#237;duos com fun&#231;&#227;o sist&#243;lica preservada do VE<sup>7</sup>. Felizmente, a desej&#225;vel reperfus&#227;o precoce obtida pelos avan&#231;os recentes nas t&#233;cnicas de ATC tem resultado em melhores desfechos cl&#237;nicos e superior recupera&#231;&#227;o da fun&#231;&#227;o ventricular esquerda<sup>8</sup>. Por outro lado, a raz&#227;o entre a velocidade diast&#243;lica precoce do fluxo mitral ao Doppler puls&#225;til convencional (E) e a velocidade diast&#243;lica precoce do anel mitral ao Doppler tecidual (e'), conhecida como rela&#231;&#227;o E/e', teve forte correla&#231;&#227;o com a press&#227;o de enchimento do VE invasivamente determinada<sup>7</sup>, mesmo em indiv&#237;duos com fra&#231;&#227;o de eje&#231;&#227;o (FE) preservada.</p>
    <p>A hip&#243;tese deste estudo foi que a rela&#231;&#227;o E/e' aumentada (marcador n&#227;o invasivo da eleva&#231;&#227;o das press&#245;es de enchimento do VE) est&#225; associada com maior ocorr&#234;ncia de dilata&#231;&#227;o do VE em pacientes com reperfus&#227;o de sucesso ap&#243;s IAM. Portanto, o objetivo deste estudo foi definir se a rela&#231;&#227;o E/e' prediz remodela&#231;&#227;o do VE infartado e adiciona informa&#231;&#227;o &#224; abordagem cl&#237;nica, laboratorial e ecocardiogr&#225;fica tradicional.</p>
    <p>
      <bold>M&#233;todos</bold>
    </p>
    <p>
      <bold>Popula&#231;&#227;o</bold>
    </p>
    <p>Pacientes consecutivos, admitidos na unidade coronariana de nossa institui&#231;&#227;o, com diagn&#243;stico de primeiro IAM, foram avaliados para ingresso no estudo. O diagn&#243;stico do IAM foi definido pelas recomenda&#231;&#245;es da European American College of Cardiology/American Heart Association<sup>9</sup>. Os crit&#233;rios de inclus&#227;o foram: 1) cinecoronariografia ap&#243;s ATC mostrando art&#233;ria relacionada ao IAM patente, com fluxo TIMI grau III<sup>10</sup>; 2) ecocardiograma demonstrando acinesia em parede relacionada ao territ&#243;rio arterial comprometido. Os crit&#233;rios de exclus&#227;o foram: 1) necessidade de suporte hemodin&#226;mico com bal&#227;o intra-a&#243;rtico; 2) arritmia sustentada, impossibilitando aferi&#231;&#227;o dos &#237;ndices ecodopplercardiogr&#225;ficos; 3) janela ac&#250;stica tor&#225;cica inadequada; 4) n&#227;o concord&#226;ncia em participar do estudo.</p>
    <p>O estudo foi aprovado pelo comit&#234; de &#233;tica e os pacientes foram inclu&#237;dos ap&#243;s assinatura do termo de consentimento livre e esclarecido.</p>
    <p>
      <bold>Ecocardiografia</bold>
    </p>
    <p>Completa avalia&#231;&#227;o ecocardiogr&#225;fica foi realizada em s&#233;rie consecutiva de pacientes com primeiro IAM em dois momentos: 48 horas ap&#243;s ATC com recanaliza&#231;&#227;o de &#234;xito do vaso culpado e, aproximadamente, 60 dias ap&#243;s o IAM. Em nossa institui&#231;&#227;o, todos os pacientes s&#227;o diretamente tratados com ATC prim&#225;ria e n&#227;o tromb&#243;lise. Portanto, o valor de E/e' para o desfecho pesquisado foi testado nessas circunst&#226;ncias para todos os indiv&#237;duos do estudo. Os ecocardiogramas foram realizados pelo mesmo examinador utilizando ecocardi&#243;grafo Ie33 Philips (Philips Medical Systems, EUA) equipado com transdutor de 2,5-4 MHz. Os cortes usuais foram realizados para permitir completo estudo pelas t&#233;cnicas de modo M, bidimensional e Doppler (puls&#225;til, cont&#237;nuo, <italic>color</italic> e tecidual).</p>
    <p>Em concord&#226;ncia com as recomenda&#231;&#245;es da American Society of Echocardiography (ASE)<sup>11</sup>, os seguintes par&#226;metros foram determinados: espessura do septo interventricular e da parede inferolateral do VE na di&#225;stole, dimens&#245;es sist&#243;lica e diast&#243;lica do VE. O escore de motilidade parietal (EMP) foi calculado levando em conta o modelo-padr&#227;o de 16 segmentos e graduado em escala de quatro pontos: 1 = normal, 2 = hipocin&#233;tico, 3 = acin&#233;tico, 4 = discin&#233;tico. A massa do VE foi calculada por meio da f&#243;rmula da ASE e indexada pela superf&#237;cie corp&#243;rea (m&#233;todo de DuBois e DuBois). Os volumes e a FE foram calculados pelo m&#233;todo biplanar de Simpson. Remodela&#231;&#227;o do VE foi definida, prospectivamente, como aumento <sup>&gt;</sup> 15% no volume sist&#243;lico final<sup>12</sup>.</p>
    <p>As velocidades do fluxo mitral foram medidas pelo Doppler puls&#225;til no corte apical de quatro c&#226;maras, com a amostra de volume posicionada entre as pontas das c&#250;spides da valva mitral, e o paciente instru&#237;do a segurar a respira&#231;&#227;o, quando poss&#237;vel. Foram determinadas as velocidades diast&#243;licas precoce (E) e de contra&#231;&#227;o atrial (A), bem como a rela&#231;&#227;o E/A e o TD. As velocidades anulares diast&#243;licas precoce (e') e atrial (a') foram registradas pelo Doppler tecidual nos cortes apicais de quatro e duas c&#226;maras, com amostra de volume de 1-2 mm colocada na jun&#231;&#227;o da parede do VE com quatro s&#237;tios do anel mitral (septal, lateral, anterior e inferior). A m&#233;dia das velocidades nos quatro s&#237;tios representou as ondas e' e a' utilizadas para an&#225;lise no estudo, assim como a rela&#231;&#227;o E/e'. Todas as medidas representaram a m&#233;dia de tr&#234;s ciclos card&#237;acos.</p>
    <p>A fun&#231;&#227;o diast&#243;lica do VE foi graduada de acordo com a interpreta&#231;&#227;o combinada dos &#237;ndices derivados do Doppler puls&#225;til convencional do fluxo mitral e do Doppler tecidual. Relaxamento anormal foi diagnosticado com a presen&#231;a de rela&#231;&#227;o E/A &lt; 0,9 e e' &lt; 10 cm/s; o fluxo restritivo foi determinado com rela&#231;&#227;o E/A &gt; 2, TD &lt; 140 ms e e' &lt; 8 cm/s<sup>13</sup>. Na diferencia&#231;&#227;o entre padr&#227;o normal e pseudonormal, a presen&#231;a de e' &lt; 8 cm/s e E/e' <sup>&gt;</sup> 15 foi usada<sup>13</sup>. O volume de &#225;trio esquerdo indexado (VAEI) foi aferido por meio da t&#233;cnica de Simpson biplanar seguida da indexa&#231;&#227;o pela superf&#237;cie corp&#243;rea.</p>
