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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 pub-id-type="publisher-id" specific-use="scielo-v3">Q3wWwYpfdt8MNDtvm57pMBn</article-id>
      <article-id pub-id-type="other">01197</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2020001401197</article-id>
      <article-id pub-id-type="publisher-id">abc.20201205</article-id>
      <article-id pub-id-type="doi">10.36660/abc.20201205</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Carta Cient&#237;fica</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>T&#243;picos Emergentes em Insufici&#234;ncia Card&#237;aca: Perspectivas Futuras</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-9413-3792</contrib-id>
          <name>
            <surname>Oliveira</surname>
            <given-names>Mucio Tavares de</given-names>
            <suffix>Jr</suffix>
          </name>
          <xref ref-type="aff" rid="aff1">
            <sup>1</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-1654-4531</contrib-id>
          <name>
            <surname>Villacorta</surname>
            <given-names>Humberto</given-names>
          </name>
          <xref ref-type="aff" rid="aff2">
            <sup>2</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-1206-9489</contrib-id>
          <name>
            <surname>Bittencourt</surname>
            <given-names>Marcelo Imbroinise</given-names>
          </name>
          <xref ref-type="aff" rid="aff3">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Barretto</surname>
            <given-names>Ant&#244;nio Carlos Pereira</given-names>
          </name>
          <xref ref-type="aff" rid="aff4">
            <sup>4</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-7452-3870</contrib-id>
          <name>
            <surname>Mesquita</surname>
            <given-names>Evandro Tinoco</given-names>
          </name>
          <xref ref-type="aff" rid="aff2">
            <sup>2</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-6557-393X</contrib-id>
          <name>
            <surname>Rohde</surname>
            <given-names>Luis Eduardo</given-names>
          </name>
          <xref ref-type="aff" rid="aff5">
            <sup>5</sup>
          </xref>
          <xref ref-type="aff" rid="aff6">
            <sup>6</sup>
          </xref>
        </contrib>
      </contrib-group>
      <aff id="aff1">
        <label>1</label>
        <institution content-type="orgdiv2">Instituto do Cora&#231;&#227;o</institution>
        <institution content-type="orgdiv1">Hospital das Cl&#237;nicas</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 do Hospital das Cl&#237;nicas da Universidade de S&#227;o Paulo,S&#227;o Paulo, SP - Brasil</institution>
      </aff>
      <aff id="aff2">
        <label>2</label>
        <institution content-type="orgdiv1">Faculdade de Medicina</institution>
        <institution content-type="orgname">Universidade Federal Fluminense</institution>
        <addr-line>
          <named-content content-type="city">Niter&#243;i</named-content>
          <named-content content-type="state">RJ</named-content>
        </addr-line>
        <country country="BR">Brasil</country>
        <institution content-type="original">Faculdade de Medicina - Universidade Federal Fluminense, Niter&#243;i, RJ - Brasil</institution>
      </aff>
      <aff id="aff3">
        <label>3</label>
        <institution content-type="orgdiv2">Cl&#237;nica de Insufici&#234;ncia Card&#237;aca e Cardiomiopatias</institution>
        <institution content-type="orgdiv1">Hospital Universit&#225;rio Pedro Ernesto</institution>
