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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">Y9hYksbPMQDr9cdHqvMR7md</article-id>
      <article-id specific-use="scielo-v2" pub-id-type="publisher-id">S0066-782X2021000600926</article-id>
      <article-id pub-id-type="publisher-id">abc.20210205</article-id>
      <article-id pub-id-type="doi">10.36660/abc.20210205</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Minieditorial</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Mapeamento de T1 na Insufici&#234;ncia Card&#237;aca: Implica&#231;&#245;es Progn&#243;sticas</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="editor">
          <contrib-id contrib-id-type="orcid">0000-0002-8007-0476</contrib-id>
          <name>
            <surname>Moharem-Elgamal</surname>
            <given-names>Sarah</given-names>
          </name>
          <xref ref-type="aff" rid="aff1">
            <sup>1</sup>
          </xref>
          <xref ref-type="aff" rid="aff2">
            <sup>2</sup>
          </xref>
          <xref ref-type="corresp" rid="c1"/>
        </contrib>
        <aff id="aff1">
          <label>1</label>
          <institution content-type="orgname">Liverpool Heart and Chest Hospital</institution>
          <addr-line>
            <named-content content-type="city">Liverpool</named-content>
          </addr-line>
          <country country="GB">Reino Unido</country>
          <institution content-type="original">Liverpool Heart and Chest Hospital, Liverpool - Reino Unido</institution>
        </aff>
        <aff id="aff2">
          <label>2</label>
          <institution content-type="orgname">National Heart Institute</institution>
          <addr-line>
            <named-content content-type="city">Giza</named-content>
          </addr-line>
          <country country="EG">Egito</country>
          <institution content-type="original">National Heart Institute, Giza - Egito</institution>
        </aff>
      </contrib-group>
      <author-notes>
        <corresp id="c1"><bold>Correspond&#234;ncia: Sarah Moharem-Elgamal</bold> &#8226; Cardiology Department- Liverpool Heart and Chest Hospital Thomas Drive Liverpool L14 3PE - Reino Unido. E-mail: <email>sarahmoharem@hotmail.com</email></corresp>
      </author-notes>
      <pub-date publication-format="electronic" date-type="pub">
        <day>17</day>
        <month>05</month>
        <year>2021</year>
      </pub-date>
      <pub-date publication-format="electronic" date-type="collection">
        <month>05</month>
        <year>2021</year>
      </pub-date>
      <volume>116</volume>
      <issue>5</issue>
      <fpage>926</fpage>
      <lpage>927</lpage>
      <permissions>
        <license license-type="open-access" xml:lang="en" xlink:href="https://creativecommons.org/licenses/by/4.0/">
          <license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License</license-p>
        </license>
      </permissions>
      <kwd-group xml:lang="pt">
        <title>Palavras-chave</title>
        <kwd>Fibrose Endomioc&#225;rdica</kwd>
        <kwd>Insufici&#234;ncia Card&#237;aca</kwd>
        <kwd>Mortalidade</kwd>
        <kwd>Proteina de Suscetibilidade a Apoptose Celular</kwd>
        <kwd>Fibroblastos</kwd>
        <kwd>Resson&#226;ncia Magn&#233;tica/m&#233;todos</kwd>
      </kwd-group>
      <counts>
        <fig-count count="0"/>
        <table-count count="0"/>
        <equation-count count="0"/>
        <ref-count count="6"/>
        <page-count count="2"/>
      </counts>
    </article-meta>
  </front>
  <body>