    <p>
      <bold>Dados cl&#237;nicos basais e seguimento</bold>
    </p>
    <p>Dados cl&#237;nicos e demogr&#225;ficos foram obtidos por detalhada revis&#227;o de prontu&#225;rio. Foi feito o registro de idade, g&#234;nero, peso, altura, &#237;ndice de massa corp&#243;rea (IMC), hist&#243;ria pregressa de diabetes, hipertens&#227;o arterial, dislipidemia, tabagismo, drogas em uso e ATC pr&#233;via. O tempo transcorrido do in&#237;cio dos sintomas at&#233; a recanaliza&#231;&#227;o do vaso culpado, o local (parede do VE comprometida), a classifica&#231;&#227;o de Killip, press&#227;o arterial no momento da admiss&#227;o e picos enzim&#225;ticos de isoenzima MB creatina quinase (CK-MB) e troponina foram tamb&#233;m anotados. Durante e ap&#243;s a realiza&#231;&#227;o da ATC, todos os pacientes foram tratados com as doses recomendadas de aspirina, clopidogrel, heparina n&#227;o fracionada e abxicimabe<sup>9</sup>. O tratamento medicamentoso ap&#243;s o evento foi conduzido pelo m&#233;dico do paciente, recomendando-se a administra&#231;&#227;o de inibidores da enzima conversora (ou bloqueadores do receptor da angiotensina II), betabloqueadores e diur&#233;ticos, de acordo com as diretrizes vigentes<sup>9</sup>. O desfecho prim&#225;rio foi a remodela&#231;&#227;o do VE ap&#243;s 60 dias do IAM.</p>
    <p>
      <bold>An&#225;lise estat&#237;stica</bold>
    </p>
    <p>O c&#225;lculo estimado da amostra foi de 51 pacientes, considerando incid&#234;ncia de remodela&#231;&#227;o de aproximadamente 30%<sup>1</sup>, poder estat&#237;stico (<italic>power</italic>) de 90% e n&#237;vel de signific&#226;ncia de 5%. Os dados s&#227;o apresentados em m&#233;dia com desvio-padr&#227;o (vari&#225;veis cont&#237;nuas) e porcentuais (vari&#225;veis categ&#243;ricas). As diferen&#231;as entre os grupos com e sem remodela&#231;&#227;o foram determinadas por meio dos testes <italic>t</italic> de Student pareado (vari&#225;veis cont&#237;nuas com distribui&#231;&#227;o normal), Mann-Whitney (cont&#237;nuas com distribui&#231;&#227;o n&#227;o normal) e qui-quadrado (categ&#243;ricas).</p>
    <p>As correla&#231;&#245;es entre os &#237;ndices ecodopplercardiogr&#225;ficos e as mudan&#231;as no volume sist&#243;lico final foram analisadas pelo coeficiente de Pearson. Curva receptor-operador (ROC) foi constru&#237;da para determinar E/e' como preditor de remodela&#231;&#227;o, bem como sensibilidade e especificidade. Por fim, an&#225;lise de regress&#227;o log&#237;stica multivariada foi empregada para identificar o valor independente de E/e' em rela&#231;&#227;o a diversas vari&#225;veis tradicionais. Signific&#226;ncia estat&#237;stica foi definida como valor de p &lt; 0,05. As an&#225;lises foram processadas usando o programa de estat&#237;stica <italic>SPSS 13.0 for Windows</italic> (SPSS INC, Chicago, Illinois).</p>
    <p>
      <bold>Resultados</bold>
    </p>
    <p>Foram inclu&#237;dos 55 pacientes, com idade 58 &#177; 11 anos, 43 homens, detectando-se remodela&#231;&#227;o (grupo I) em 13 indiv&#237;duos (24%), os quais foram comparados com o grupo sem remodela&#231;&#227;o (grupo II), composto por 42 indiv&#237;duos.</p>
    <p>As caracter&#237;sticas cl&#237;nicas, demogr&#225;ficas e laboratoriais da popula&#231;&#227;o do estudo (e seus subgrupos) est&#227;o dispostas na <xref ref-type="table" rid="aop_5219tab01">Tabela 1</xref>. O grupo I teve maior percentual de hist&#243;ria pr&#233;via de hipertens&#227;o arterial sist&#234;mica (60% <italic>versus</italic> 38%, p = 0,02) e maior pico de troponina (20 &#177; 12 <italic>versus</italic> 7 &#177; 8 ng/ml, p = 0,005) em compara&#231;&#227;o ao grupo II. Houve tamb&#233;m tend&#234;ncia a maiores picos de CK-MB (p = 0,06) e tempo entre sintoma e recanaliza&#231;&#227;o do vaso (p = 0,08) no grupo I. N&#227;o houve diferen&#231;as estatisticamente significativas entre os grupos em rela&#231;&#227;o a idade, g&#234;nero, IMC, diabetes, dislipidemia, tabagismo, uso pr&#233;vio de inibidores da enzima conversora/bloqueadores do receptor da angiotensina II, ATC pr&#233;via, infarto localizado em parede anterior, Killip II na admiss&#227;o, press&#227;o arterial na admiss&#227;o e n&#237;veis s&#233;ricos de hemoglobina, glicose e creatinina (todos com p &gt; 0,05).</p>
    <p content-type="asset">
      <table-wrap id="aop_5219tab01">
        <graphic xlink:href="1678-4170-abc-100-06-0531-30092-gt01.jpg"/></table-wrap>
    </p>
    <p>A <xref ref-type="table" rid="aop_5219tab02">Tabela 2</xref> mostra as principais caracter&#237;sticas Doppler-ecocardiogr&#225;ficas da amostra estudada. O grupo I teve maior dimens&#227;o sist&#243;lica do VE (p = 0,02), menor FE (p = 0,01), maior EMP (p &lt; 0,001), menores e' (p = 0,02) e a' (p 0,03), e maior rela&#231;&#227;o E/e' (p &lt; 0,001). N&#227;o foram encontradas diferen&#231;as de dimens&#227;o diast&#243;lica de VE, IMVE, rela&#231;&#227;o E/A, TD e VAEI (todos p &gt; 0,05) entre os grupos.</p>
    <p content-type="asset">
      <table-wrap id="aop_5219tab02">
        <graphic xlink:href="1678-4170-abc-100-06-0531-30092-gt02.jpg"/></table-wrap>
    </p>
    <p>Houve correla&#231;&#227;o entre a varia&#231;&#227;o do volume sist&#243;lico final ap&#243;s 60 dias (r = 0,26, p = 0,03) e E/e', mas n&#227;o com as demais vari&#225;veis. A curva ROC (<xref ref-type="fig" rid="aop_5219fig01">Figura 1</xref>) indicou E/e' como preditor de remodela&#231;&#227;o (&#225;rea sob a curva = 0,81, 95% de intervalo de confian&#231;a 0,68-0,94, p = 0,001). O valor de corte para E/e' &gt; 15 demonstrou sensibilidade de 70% e especificidade de 98% para aumento &gt; 15% do volume sist&#243;lico final do VE.</p>