        <institution content-type="orgname">Universidade do Estado do Rio de Janeiro</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">Cl&#237;nica de Insufici&#234;ncia Card&#237;aca e Cardiomiopatias - Hospital Universit&#225;rio Pedro Ernesto - Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ - Brasil</institution>
      </aff>
      <aff id="aff4">
        <label>4</label>
        <institution content-type="orgdiv1">Faculdade de Medicina</institution>
        <institution content-type="orgname">Universidade de S&#227;o Paulo</institution>
        <institution content-type="orgdiv2">Servi&#231;o de Preven&#231;&#227;o e Reabilita&#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">Faculdade de Medicina da Universidade de S&#227;o Paulo - Servi&#231;o de Preven&#231;&#227;o e Reabilita&#231;&#227;o do Instituto do Cora&#231;&#227;o, S&#227;o Paulo, SP - Brasil</institution>
      </aff>
      <aff id="aff5">
        <label>5</label>
        <institution content-type="orgdiv2">Grupo de Insufici&#234;ncia Card&#237;aca Avan&#231;ada</institution>
        <institution content-type="orgdiv1">Servi&#231;o de Cardiologia</institution>
        <institution content-type="orgname">Hospital de Cl&#237;nicas 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">Grupo de Insufici&#234;ncia Card&#237;aca Avan&#231;ada do Servi&#231;o de Cardiologia do Hospital de Cl&#237;nicas de Porto Alegre, Porto Alegre, RS - Brasil</institution>
      </aff>
      <aff id="aff6">
        <label>6</label>
        <institution content-type="orgdiv1">Faculdade de Medicina</institution>
        <institution content-type="orgname">Universidade Federal do Rio Grande do Sul</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">Faculdade de Medicina da Universidade Federal do Rio Grande do Sul, Porto Alegre, RS - Brasil</institution>
      </aff>
      <author-notes>
        <corresp id="c01"> Correspond&#234;ncia: Mucio Tavares de Oliveira Jr &#8226; Instituto do Cora&#231;&#227;o &#8211; HC-FMUSP - Hospital Dia e Centro de Infus&#227;o Dr. Eneas Aguiar, 44. CEP 05403900, S&#227;o Paulo, SP &#8211; Brasil E-mail: <email>mucio@incor.usp.br</email>
				</corresp>
        <fn fn-type="con">
          <p>Contribui&#231;&#227;o dos autores</p>
          <p>Reda&#231;&#227;o do manuscrito e Revis&#227;o cr&#237;tica do manuscrito quanto ao conte&#250;do intelectual importante: Oliveira Jr MT, Villacorta H, Bittencourt MI, Barretto ACP, Mesquita ET, Rohde LE.</p>
        </fn>
        <fn fn-type="conflict">
          <p>Potencial conflito de interesses</p>
          <p>Declaro n&#227;o haver conflito de interesses pertinentes.</p>
        </fn>
      </author-notes>
      <pub-date date-type="pub" publication-format="electronic">
        <day>18</day>
        <month>01</month>
        <year>2021</year>
      </pub-date>
      <pub-date date-type="collection" publication-format="electronic">
        <month>12</month>
        <year>2020</year>
      </pub-date>
      <volume>115</volume>
      <issue>6</issue>
      <fpage>1197</fpage>
      <lpage>1200</lpage>
      <history>
        <date date-type="received">
          <day>12</day>
          <month>11</month>
          <year>2020</year>
        </date>
        <date date-type="rev-recd">
          <day>12</day>
          <month>11</month>
          <year>2020</year>
        </date>
        <date date-type="accepted">
          <day>12</day>
          <month>11</month>
          <year>2020</year>
        </date>
      </history>
      <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 Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. </license-p>