    <p>A fibrose mioc&#225;rdica leva ao comprometimento da fun&#231;&#227;o diast&#243;lica e sist&#243;lica e est&#225; associada ao aumento de eventos cardiovasculares adversos maiores. &#201; um correlato estrutural que pode ser encontrado nas diferentes fases da insufici&#234;ncia card&#237;aca. Os dois principais tipos de fibrose mioc&#225;rdica s&#227;o a fibrose intersticial e a fibrose de substitui&#231;&#227;o. A fibrose intersticial &#233; um processo revers&#237;vel que ocorre no in&#237;cio do processo da doen&#231;a como aumento da s&#237;ntese de col&#225;geno em distribui&#231;&#227;o microsc&#243;pica difusa dentro do mioc&#225;rdio e &#224;s vezes por distribui&#231;&#227;o perivascular localizada. A fibrose de substitui&#231;&#227;o tipicamente ocorre nos est&#225;gios mais avan&#231;ados da doen&#231;a, ap&#243;s les&#227;o irrevers&#237;vel do mi&#243;cito ou morte, na qual a apoptose celular desencadeia o aparecimento de fibroblastos e promove deposi&#231;&#227;o macrosc&#243;pica de tecido fibroso de col&#225;geno no mioc&#225;rdio.</p>
    <p>A resson&#226;ncia magn&#233;tica card&#237;aca (RMC) tem a capacidade de quantificar com precis&#227;o os volumes ventriculares e a fra&#231;&#227;o de eje&#231;&#227;o, bem como a caracteriza&#231;&#227;o n&#227;o-invasiva do mioc&#225;rdio. Essas caracter&#237;sticas &#250;nicas levaram ao aumento do uso de RMC na avalia&#231;&#227;o de pacientes com insufici&#234;ncia card&#237;aca (IC). A RMC pode detectar a presen&#231;a e extens&#227;o da fibrose de substitui&#231;&#227;o atrav&#233;s de imagem de realce tardio com gadol&#237;nio e fibrose intersticial difusa por mapeamento de T1 nativo. A fibrose intersticial identificada pelo mapeamento de T1 nativo tem sido utilizada como marcador de atividade da doen&#231;a,<xref ref-type="bibr" rid="B1"><sup>1</sup></xref><sup>&#8211;</sup><xref ref-type="bibr" rid="B3"><sup>3</sup></xref> na estratifica&#231;&#227;o de risco<xref ref-type="bibr" rid="B4"><sup>4</sup></xref> e no monitoramento do manejo terap&#234;utico em pacientes com IC.<xref ref-type="bibr" rid="B5"><sup>5</sup></xref></p>
    <p>Nesta edi&#231;&#227;o dos Arquivos Brasileiros de Cardiologia, Marques et al.,<xref ref-type="bibr" rid="B6"><sup>6</sup></xref> relatam a viabilidade da avalia&#231;&#227;o do mapeamento de T1 nativo em pacientes com IC em um hospital de refer&#234;ncia em cardiologia e sua associa&#231;&#227;o com par&#226;metros estruturais e perfil funcional.<xref ref-type="bibr" rid="B6"><sup>6</sup></xref> Eles inclu&#237;ram 134 pacientes com insufici&#234;ncia card&#237;aca de diferentes etiologias de um &#250;nico centro. A maior parte da etiologia da popula&#231;&#227;o do estudo foi de pacientes n&#227;o isqu&#234;micos [n = 95 (70,9%)]. O realce tardio com gadol&#237;nio foi observado em 59% (56 pacientes) com cardiomiopatia n&#227;o-isqu&#234;mica e 87% (34 de 39) de pacientes com cardiomiopatia isqu&#234;mica. Valores aumentados de T1 nativo do mioc&#225;rdio foram associados a maiores di&#226;metros do VE (p = 0,007) e volumes ventriculares (p &lt;0,01). Um valor de T1 significativamente maior foi observado em pacientes com FEVE &lt;35% (p &lt;0,001). Ao comparar os valores de T1 em rela&#231;&#227;o &#224; gravidade da disfun&#231;&#227;o sist&#243;lica, o T1 significativamente maior foi observado na ICFEr do que na ICFEi (p = 0,004) e ICFEp (p &lt;0,001). T1 elevado foi observado em 55,2% dos pacientes com ICFEp (p &lt;0,01).</p>
    <p>Al&#233;m disso, o mapeamento de T1 estava elevado independentemente da etiologia da IC (89,7% em isqu&#234;micos e 81,1% em n&#227;o-isqu&#234;micos), com um maior valor de T1 observado em pacientes isqu&#234;micos <italic>vs.</italic> n&#227;o isqu&#234;micos (p = 0,004). Um dado interessante neste estudo, foi o fato de os autores inclu&#237;ram a cardiomiopatia chag&#225;sica. Eles demonstraram que 13 pacientes com cardiomiopatia chag&#225;sica com T1 nativo aumentado (1.077,1 &#177; 61,1ms) estavam associados &#224; redu&#231;&#227;o da FEVE (27,6 &#177; 16,8%) e aumento dos di&#226;metros e volumes do VE. Al&#233;m das diferentes etiologias e da gravidade da insufici&#234;ncia card&#237;aca, o tabagismo foi a &#250;nica comorbidade identificada com valores elevados de T1 estatisticamente significativos (p = 0,032).</p>