    <p content-type="asset">
      <fig id="aop_5219fig01">
        <graphic xlink:href="1678-4170-abc-100-06-0531-30092-gf01.jpg"/></fig>
    </p>
    <p>An&#225;lises de regress&#227;o multivariada contendo vari&#225;veis cl&#237;nicas (hist&#243;ria de hipertens&#227;o arterial, tempo dos sintomas), laboratoriais (troponina e CK-MB) e Doppler-ecocardiogr&#225;ficas (dimens&#227;o sist&#243;lica de VE, FE, EMP, a', E/e' e local do IAM) confirmaram E/e' como &#250;nico preditor independente de remodela&#231;&#227;o (<italic>odds ratio</italic> 1,42, 95% de intervalo de confian&#231;a 1,1-1,9, p = 0,01), acima e al&#233;m dos demais par&#226;metros. An&#225;lises especulativas, for&#231;ando no modelo a entrada de outras vari&#225;veis tradicionalmente utilizadas, como idade, g&#234;nero, TD e localiza&#231;&#227;o do IAM em parede anterior, n&#227;o modificaram o valor preditivo independente da rela&#231;&#227;o E/e'. </p>
    <p>
      <bold>Discuss&#227;o</bold>
    </p>
    <p>O principal achado deste estudo foi que a rela&#231;&#227;o E/e' parece ser um preditor independente da remodela&#231;&#227;o ventricular esquerda, ap&#243;s IAM tratado com reperfus&#227;o de sucesso por ATC. Em especial, a evid&#234;ncia ecocardiogr&#225;fica de eleva&#231;&#227;o de press&#245;es de enchimento do VE, proporcionada por E/e &gt; 15, associou-se fortemente com dilata&#231;&#227;o do VE, com valor superior aos par&#226;metros cl&#237;nicos, laboratoriais e ecocardiogr&#225;ficos previamente estabelecidos. Consider&#225;vel volume de evid&#234;ncias demonstrou que a presen&#231;a do fluxo mitral restritivo (TD encurtado) &#233; forte preditor progn&#243;stico, ap&#243;s IAM, uma vez que se associa em geral com maior &#225;rea de acinesia de parede do VE e press&#227;o diast&#243;lica final aumentada<sup>4-6</sup>. Entretanto, o TD tem reconhecidas limita&#231;&#245;es em indiv&#237;duos com fun&#231;&#227;o sist&#243;lica preservada<sup>7</sup>, situa&#231;&#227;o cada vez mais frequente ap&#243;s os avan&#231;os obtidos com a pronta interven&#231;&#227;o percut&#226;nea na terapia do IAM. Em paralelo, demonstrou-se que a rela&#231;&#227;o E/e' foi o melhor indicador da presen&#231;a de press&#227;o diast&#243;lica final elevada na compara&#231;&#227;o entre m&#250;ltiplos par&#226;metros ecocardiogr&#225;ficos e a press&#227;o medida por cateter de hemodin&#226;mica<sup>7,14</sup>. </p>
    <p>O presente estudo indica que a rela&#231;&#227;o E/e' pode ser superior ao TD para prever remodela&#231;&#227;o quando avaliamos uma popula&#231;&#227;o de pacientes com FE relativamente preservada (amostra geral com porcentual de FE m&#233;dia 55 &#177; 12). Outro achado intrigante foi que a rela&#231;&#227;o E/e', representativa dos efeitos agudos da eleva&#231;&#227;o das press&#245;es de enchimento do VE, teve melhor desempenho para prever remodela&#231;&#227;o p&#243;s-IAM do que o VAEI, &#237;ndice tradicionalmente associado &#224; eleva&#231;&#227;o cr&#244;nica de press&#245;es de enchimento. Embora o VAEI seja um preditor inequ&#237;voco de mortalidade ap&#243;s IAM<sup>15</sup>, seu impacto na remodela&#231;&#227;o n&#227;o foi evidenciado em nosso estudo. </p>
    <p>&#201; poss&#237;vel que pacientes com aumento cr&#244;nico do VAEI j&#225; tenham sofrido anteriormente ao IAM algum grau de remodela&#231;&#227;o ventricular esquerda, atenuando os efeitos gerados pela les&#227;o isqu&#234;mica mais recente. Portanto, o impacto do VAEI aumentado na remodela&#231;&#227;o do VE n&#227;o seria aparente para uma coorte relativamente pequena e com curto tempo de seguimento como a nossa. Alternativamente, pode-se especular que a rela&#231;&#227;o entre a remodela&#231;&#227;o do VE e o aumento agudo das press&#245;es de enchimento seja mais importante do que entre a remodela&#231;&#227;o e o aumento cr&#244;nico. No contexto de isquemia mioc&#225;rdica e infarto, o Doppler tecidual (do qual deriva a velocidade e' e, em &#250;ltima inst&#226;ncia, a rela&#231;&#227;o E/e') mostra baixas velocidades sist&#243;licas e diast&#243;licas no anel mitral<sup>16</sup>. Essas velocidades decrescem com a hipoperfus&#227;o regional, recuperam com a reperfus&#227;o e diferenciam entre infarto transmural e n&#227;o transmural<sup>17</sup>. Ap&#243;s o IAM, os efeitos agudos de isquemia e necrose provocam perda da integridade dos mi&#243;citos e desarranjo da geometria do VE, levando a queda do desempenho global e aumento na press&#227;o diast&#243;lica final do VE. A dilata&#231;&#227;o/remodela&#231;&#227;o do VE emerge desse processo como mecanismo compensat&#243;rio para tentar restaurar a press&#227;o de enchimento para o n&#237;vel normal (ou pr&#243;ximo do normal). Isso poderia explicar por que um marcador substituto da medida <italic>aguda</italic> da press&#227;o de enchimento do VE funciona melhor na predi&#231;&#227;o da remodela&#231;&#227;o.</p>
    <p>Al&#233;m de estimar a fun&#231;&#227;o card&#237;aca e as press&#245;es de enchimento, alguns autores t&#234;m investigado o valor progn&#243;stico da rela&#231;&#227;o E/e' no IAM. Em 250 pacientes acompanhados por per&#237;odo mediano de 13 meses ap&#243;s IAM, Hillis e cols.<sup>18</sup> mostraram que E/e' &gt; 15 foi um forte indicador de menor sobrevida, com valor incremental aos par&#226;metros cl&#237;nicos e &#237;ndices ecocardiogr&#225;ficos tradicionais de fun&#231;&#227;o sist&#243;lica e diast&#243;lica. Certamente a remodela&#231;&#227;o ventricular esquerda exerce importante papel na fisiopatologia dos fen&#244;menos envolvidos na diminui&#231;&#227;o da sobrevida nesse grupo. Esses estudiosos publicaram um estudo na mesma linha investigativa que o nosso, mostrando que E/e' &gt; 15 identificava indiv&#237;duos com maior risco de desenvolver dilata&#231;&#227;o do VE ap&#243;s IAM<sup>19</sup>.</p>