        </license>
      </permissions>
      <kwd-group xml:lang="pt">
        <kwd>Biomarcadores</kwd>
        <kwd>Avalia&#231;&#227;o Gen&#233;tica</kwd>
        <kwd>Omecamtiv Mecarbil</kwd>
        <kwd>Mavacamten</kwd>
        <kwd>Telemedicina</kwd>
        <kwd>Imuniza&#231;&#227;o</kwd>
        <kwd>Vacinas</kwd>
        <kwd>Danon</kwd>
        <kwd>Fabry</kwd>
        <kwd>Amiloidose</kwd>
      </kwd-group>
      <counts>
        <fig-count count="0"/>
        <table-count count="0"/>
        <equation-count count="0"/>
        <ref-count count="15"/>
        <page-count count="4"/>
      </counts>
    </article-meta>
  </front>
  <body>
    <sec sec-type="intro">
      <title>Introdu&#231;&#227;o</title>
      <p>O <italic>Heart Failure Summit 2020</italic> abordou novas perspectivas de avalia&#231;&#227;o, diagn&#243;stico, estratifica&#231;&#227;o de risco e tratamento da insufici&#234;ncia card&#237;aca (IC), as quais em breve poder&#227;o estar dispon&#237;veis para ampla aplicabilidade cl&#237;nica. Essas estrat&#233;gias envolvem o uso de novos biomarcadores, a avalia&#231;&#227;o gen&#233;tica, novos potenciais alvos terap&#234;uticos e a medicina personalizada.</p>
      <sec>
        <title>Novos Biomarcadores</title>
        <p>Entre os novos biomarcadores, citamos dois relacionados ao processo de fibrose. A galectina-3 (Gal-3) &#233; expressa em v&#225;rios tecidos e c&#233;lulas, incluindo o mioc&#225;rdio. No cora&#231;&#227;o, ela ativa fibroblastos quiescentes, transformando-os em miofibroblastos que alteram a matriz extracelular, produzindo fibrose, sendo preditora de remodelamento na IC. Al&#233;m de ser um marcador de risco, a Gal-3 parece participar ativamente do processo de fibrose, sendo um potencial alvo terap&#234;utico.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> O ST2 sol&#250;vel &#233; outro marcador de fibrose na IC, fornecendo informa&#231;&#245;es adicionais aos pept&#237;deos natriur&#233;ticos e troponinas.<sup><xref ref-type="bibr" rid="B2">2</xref></sup> Mais recentemente, o fator de diferencia&#231;&#227;o de crescimento-15 (GDF-15) tem-se mostrado preditor de eventos na IC.<sup><xref ref-type="bibr" rid="B3">3</xref></sup></p>
        <p>Embora esses biomarcadores sejam promissores, ainda n&#227;o temos um grande estudo mostrando que adicionam informa&#231;&#227;o ao manuseio convencional.</p>
      </sec>
      <sec>
        <title>Avalia&#231;&#227;o Gen&#233;tica</title>
        <p>Os avan&#231;os na gen&#233;tica est&#227;o melhorando a compreens&#227;o das diversas cardiopatias heredit&#225;rias, em especial as cardiomiopatias, causas frequentes de IC. Doen&#231;as como cardiomiopatia dilatada e cardiomiopatia hipertr&#243;fica t&#234;m sido impactadas nesse sentido.<sup><xref ref-type="bibr" rid="B4">4</xref></sup> Evid&#234;ncias nessa &#225;rea v&#234;m esclarecendo aspectos etiopatog&#234;nicos, como variantes em truncamento de genes. Outro cen&#225;rio que a gen&#233;tica ajudou a mudar nossa forma de avalia&#231;&#227;o foi a cardiomiopatia arritmog&#234;nica, tema de consenso recentemente publicado.<sup><xref ref-type="bibr" rid="B5">5</xref></sup> Antigamente associada exclusivamente a cardiomiopatia do ventr&#237;culo direito determinada por muta&#231;&#245;es desmossomais, hoje sabemos que abrange um amplo espectro de doen&#231;as gen&#233;ticas, sist&#234;micas e inflamat&#243;rias. A incorpora&#231;&#227;o do sequenciamento de &#250;ltima gera&#231;&#227;o vem aumentando a sensibilidade dos testes gen&#233;ticos, o que possibilita diagn&#243;stico precoce com perspectiva de interven&#231;&#227;o. Entretanto, nem todos est&#227;o cientes da aplicabilidade dessa ferramenta, assim como das armadilhas que surgem com a sua incorpora&#231;&#227;o. Fica clara a necessidade de buscar formas mais eficientes da utiliza&#231;&#227;o da gen&#233;tica, especialmente no aconselhamento familiar, trazendo resultados seguros e sustent&#225;veis na gest&#227;o do cuidado desses pacientes e suas fam&#237;lias.</p>