    <p>Esses achados enfatizam o fato de que o aumento dos valores de mapeamento de T1 nativo apresentaram uma associa&#231;&#227;o direta com os par&#226;metros tradicionais utilizados para avaliar a gravidade da doen&#231;a, independentemente da etiologia subjacente. Os autores reconheceram que o tamanho limitado da amostra, outras patologias tais como edema, infiltra&#231;&#227;o, e inflama&#231;&#227;o podem afetar os valores de T1, bem como a falta de c&#225;lculo do volume extracelular. Apesar disso, o mapeamento de T1 nativo oferece um m&#233;todo n&#227;o invasivo para caracterizar a patologia difusa. Seus achados apoiam o uso do mapeamento de T1 nativo como um biomarcador n&#227;o invasivo para estratifica&#231;&#227;o de risco na insufici&#234;ncia card&#237;aca.</p>
  </body>
  <back>
    <fn-group>
      <fn fn-type="other" id="fn1">
        <p>Minieditorial referente ao artigo: Estratifica&#231;&#227;o da Insufici&#234;ncia Card&#237;aca Cl&#237;nica atrav&#233;s do Mapa T1 Nativo: Experi&#234;ncia de um Servi&#231;o de Refer&#234;ncia</p>
      </fn>
    </fn-group>
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  </back>
  <sub-article article-type="translation" id="S01" xml:lang="en">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Short Editorial</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>T1 Mapping in Heart Failure: Prognostic Implications</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="editor">
          <contrib-id contrib-id-type="orcid">0000-0002-8007-0476</contrib-id>
          <name>
            <surname>Moharem-Elgamal</surname>
            <given-names>Sarah</given-names>
          </name>
          <xref ref-type="aff" rid="aff3">
            <sup>1</sup>
          </xref>
          <xref ref-type="aff" rid="aff4">
            <sup>2</sup>
          </xref>
          <xref ref-type="corresp" rid="c2"/>
        </contrib>
        <aff id="aff3">
          <label>1</label>
          <addr-line>
            <named-content content-type="city">Liverpool</named-content>
          </addr-line>
          <country country="GB">United Kingdom</country>
          <institution content-type="original">Liverpool Heart and Chest Hospital, Liverpool - United Kingdom</institution>
        </aff>
        <aff id="aff4">
          <label>2</label>
          <addr-line>
            <named-content content-type="city">Giza</named-content>
          </addr-line>
          <country country="EG">Egypt</country>
          <institution content-type="original">National Heart Institute, Giza - Egypt</institution>
        </aff>
      </contrib-group>
      <author-notes>
        <corresp id="c2"><bold>Mailing Address: Sarah Moharem-Elgamal</bold> &#8226; Cardiology Department- Liverpool Heart and Chest Hospital Thomas Drive Liverpool L14 3PE - United Kingdom E-mail: <email>sarahmoharem@hotmail.com</email></corresp>
      </author-notes>
      <kwd-group xml:lang="en">
        <title>Keywords</title>
        <kwd>Endomyocardial Fibrosis</kwd>
        <kwd>Heart Failure</kwd>
        <kwd>Mortality</kwd>
        <kwd>Cellular Apoptose Susceptibility Protein</kwd>
        <kwd>Fibroblasts</kwd>
        <kwd>Magnetic Resonance Spectroscopy/methods</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>Myocardial fibrosis leads to impaired diastolic and systolic function and is associated with increased major adverse cardiovascular events. It is a structural correlate that can be found in the different stages of heart failure. The two main types of myocardial fibrosis are interstitial fibrosis and replacement fibrosis. Interstitial fibrosis is a reversible process that occurs early in the disease process as increased collagen synthesis in diffuse microscopic distribution within the myocardium and sometimes by localized perivascular distribution. Replacement fibrosis typically occurs in the later stages of the disease after irreversible myocyte injury or death, in which cell apoptosis triggers fibroblasts and promotes macroscopic deposition of collagen fibrous tissue in the myocardium.</p>