    <p>Entretanto, h&#225; diversas diferen&#231;as metodol&#243;gicas entre tal relato e o presente estudo que devem ser salientadas. Em primeiro lugar, a popula&#231;&#227;o estudada por Hillis e cols.<sup>18</sup> foi composta de 47 indiv&#237;duos, sendo apenas 22 pacientes (47%) tratados com ATC prim&#225;ria e 25 (53%) tratados com tromb&#243;lise<sup>19</sup>. Em contraste, todos os pacientes do nosso grupo passaram por interven&#231;&#227;o percut&#226;nea, reconhecidamente capaz de proporcionar melhor evolu&#231;&#227;o<sup>8</sup>. Al&#233;m disso, os crit&#233;rios para definir remodela&#231;&#227;o do VE foram d&#237;spares: aumento <sup>&gt;</sup> 15% no volume sist&#243;lico final do VE em nosso estudo, em contraste com aumento <sup>&gt;</sup> 15% no volume diast&#243;lico final no artigo supracitado. N&#227;o h&#225; consenso na literatura se a varia&#231;&#227;o do volume sist&#243;lico ou diast&#243;lico final do VE deva ser usada no diagn&#243;stico da remodela&#231;&#227;o, e outros autores tamb&#233;m t&#234;m utilizado nossa op&#231;&#227;o como refer&#234;ncia<sup>12</sup>. A op&#231;&#227;o pelo emprego da varia&#231;&#227;o no volume sist&#243;lico final deveu-se &#224; evid&#234;ncia pr&#233;via de que tal par&#226;metro &#233; superior ao volume diast&#243;lico final e &#224; pr&#243;pria fra&#231;&#227;o de eje&#231;&#227;o como preditor prim&#225;rio do progn&#243;stico ap&#243;s IAM<sup>12</sup>. Finalmente, &#233; importante sublinhar que, no estudo de Hillis e cols.<sup>18</sup>, a rela&#231;&#227;o E/e' foi obtida a partir da medida da velocidade e' realizada, exclusivamente, no lado septal do anel mitral, enquanto em nossa investiga&#231;&#227;o empregamos a m&#233;dia de quatro lados do anel mitral (septal, lateral, anterior e inferior). Tal conduta &#233; fundamental para diminuir discrep&#226;ncias na vig&#234;ncia de disfun&#231;&#227;o mioc&#225;rdica regional<sup>13</sup>.</p>
    <p>Nossa abordagem tem algumas limita&#231;&#245;es. Sabe-se que as velocidades do Doppler tecidual s&#227;o afetadas pela transla&#231;&#227;o, tra&#231;&#227;o e <italic>arrastamento</italic> (<italic>tethering</italic>) dos segmentos mioc&#225;rdicos adjacentes<sup>20</sup>, portanto bastante dependentes do &#226;ngulo. Novos m&#233;todos de imagem, como o <italic>speckle-tracking</italic> ecocardiogr&#225;fico<sup>21</sup> e a resson&#226;ncia nuclear magn&#233;tica<sup>22</sup>, sem essa limita&#231;&#227;o, t&#234;m demonstrado extraordin&#225;rio valor na predi&#231;&#227;o da remodela&#231;&#227;o ap&#243;s IAM. Entretanto, sua aplicabilidade cl&#237;nica ainda &#233; bastante restrita por v&#225;rias raz&#245;es, entre elas a disponibilidade, o que torna a rela&#231;&#227;o E/e' a melhor escolha em termos de custo-benef&#237;cio no momento. Outra limita&#231;&#227;o relativa foi o fato de todos os exames terem sido realizados por um s&#243; examinador, impossibilitando a aferi&#231;&#227;o da variabilidade interobservador.</p>
    <p>Assim, a rela&#231;&#227;o E/e', marcador n&#227;o invasivo da eleva&#231;&#227;o das press&#245;es de enchimento do VE, pode ser um preditor &#250;til no cen&#225;rio da dilata&#231;&#227;o/remodela&#231;&#227;o ventricular ap&#243;s IAM, indicando pacientes com maior risco cardiovascular e possibilitando interven&#231;&#227;o precoce.</p>
    <p>
      <bold>Potencial Conflito de Interesses</bold>
    </p>
    <p>Declaro n&#227;o haver conflito de interesses pertinentes.</p>
    <p>
      <bold>Fontes de Financiamento</bold>
    </p>
    <p>O presente estudo n&#227;o teve fontes de financiamento externas.</p>
    <p>
      <bold>Vincula&#231;&#227;o Acad&#234;mica</bold>
    </p>
    <p>N&#227;o h&#225; vincula&#231;&#227;o deste estudo a programas de p&#243;s-gradua&#231;&#227;o.</p>
    <p>
      <fn id="corresp" fn-type="corresp">
        <label>
          <bold>Correspond&#234;ncia:</bold>
        </label>
        <p> Silvio Henrique Barberato </p>
        <p> Rua Rezala Sim&#227;o, 1316, casa 28, Santa Quit&#233;ria </p>
        <p> CEP 80330-180, Curitiba, PR- Brasil </p>
        <p> E-mail: </p>
        <p><email xlink:href="silviohb@cardiol.br">silviohb@cardiol.br</email>; </p>
        <p>
          <email xlink:href="msbarberato@terra.com.br">msbarberato@terra.com.br</email>
        </p>
      </fn>
    </p>
    <p>Artigo recebido em 22/10/12; revisado em 13/01/13; aceito em 05/02/13.</p>
  </body>
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  <sub-article article-type="translation" id="TRen" xml:lang="en">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Original Articles</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="en">Non invasive assessment of left ventricular filling pressure and remodeling after acute myocardial infarction</article-title>
      </title-group>
      <abstract xml:lang="en">