      </sec>
      <sec>
        <title>Novos Alvos Terap&#234;uticos</title>
        <p>A miosina como alvo de tratamento nos traz duas novas drogas com resultados promissores nos estudos iniciais de fase 1 e 2 no tratamento da IC e da cardiomiopatia hipertr&#243;fica.</p>
        <sec>
          <title>Omecamtiv mecarbil</title>
          <p>&#201; um ativador seletivo da miosina, e essa ativa&#231;&#227;o trataria a altera&#231;&#227;o central da disfun&#231;&#227;o ventricular, melhorando a contra&#231;&#227;o ventricular comprometida nos casos de IC com fra&#231;&#227;o de eje&#231;&#227;o reduzida. Seu mecanismo de a&#231;&#227;o &#233; diferente dos tratamentos atuais que bloqueiam a elevada estimula&#231;&#227;o neuro-hormonal. Os estudos mecan&#237;sticos, como o ATOMIC-AHF ( <italic>Acute Treatment with Omecamtiv Mecarbil to Increase Contractility in Acute Heart Failure</italic> ) e o COSMIC-HF ( <italic>Chronic Oral Study of Myosin Activation to Increase Contractility in Heart Failure</italic> ), mostraram que a droga melhora a contratilidade, melhorando a fra&#231;&#227;o de eje&#231;&#227;o, o volume ejetado e o d&#233;bito card&#237;aco, al&#233;m de outros par&#226;metros que indicam melhora da fun&#231;&#227;o card&#237;aca. Os estudos mostraram que promove redu&#231;&#227;o dos n&#237;veis de NT-proBNP. Identificou-se tamb&#233;m eleva&#231;&#227;o dos n&#237;veis de troponina, sem altera&#231;&#245;es cl&#237;nicas nos estudos realizados. O estudo ATOMIC-AHF, entretanto, em pacientes com IC aguda, n&#227;o documentou redu&#231;&#227;o da dispneia nos pacientes tratados. O estudo GALACTIC-HF (Registrational Study With Omecamtiv Mecarbil/AMG 423 to Treat Chronic Heart Failure With Reduced Ejection Fraction) n&#227;o demonstrou benef&#237;cio da droga na mortalidade a longo prazo e uma redu&#231;&#227;o de apenas 5% para primeira hospitaliza&#231;&#227;o.<sup><xref ref-type="bibr" rid="B6">6</xref></sup> Estudos em popula&#231;&#245;es com IC aguda e com IC terminal s&#227;o necess&#225;rios para definir a utilidade da droga.</p>
        </sec>
        <sec>
          <title>Mavacamten</title>
          <p>O mavacamten &#233; um inibidor espec&#237;fico da miosina, e estudos v&#234;m mostrando que a sua prescri&#231;&#227;o promove melhora no desempenho f&#237;sico dos portadores de cardiomiopatia hipertr&#243;fica obstrutiva, com melhora do consumo de oxig&#234;nio.<sup><xref ref-type="bibr" rid="B7">7</xref></sup> Com sua prescri&#231;&#227;o, documentou-se redu&#231;&#227;o dos n&#237;veis de NT-proBNP e de troponina, sugerindo redu&#231;&#227;o do estresse na parede mioc&#225;rdica, redu&#231;&#227;o da obstru&#231;&#227;o ventricular e redu&#231;&#227;o da fra&#231;&#227;o de eje&#231;&#227;o. No estudo MAVERICK, os eventos colaterais foram frequentes e um percentual n&#227;o desprez&#237;vel de pacientes apresentou redu&#231;&#227;o exagerada da fra&#231;&#227;o de eje&#231;&#227;o, revers&#237;vel com a suspens&#227;o da droga. O acerto da dose parece ser fundamental e se prop&#245;e que seja avaliado com base na resposta da fra&#231;&#227;o de eje&#231;&#227;o. Precisamos aguardar os estudos de sobrevida para ter certeza de que a droga &#233; segura e entender melhor como avaliar a redu&#231;&#227;o da contratilidade e da fra&#231;&#227;o de eje&#231;&#227;o com o medicamento.</p>