      <p>Cardiac magnetic resonance (CMR) has the capability to accurately quantify ventricular volumes and ejection fraction, as well as the non-invasive characterization of the myocardium. These unique features have led to the increased use of CMR in the assessment of patients with heart failure (HF). CMR can detect the presence and extent of replacement fibrosis through late gadolinium enhancement imaging and diffuse interstitial fibrosis through native T1 mapping. Interstitial fibrosis identified by native T1 mapping has been used as a marker of disease activity,<xref ref-type="bibr" rid="B1"><sup>1</sup></xref><sup>&#8211;</sup><xref ref-type="bibr" rid="B3"><sup>3</sup></xref> risk stratification<xref ref-type="bibr" rid="B4"><sup>4</sup></xref> and monitoring of the therapeutic management in heart failure patients.<xref ref-type="bibr" rid="B5"><sup>5</sup></xref></p>
      <p>In this issue of the Brazilian Archives of Cardiology, Marques et al.<xref ref-type="bibr" rid="B6"><sup>6</sup></xref> report the feasibility of native T1 mapping assessment in patients with HF in a cardiology referral hospital and its association with structural parameters and functional profile.<xref ref-type="bibr" rid="B6"><sup>6</sup></xref> They enrolled 134 patients with heart failure of different etiologies from a single center. Most of the study population's etiology comprised non-ischemic patients [n=95 (70.9%)]. Late gadolinium enhancement was observed in 59% (56 patients) with non-ischemic cardiomyopathy and 87% (34 of 39) ischemic cardiomyopathy patients. Increased native myocardial T1 values were associated with larger LV diameters (p = 0.007) and ventricular volumes (p &lt;0.01). A significantly higher T1 value was observed in patients with LVEF &lt;35% (p &lt;0.001). Upon comparing the T1 values in relation to systolic dysfunction severity, significantly higher T1 was observed in HFrEF than in HFmrEF (p = 0.004); and HFpEF (p &lt;0.001). Elevated T1 was observed in 55.2% of patients with HFpEF (p &lt;0.01).</p>
      <p>Furthermore, T1 mapping was elevated regardless of the HF etiology (89.7% in ischemic and 81.1% in non-ischemic cases), with a higher T1 value observed in ischemic vs. non-ischemic patients (p = 0.004). Unique to this study, the authors have included Chagas cardiomyopathy. They demonstrated that 13 Chagas cardiomyopathy patients with increased native T1 (1077.1 &#177; 61.1ms) was associated with reduced LVEF (27.6 &#177; 16.8%) and increased LV diameters and volumes. In addition to the different etiologies and the severity of heart failure, smoking was the only comorbidity identified with a statistically significant elevated T1 values (p = 0.032).</p>
      <p>These findings emphasize that the increased native T1 mapping values had a direct association with traditional parameters used to assess disease severity regardless of the underlying etiology. The authors have acknowledged that the limited sample size, other pathologies such as edema, infiltration, and inflammation may affect T1 values, as well as the lack of extracellular volume calculation. Nonetheless, native T1 mapping offers a noninvasive method to characterize diffuse pathology. Their findings support the use of native T1 mapping as a non-invasive biomarker for risk stratification in heart failure.</p>
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          <p>Short Editorial related to the article: Clinical Heart Failure Stratification Through Native T1 Mapping: Experience of a Referral Service</p>
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