        <p>BACKGROUND: Left ventricular (LV) dilation after acute myocardial infarction (AMI) is an important determinant of prognosis. The ratio of early mitral inflow velocity (E) and peak early diastolic annular velocity (e') provides the best single index for noninvasive detection of acute elevation of LV filling pressure. OBJECTIVE: To assess whether E/e' ratio predicts LV remodeling after properly treated AMI compared with traditional clinical, laboratory and echocardiographic data. METHODS: Comprehensive echocardiograms were performed in a series of consecutive patients with first AMI successfully treated with primary percutaneous transluminal angioplasty (PTCA), both 48 hours after intervention and 60 days later. Mean E/e' was determined from four sites of the mitral annulus. LV remodeling was defined as more than 15% increase in end-systolic volume estimated by Simpson method. Statistical analysis included Student's t test, receiver-operator curves (ROC) and multivariate logistic regression (all significant with p &lt; 0.05). RESULTS: Fifty-five patients were included, with mean age 58 &#177; 11 years, 43 men. The group of patients who underwent LV remodeling (n = 13) had higher baseline E/e' than those without (13 &#177; 4 versus 8.5 &#177; 2, p &lt; 0.001). The ROC curve showed E/e' &gt; 15 as a predictor of remodeling (AUC = 0.81, p = 0.001). In addition, regression analysis (comprising clinical, laboratory and echocardiographic variables along with AMI site) confirmed the independent value of E/e' in the prediction of LV remodeling (odds ratio 1.42, p = 0.01). CONCLUSION: The E/e' ratio is a useful predictor of LV remodeling after AMI, indicating patients with increased cardiovascular risk.</p>
      </abstract>
      <kwd-group xml:lang="en">
        <kwd>Ventricular Remodeling</kwd>
        <kwd>Myocardial Infarction</kwd>
        <kwd>Echocardiography</kwd>
        <kwd>Stroke Volume</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>
        <fn id="inicio-body2">
          <label>
            <bold>Non invasive assessment of left ventricular filling pressure and remodeling after acute myocardial infarction</bold>
          </label>
          <p>
            <bold>Silvio Henrique Barberato; Admar Moraes de Souza; Costantino Ortiz Costantini; Costantino Roberto Costantini</bold>
          </p>
        </fn>
      </p>
      <p>Hospital Cardiol&#243;gico Costantini, Curitiba, PR - Brazil</p>
      <p>Mailing Address</p>
      <p>
        <bold>ABSTRACT</bold>
      </p>
      <p><bold>BACKGROUND:</bold> Left ventricular (LV) dilation after acute myocardial infarction (AMI) is an important determinant of prognosis. The ratio of early mitral inflow velocity (E) and peak early diastolic annular velocity (e') provides the best single index for noninvasive detection of acute elevation of LV filling pressure.</p>
      <p><bold>OBJECTIVE:</bold> To assess whether E/e' ratio predicts LV remodeling after properly treated AMI compared with traditional clinical, laboratory and echocardiographic data.</p>
      <p><bold>METHODS:</bold> Comprehensive echocardiograms were performed in a series of consecutive patients with first AMI successfully treated with primary percutaneous transluminal angioplasty (PTCA), both 48 hours after intervention and 60 days later. Mean E/e' was determined from four sites of the mitral annulus. LV remodeling was defined as more than 15% increase in end-systolic volume estimated by Simpson method. Statistical analysis included Student's t test, receiver-operator curves (ROC) and multivariate logistic regression (all significant with p &lt; 0.05).</p>
      <p><bold>RESULTS:</bold> Fifty-five patients were included, with mean age 58 &#177; 11 years, 43 men. The group of patients who underwent LV remodeling (n = 13) had higher baseline E/e' than those without (13 &#177; 4 versus 8.5 &#177; 2, p &lt; 0.001). The ROC curve showed E/e' &gt; 15 as a predictor of remodeling (AUC = 0.81, p = 0.001). In addition, regression analysis (comprising clinical, laboratory and echocardiographic variables along with AMI site) confirmed the independent value of E/e' in the prediction of LV remodeling (odds ratio 1.42, p = 0.01).</p>
      <p><bold>CONCLUSION:</bold> The E/e' ratio is a useful predictor of LV remodeling after AMI, indicating patients with increased cardiovascular risk.</p>
      <p><bold>Keywords:</bold> Ventricular Remodeling; Myocardial Infarction; Echocardiography / utilization; Stroke Volume / physiopathology.</p>
      <p>
        <bold>Introduction</bold>
      </p>
      <p>Dilation of the left ventricle (LV) after acute myocardial infarction (AMI) may occur even after successful transluminal coronary angioplasty (TCA). Previous studies have observed significant LV dilation in approximately one third of patients, despite the patency of the artery affected by the AMI<sup>1,2</sup>. The increase in the left ventricular cavity in response to injury is often accompanied by alterations in geometry and decrease in overall chamber performance, which is conventionally called remodeling. Such LV dilation after AMI is an important determinant of prognosis, increasing the risk of heart failure and sudden death<sup>3</sup>.</p>
      <p>Several indices derived from Doppler echocardiography have been used to predict outcomes in patients after AMI. The presence of restrictive mitral flow, characterized by shortened deceleration time (DT) of the mitral flow E-wave secondary to increased end diastolic pressure, was associated with increased risk of LV dilation after AMI<sup>4,5</sup>. Elevated filling pressures, as suggested by DT &lt; 130-140 ms, usually indicates larger infarctions, with more pronounced systolic dysfunction and particular predisposition to remodeling<sup>6</sup>.</p>
      <p>However, the velocities of mitral flow and DT are of limited value in patients with preserved LV systolic function<sup>7</sup>. Fortunately, the desirable early reperfusion obtained by recent advances in TCA techniques has resulted in better clinical outcomes and better recovery of left ventricular function<sup>8</sup>. On the other hand, the ratio between the early diastolic mitral flow velocity at conventional pulsed Doppler (E) and early diastolic mitral annular velocity at tissue Doppler (e'), known as the E/e', showed a strong correlation with invasively determined LV filling pressure<sup>7</sup>, even in subjects with preserved ejection fraction (EF).</p>