        </sec>
      </sec>
    </sec>
    <sec>
      <title>Telemedicina</title>
      <p>A telemedicina &#233; uma ampla plataforma de estrat&#233;gias singulares com complexidades variadas que surgiram na &#225;rea m&#233;dica como uma ferramenta promissora para melhorar a ades&#227;o de pacientes com doen&#231;as cr&#244;nicas e reduzir as desigualdades em sa&#250;de. Infelizmente, a aplicabilidade da telemedicina tem sido err&#225;tica na Am&#233;rica Latina e em muitas partes do mundo, devido &#224;s dificuldades log&#237;sticas para estabelecer estruturas tecnol&#243;gicas de suporte que sejam eficientes e vi&#225;veis para muitos pacientes. Al&#233;m disso, v&#225;rias estrat&#233;gias de telemonitoramento foram testadas em IC com resultados inconsistentes. A falta de efic&#225;cia de forma conclusiva pode ser explicada por diferen&#231;as no conte&#250;do e intensidade de cada interven&#231;&#227;o e pela natureza heterog&#234;nea das popula&#231;&#245;es de pacientes inclu&#237;dos em diferentes estudos. A maioria dos estudos que demonstram os efeitos ben&#233;ficos das estrat&#233;gias de telemedicina na IC envolveu pacientes inst&#225;veis e vulner&#225;veis com uma hospitaliza&#231;&#227;o recente. Tamb&#233;m parece essencial que estrat&#233;gias espec&#237;ficas sejam adaptadas para cada ambiente de sa&#250;de, considerando aspectos sociais, econ&#244;micos, cognitivos e culturais. Uma an&#225;lise de 15 revis&#245;es sistem&#225;ticas sobre a efic&#225;cia dessas estrat&#233;gias para pacientes com IC sugere que as interven&#231;&#245;es de telemonitoramento domiciliar reduzem o risco relativo de mortalidade por todas as causas e hospitaliza&#231;&#245;es relacionadas &#224; IC em compara&#231;&#227;o com o tratamento usual. As redu&#231;&#245;es de risco na mortalidade e hospitaliza&#231;&#245;es por todas as causas pareceram ser maiores em pacientes que receberam alta recentemente (&#8804; 28 dias) em cen&#225;rios de descompensa&#231;&#245;es agudos ap&#243;s uma exacerba&#231;&#227;o recente de IC.<sup><xref ref-type="bibr" rid="B8">8</xref></sup></p>
    </sec>
    <sec>
      <title>Novas Terapias na Insufici&#234;ncia Card&#237;aca com Fra&#231;&#227;o de Eje&#231;&#227;o Preservada (ICFEP)</title>
      <p>Entre as terapias para ICFEp, as que mais t&#234;m chamado a aten&#231;&#227;o e curiosidade s&#227;o os inibidores do cotransportador de s&#243;dio-glicose (iSGLT2), como a empaglifozina [EMPEROR-Preserved ( <italic>Empagliflozin outcome trial in patients with chronic heart failure with preserved ejection fraction</italic> ) e EMBRACE-HF ( <italic>Empagliflozin impact on hemodynamics in patients with heart failure</italic> )], a dapaglifozina [PRESERVED-HF ( <italic>Dapagliflozin in preserved ejection fraction heart failure</italic> )] e a ertuglifozina [ERADICATE-HF ( <italic>Ertugliflozin trial in diabetes with preserved or reduced ejection fraction mechanistic evaluation in heart failure</italic> )]. Outras drogas tamb&#233;m est&#227;o em fase de avalia&#231;&#227;o, como TRC4186 (inibidor dos produtos finais de glicoliza&#231;&#227;o avan&#231;ada), trimetazidina, praliciguat e vericiguat (estimulante da guanilato ciclase sol&#250;vel), neladenoson (agonista parcial do receptor A1 da adenosina) e o pirfenidone (agente antifibr&#243;tico), como tamb&#233;m o procedimento de abertura de uma comunica&#231;&#227;o interatrial por cateter a fim de aliviar a press&#227;o elevada do &#225;trio esquerdo.</p>
    </sec>
    <sec>
      <title>Imuniza&#231;&#245;es na IC</title>
      <p>At&#233; pouco tempo, n&#227;o havia dados sobre o impacto da <italic>influenza</italic> sobre os desfechos em pacientes com IC,<sup><xref ref-type="bibr" rid="B9">9</xref></sup> mas ficou demonstrado em estudo populacional a rela&#231;&#227;o entre a esta&#231;&#227;o de <italic>influenza</italic> e a ocorr&#234;ncia de maior n&#250;mero de interna&#231;&#245;es por IC, coincidindo em quatro per&#237;odos consecutivos. Em uma suban&#225;lise do estudo PARADIGM (P <italic>rospective comparison of ARNI with ACEI to determine impact on global mortality and morbidity</italic> ), 21% dos participantes receberam vacina&#231;&#227;o contra <italic>influenza</italic> e nestes houve uma redu&#231;&#227;o de morte total de 19% ap&#243;s ajuste de propens&#227;o. Em um estudo de coorte dinamarqu&#234;s com 134.048 pacientes com IC, uma ou mais vacina&#231;&#245;es entre 2003 e 2015 resultaram igualmente em redu&#231;&#227;o de 18% na mortalidade total e mortalidade por todas as causas e mais de tr&#234;s vacina&#231;&#245;es, a uma redu&#231;&#227;o de 28% na mortalidade total e de 29% na mortalidade cardiovascular.<sup><xref ref-type="bibr" rid="B10">10</xref></sup> Um estudo com banco de dados de 6.435 pacientes com IC, sendo 695 vacinados antes ou durante o inverno de 2017/2018, houve redu&#231;&#227;o de 22% na morte total e 17% em morte cardiovascular ou interna&#231;&#227;o por IC, sendo o benef&#237;cio da vacina&#231;&#227;o sobre a morte total maior em pacientes com mais de 70 anos, com redu&#231;&#227;o de mais de 25%.<sup><xref ref-type="bibr" rid="B11">11</xref></sup> N&#227;o h&#225; estudos sobre o impacto da vacina&#231;&#227;o para pneumococo. Diversos estudos prospectivos est&#227;o em fase de inclus&#227;o de pacientes.</p>
    </sec>
    <sec>
      <title>IC Personalizada</title>
      <p>A promessa da medicina personalizada na IC vai progressivamente se tornando uma nova realidade e um novo campo apoiado na cardioimagem, na gen&#244;mica e nas ci&#234;ncias de dados. Na presente d&#233;cada, ocorreu um importante desafio do governo norte-americano, apoiando iniciativas de pesquisa para doen&#231;as cr&#244;nicas visando incorporar o paradigma da medicina de precis&#227;o, e esse esfor&#231;o tem apresentado importantes avan&#231;os em diferentes centros acad&#234;micos. A ICFEp &#233; hoje um dos maiores desafios na pr&#225;tica cl&#237;nica pela aus&#234;ncia de medicamentos capazes de reduzir a morbimortalidade. A ICFEp vem sendo estudada com um novo olhar, apoiando-se nas t&#233;cnicas de bioinform&#225;tica, identificando redes fenot&#237;picas e buscando identificar padr&#245;es que possam cursar com diferentes progn&#243;sticos e, possivelmente, apresentar respostas diferentes frente aos medicamentos.<sup><xref ref-type="bibr" rid="B12">12</xref></sup></p>
      <p>Apoiando-se nas t&#233;cnicas de bioinform&#225;tica e de cientistas de dados, tem sido poss&#237;vel predizer a evolu&#231;&#227;o cl&#237;nica das cardiomiopatias heredit&#225;rias, como as doen&#231;as de Danon e Fabry.<sup><xref ref-type="bibr" rid="B13">13</xref></sup> A miocardiopatia hipertr&#243;fica tem apresentado grandes avan&#231;os com a possibilidade de caracterizar fenoc&#243;pias &#8211; condi&#231;&#245;es que simulam a apresenta&#231;&#227;o morfol&#243;gica da miocardiopatia hipertr&#243;fica, tais como a doen&#231;a de Fabry, amiloidose card&#237;aca, doen&#231;a de Pompe, doen&#231;a de Danon, entre outras. As t&#233;cnicas que manipulam o c&#243;digo gen&#233;tico, como o sistema de repeti&#231;&#245;es palindr&#244;micas curtas agrupadas e regularmente interespa&#231;adas (CRISPR), t&#234;m o potencial futuro de tratarem doen&#231;as monog&#234;nicas e est&#227;o sendo empregadas em modelos animais.</p>