      <p>Our hypothesis was that an increased E/e' ratio (noninvasive marker of elevated LV filling pressure) is associated with higher incidence of LV dilation in patients with successful reperfusion after AMI. Therefore, the aim of this study was to determine whether the E/e' ratio predicts infarcted LV remodeling and adds information to the traditional clinical, laboratory and echocardiographic approach.</p>
      <p>
        <bold>Methods</bold>
      </p>
      <p>
        <bold>Study population</bold>
      </p>
      <p>Consecutive patients admitted to the coronary care unit of our hospital with a diagnosis of first AMI were evaluated for study enrollment. The diagnosis of AMI was defined by the recommendations of the European American College of Cardiology/ American Heart Association<sup>9</sup>. Inclusion criteria were: 1) coronary angiography after TCA showing patent artery related to the AMI, with TIMI flow grade III<sup>10</sup>; 2) echocardiogram showing wall akinesia related to compromised arterial site. Exclusion criteria were: 1) need for hemodynamic support with intra-aortic balloon, 2) sustained arrhythmia, precluding measurement of Doppler echocardiographic indices, 3) inadequate thoracic acoustic window; 4) refusal to participate in the study. </p>
      <p>The study was approved by the ethics committee and patients were included in the study after signing the free and informed consent form.</p>
      <p>
        <bold>Echocardiography</bold>
      </p>
      <p>Complete echocardiographic assessment was carried out in a consecutive series of patients with first AMI at two times: 48 hours after TCA with successful recanalization of the culprit vessel and approximately 60 days after AMI. At our institution, all patients are directly treated with primary TCA and not thrombolysis. Therefore, the value of E/e' for the studied outcome was tested under these circumstances for all study subjects. Echocardiograms were performed by the same examiner using a Philips IE33 echocardiograph (Philips Medical Systems, USA) equipped with a 2.5-4 MHz transducer. The usual slices were made to allow a detailed study by M-mode, two-dimensional and Doppler techniques (pulsed, continuous, color and tissue).</p>
      <p>Consistent with the recommendations of the American Society of Echocardiography (ASE)<sup>11</sup>, the following parameters were determined: LV interventricular septal thickness and inferolateral wall in diastole, LV systolic and diastolic dimensions. The score of parietal motility (SPM) was calculated taking into account the standard model of 16 segments and graduated in a four-point scale: 1 = normal, 2 = hypokinetic, 3 = akinetic, 4 = dyskinetic. LV mass was calculated using the formula of the ASE and indexed by body surface area (DuBois and DuBois method). The volumes and ejection fraction (EF) were calculated using the biplane Simpson method. LV remodeling was defined prospectively as an increase <underline>&gt;</underline> 15% in end-systolic volume<sup>12</sup>.</p>
      <p>The mitral flow velocities were measured by pulsed Doppler in the apical four-chamber view, with the sample volume positioned between the tips of the mitral valve leaflets, and patients were instructed to hold their breath when possible. We determined early diastolic (E) and atrial contraction (A) velocities as well as the E / A ratio and the DT. The early diastolic annular (e') and atrial (a') velocities were recorded by tissue Doppler in the apical four and two-chamber view, with a sample volume of 1-2 mm placed at the junction of the LV wall with four sites of the mitral annulus (septal, lateral, anterior and inferior). The mean of the velocities at the four sites represented the e' and a' waves used for analysis in this study, as well as the E/e' ratio. All measurements represent the mean of three cardiac cycles.</p>
      <p>LV diastolic function was graded according to the combined interpretation of the indices derived from conventional pulsed Doppler of mitral flow and tissue Doppler. Abnormal relaxation was diagnosed with the presence of E / A ratio &lt; 0.9 and e' &lt;10 cm /s; restrictive flow was determined with the E / A &gt; 2, DT &lt; 140 ms and e' &lt; 8 cm/s<sup>13</sup>. When differentiating between normal and pseudo-normal pattern, the presence of e' &lt; 8 cm and E/e' <underline>&gt;</underline> 15 was used<sup>13</sup>. The left atrial volume index (LAVi) was measured using the biplane Simpson's technique followed by body surface indexation.</p>
      <p>
        <bold>Basal clinical data and follow-up</bold>
      </p>
      <p>Demographic and clinical data were obtained by detailed chart review. Data such as age, gender, weight, height, body mass index (BMI), history of diabetes, hypertension, dyslipidemia, smoking, drug use and prior TCA were recorded. The time from symptom onset to recanalization of the culprit vessel, location (compromised LV wall), Killip classification, blood pressure on admission, peak creatine kinase MB isoenzyme (CK-MB) and troponin levels were also recorded. During and after completion of the TCA, all patients were treated with the recommended doses of aspirin, clopidogrel, unfractionated heparin and abciximab<sup>9</sup>. Drug treatment after the event was conducted by the patient's physician, recommending the administration of angiotensin-converting enzyme inhibitors (or angiotensin receptor blockers II), beta-blockers and diuretics, according to current guidelines<sup>9</sup>. The primary endpoint was LV remodeling 60 days after the AMI.</p>
      <p>
        <bold>Statistical Analysis</bold>
      </p>
      <p>The estimated sample size was calculated as 51 patients, considering an incidence of remodeling of approximately 30%<sup>1</sup>, statistical power of 90% and a significance level of 5%. Data are shown as mean and standard deviation (continuous variables) and percentages (categorical variables). The differences between the groups with and without remodeling were determined by Student's <italic>t</italic> test (continuous variables with normal distribution), Mann-Whitney test (continuous variables with non-normal distribution) and Chi-square (categorical variables).</p>