      <p>O maior avan&#231;o da presente d&#233;cada tem sido a realiza&#231;&#227;o do diagn&#243;stico da amiloidose card&#237;aca e da caracteriza&#231;&#227;o de seus principais tipos, combinando imagem molecular, biomarcadores e testes gen&#233;ticos.<sup><xref ref-type="bibr" rid="B14">14</xref></sup> H&#225; algoritmos que empregam dosagem s&#233;rica das cadeias leves de imunoglobulina e imunofixa&#231;&#227;o no sangue e urina, cintilografia card&#237;aca com pirofosfato de tecn&#233;cio em associa&#231;&#227;o com abordagem multimodal com t&#233;cnicas avan&#231;adas de ecodopplercardiografia com <italic>speckle tracking</italic> e da resson&#226;ncia card&#237;aca em combina&#231;&#227;o com teste gen&#233;tico. Essa abordagem tem permitido a substitui&#231;&#227;o da bi&#243;psia de tecido gorduroso e/ou card&#237;aco para correta identifica&#231;&#227;o de amiloidose decorrente da muta&#231;&#227;o da transtirretina. Os novos medicamentos, como o tafamidis, e aqueles que interferem com a transcri&#231;&#227;o do RNA, como o patisiran, s&#227;o exemplos da personaliza&#231;&#227;o do tratamento. Um recente relato de caso mostra a regress&#227;o e normaliza&#231;&#227;o da cintilografia mioc&#225;rdica com pirofosfato de tecn&#233;cio no paciente tratado com esses novos medicamentos no curso da amiloidose card&#237;aca por uma muta&#231;&#227;o da TTR, representando esse novo futuro.<sup><xref ref-type="bibr" rid="B15">15</xref></sup></p>
    </sec>
    <sec>
      <title>Lista de Participantes do Heart Failure Summit Brazil 2020 / Departamento de Insufici&#234;ncia Card&#237;aca - DEIC/SBC</title>
      <p>Aguinaldo Freitas Junior, Andr&#233;ia Biolo, Antonio Carlos Pereira Barretto, Ant&#244;nio Lagoeiro Jorge, Bruno Biselli, Carlos Eduardo Montenegro, Denilson Campos de Albuquerque, Dirceu Rodrigues de Almeida, Edimar Alcides Bocchi, Edval Gomes dos Santos J&#250;nior, Est&#234;v&#227;o Lanna Figueiredo, Evandro Tinoco Mesquita, Fabiana G. Marcondes-Braga, F&#225;bio Fernandes, Fabio Serra Silveira, Felix Jos&#233; Alvarez Ramires, Fernando Atik, Fernando Bacal, Fl&#225;vio de Souza Brito, Germano Emilio Concei&#231;&#227;o Souza, Gustavo Calado de Aguiar Ribeiro, Humberto Villacorta Jr., Jefferson Luis Vieira, Jo&#227;o David de Souza Neto, Jo&#227;o Manoel Rossi Neto, Jos&#233; Albuquerque de Figueiredo Neto, L&#237;dia Ana Zytynski Moura, Livia Adams Goldraich, Lu&#237;s Beck-da- Silva, Lu&#237;s Eduardo Paim Rohde, Luiz Claudio Danzmann, Manoel Fernandes Canesin, Marcelo Bittencourt, Marcelo Westerlund Montera, Marcely Gimenes Bonatto, Marcus Vinicius Sim&#245;es, Maria da Consola&#231;&#227;o Vieira Moreira, Miguel Morita Fernandes da Silva, Monica Samuel Avila, Mucio Tavares de Oliveira Junior, Nadine Clausell, Odilson Marcos Silvestre, Otavio Rizzi Coelho Filho, Pedro Vellosa Schwartzmann, Reinaldo Bulgarelli Bestetti, Ricardo Mourilhe Rocha, Sabrina Bernadez Pereira, Salvador Rassi, Sandrigo Mangini, Silvia Marinho Martins, Silvia Moreira Ayub Ferreira, Victor Sarli Issa.</p>
    </sec>
  </body>
  <back>
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          <article-title>Amiloidose Card&#237;aca e seu Novo Fen&#243;tipo Cl&#237;nico: Insufici&#234;ncia Card&#237;aca com Fra&#231;&#227;o de Eje&#231;&#227;o Preservada</article-title>
          <source>Arq. Bras. Cardiol</source>
          <year>2017</year>
          <volume>109</volume>
          <issue>1</issue>
          <fpage>71</fpage>