      <p>The correlations between the Doppler echocardiographic indices and alterations in end-systolic volume were analyzed using Pearson's coefficient. Receiver-operator curve (ROC) was constructed to determine E/e' as a predictor of remodeling, as well as sensitivity and specificity. Finally, multivariate logistic regression analysis was used to identify the independent value of E/e' regarding several traditional variables. Statistical significance was defined as p &lt; 0.05. Analyses were processed using the statistical program SPSS 13.0 for Windows (SPSS Inc., Chicago, Illinois).</p>
      <p>
        <bold>Results</bold>
      </p>
      <p>The study included 55 patients aged 58 &#177; 11 years, 43 men, with remodeling being detected (group I) in 13 individuals (24%), which were compared with the group without remodeling (Group II), consisting of 42 individuals. </p>
      <p>The demographic, clinical and laboratory characteristics of the study population (and its subgroups) are shown in <xref ref-type="table" rid="en_aop_5219tab01-body2">Table 1</xref>. The group I had the highest percentage of prior history of hypertension (60% <italic>versus</italic> 38%, p = 0.02) and higher peak troponin level (20 &#177; 12 <italic>vs</italic>. 7 &#177; 8 ng / mL, p = 0.005) compared to group II. There was also a tendency to higher CK-MB peak (p = 0.06) and time between symptom and vessel recanalization (p = 0.08) in group I. There were no statistically significant differences between groups regarding age, gender, BMI, diabetes, dyslipidemia, smoking, prior use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers II, prior TCA, infarction located in the anterior wall, Killip II on admission, blood pressure on admission and serum levels of hemoglobin, glucose and creatinine (all with p &gt; 0.05).</p>
      <p content-type="asset">
        <table-wrap id="en_aop_5219tab01-body2">
          <graphic xlink:href="1678-4170-abc-100-06-0531-30092-gt01-en.jpg"/></table-wrap>
      </p>
      <p><xref ref-type="table" rid="en_aop_5219tab02-body2">Table 2</xref> shows the major Doppler echocardiographic characteristics of the study sample studied. Group I had higher LV systolic dimension (p = 0.02), lower EF (p = 0.01), higher SPM (p &lt; 0.001) and lower e' (p = 0.02) and a' (p = 0.03), as well as higher E / e' (p &lt; 0.001). There were no differences in LV diastolic dimension, LVMI, E/ A ratio, DT and LAVi (all with p &gt; 0.05) between the groups.</p>
      <p content-type="asset">
        <table-wrap id="en_aop_5219tab02-body2">
          <graphic xlink:href="1678-4170-abc-100-06-0531-30092-gt02-en.jpg"/></table-wrap>
      </p>
      <p>There was a correlation between the variation in end-systolic volume after 60 days (r = 0.26, p = 0.03) and E/e', but not with the other variables. The ROC curve (<xref ref-type="fig" rid="en_aop_5219fig01-body2">Figure 1</xref>) indicated E/e' as a predictor of remodeling (area under the curve = 0.81, 95% confidence interval: 0.68 - 0.94, p = 0.001). The cutoff value for E/ e' &gt; 15 showed a sensitivity of 70% and specificity of 98% for an increase of 15% in the LV end-systolic volume.</p>
      <p content-type="asset">
        <fig id="en_aop_5219fig01-body2">
          <graphic xlink:href="1678-4170-abc-100-06-0531-30092-gf01-en.jpg"/></fig>
      </p>
      <p>Multivariate regression analyses containing clinical (history of hypertension, duration of symptoms), laboratory (troponin and CK-MB levels) and Doppler echocardiographic variables (systolic dimension of LV, EF, SPM, a', E/e' ratio and location of AMI) confirmed E/e' as the sole independent predictor of remodeling (odds ratio: 1.42; 95% confidence interval: 1.1 - 1.9, p = 0.01), above and beyond all other parameters. Speculative analyses, forcing the input of other traditionally used variables into the model, such as age, gender, DT and location of the AMI in the anterior wall, did not change the independent predictive value of E/e' ratio.</p>
      <p>
        <bold>Discussion</bold>
      </p>
      <p>The main finding of this study was that the E/e' ratio seems to be an independent predictor of left ventricular remodeling after AMI successfully treated with reperfusion by TCA. In particular, echocardiographic evidence of elevated LV filling pressures, provided by E/e' &gt; 15, was strongly associated with LV dilation, with a higher value than the previously established clinical, laboratory and echocardiographic parameters. Considerable body of evidence demonstrated that the presence of restrictive mitral flow (shortened DT) is a strong predictor of prognosis after myocardial infarction, as it is generally associated with greater area of LV wall akinesia and increased end diastolic pressure<sup>4-6</sup>.</p>
      <p>However, the DT has known limitations in patients with preserved systolic function<sup>7</sup>, a situation increasingly common after the advances obtained with prompt percutaneous intervention therapy in acute myocardial infarction. In parallel, it was demonstrated that the E/e' ratio was the best indicator of the presence of elevated end-diastolic pressure in the comparison between multiple echocardiographic parameters and the pressure measured by hemodynamic catheterization<sup>7,14</sup>.</p>
      <p>The present study indicates that the E/e' ratio can be better than the DT to predict remodeling when evaluating a patient population with relatively preserved EF (overall sample with a mean percentage of EF = 55 &#177; 12). Another interesting finding was that the E/e' ratio, representing the acute effects of elevated LV filling pressures, showed a batter performance when predicting remodeling after AMI than the LAVi, an index traditionally associated with chronic elevation of filling pressures. Although LAVi is a clear predictor of mortality after AMI<sup>15</sup>, its impact on remodeling was not observed in our study. </p>
      <p>It is possible that patients with chronic LAVi increase have suffered, prior to the AMI, some degree of left ventricular remodeling, thus mitigating the effects generated by the latest ischemic injury. Therefore, the impact of increased LAVi on LV remodeling would not be apparent in a relatively small cohort with short follow-up, such as ours. Alternatively, one may speculate that the association between LV remodeling and the acute increase in filling pressures is more important than between remodeling and the chronic increase.</p>
      <p>In the context of myocardial ischemia and infarction, tissue Doppler (from which the e' velocity derives and, ultimately, the E/e' ratio) shows low systolic and diastolic velocities in the mitral annulus<sup>16</sup>. These velocities decrease with regional hypoperfusion, recover with reperfusion and differentiate between transmural and non-transmural infarction<sup>17</sup>. After the AMI, the acute effects of ischemia and necrosis cause loss of myocyte integrity and LV geometry disarray, leading to a decrease in the overall performance and increase in LV end-diastolic pressure. LV dilation/remodeling emerge from this process as a compensatory mechanism in an attempt to restore the filling pressure to the normal level (or near normal). This might explain why a surrogate marker of the <italic>acute</italic> measure of LV filling pressure works best when predicting remodeling.</p>
      <p>In addition to estimating cardiac function and filling pressures, some authors investigated the prognostic value of E/e' in AMI. In 250 patients followed for a median period of 13 months after AMI, Hillis et al<sup>18</sup> showed that E/e ' &gt; 15 was a strong predictor of poor survival, with an incremental value to the traditional clinical parameters and echocardiographic indices of systolic and diastolic function. LV remodeling certainly plays an important role in the physiopathology of the phenomena involved in the decreased survival in this group. These researchers published a study, following the same investigation line as ours, showing that E/e' &gt; 15 identified individuals with increased risk of developing LV dilation after AMI<sup>19</sup>.</p>
      <p>However, there are several methodological differences between this report and the present study that should be highlighted. First, the population studied by Hillis et al<sup>18</sup> consisted of 47 individuals, of whom only 22 patients (47%) were treated with primary TCA, whereas 25 (53%) were treated with thrombolysis<sup>19</sup>. In contrast, all patients in our group underwent percutaneous intervention, which is known as having better outcomes<sup>8</sup>. </p>
      <p>Furthermore, the criteria to define LV remodeling were dissimilar: <underline>&gt;</underline> 15% increase in LV end-systolic volume in our study, in contrast with <underline>&gt;</underline> 15% increase in end-diastolic volume in the aforementioned article. There is no consensus in the literature whether the variation in LV systolic volume or end-diastolic volume should be used in the diagnosis of remodeling and other authors have also used our choice as reference<sup>12</sup>.</p>
      <p>The choice of employing the variation in end-systolic volume was due to prior evidence that this parameter is superior to the end-diastolic volume and even to ejection fraction itself as the primary predictor of prognosis after AMI<sup>12</sup>. Finally, it is important to emphasize that, in the study by Hillis et al<sup>18</sup>, the E/e' ratio was obtained by measuring the e' velocity exclusively on the septal mitral annulus, while our study used the mean of the four sides of the mitral annulus (septal, lateral, anterior and inferior). This conduct is vital to reduce discrepancies in the presence of regional myocardial dysfunction<sup>13</sup>.</p>
      <p>Our approach has some limitations. It is known that the tissue Doppler velocities are affected by translation, traction and tethering of adjacent myocardial segments<sup>20</sup> and, therefore, it is highly dependent on the angle. New imaging methods, such as speckle-tracking echocardiography<sup>21</sup> and magnetic resonance imaging<sup>22</sup>, which do not have this limitation, have shown to be extraordinary significant to predict remodeling after AMI. However, its clinical applicability is still limited for several reasons, including availability, which makes the E/e' ratio the best choice in terms of cost-benefit at the moment. Another limitation was the fact that all assessments were performed by a single examiner, precluding the measurement of interobserver variability.</p>
      <p>Thus, the use of the E/e' ratio, a noninvasive marker of elevated LV filling pressures, may be a useful predictor of LV dilation/ remodeling scenario after AMI, indicating patients with increased cardiovascular risk and allowing early intervention.</p>
      <p>
        <bold>Potential Conflict of Interest</bold>
      </p>
      <p>No potential conflict of interest relevant to this article was reported.</p>
      <p>
        <bold>Sources of Funding</bold>
      </p>
      <p>There were no external funding sources for this study.</p>
      <p>
        <bold>Study Association</bold>
      </p>
      <p>This study is not associated with any post-graduation program.</p>
      <p>
        <bold>References</bold>
      </p>
    </body>
  </sub-article>
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