          <lpage>80</lpage>
        </element-citation>
      </ref>
      <ref id="B15">
        <label>15</label>
        <mixed-citation>15. Groothof D, Bijzet J. Regression of Bone-Tracer Uptake in Cardiac Transthyretin Amyloidosis. Mayo Clin Proc. 2020;95(2):417-426.</mixed-citation>
        <element-citation publication-type="journal">
          <person-group person-group-type="author">
            <name>
              <surname>Groothof</surname>
              <given-names>D</given-names>
            </name>
            <name>
              <surname>Bijzet</surname>
              <given-names>J</given-names>
            </name>
          </person-group>
          <article-title>Regression of Bone-Tracer Uptake in Cardiac Transthyretin Amyloidosis</article-title>
          <source>Mayo Clin Proc</source>
          <year>2020</year>
          <volume>95</volume>
          <issue>2</issue>
          <fpage>417</fpage>
          <lpage>426</lpage>
        </element-citation>
      </ref>
    </ref-list>
    <fn-group>
      <fn fn-type="other">
        <p>Carta cient&#237;fica referente ao Heart Failure Summit Brazil 2020 / Departamento de Insufici&#234;ncia Card&#237;aca &#8211; DEIC/SBC</p>
      </fn>
      <fn fn-type="other">
        <p>Vincula&#231;&#227;o acad&#234;mica</p>
        <p>N&#227;o h&#225; vincula&#231;&#227;o deste estudo a programas de p&#243;s-gradua&#231;&#227;o.</p>
      </fn>
    </fn-group>
    <fn-group>
      <fn fn-type="supported-by">
        <p><bold>Fontes de financiamento</bold> .O presente estudo n&#227;o teve fontes de financiamento externas.</p>
      </fn>
    </fn-group>
  </back>
  <sub-article article-type="translation" id="TRen" xml:lang="en">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Research Letter</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Emerging Topics in Heart Failure: Future Perspectives</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0001-9413-3792</contrib-id>
          <name>
            <surname>Oliveira</surname>
            <given-names>Mucio Tavares de</given-names>
            <suffix>Jr</suffix>
          </name>
          <xref ref-type="aff" rid="aff1001">
            <sup>1</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-1654-4531</contrib-id>
          <name>
            <surname>Villacorta</surname>
            <given-names>Humberto</given-names>
          </name>
          <xref ref-type="aff" rid="aff2001">
            <sup>2</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0003-1206-9489</contrib-id>
          <name>
            <surname>Bittencourt</surname>
            <given-names>Marcelo Imbroinise</given-names>
          </name>
          <xref ref-type="aff" rid="aff3001">
            <sup>3</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Barretto</surname>
            <given-names>Ant&#244;nio Carlos Pereira</given-names>
          </name>
          <xref ref-type="aff" rid="aff4001">
            <sup>4</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-7452-3870</contrib-id>
          <name>
            <surname>Mesquita</surname>
            <given-names>Evandro Tinoco</given-names>
          </name>
          <xref ref-type="aff" rid="aff2001">
            <sup>2</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-6557-393X</contrib-id>
          <name>
            <surname>Rohde</surname>
            <given-names>Luis Eduardo</given-names>
          </name>
          <xref ref-type="aff" rid="aff5001">
            <sup>5</sup>
          </xref>
          <xref ref-type="aff" rid="aff6001">
            <sup>6</sup>
          </xref>
        </contrib>
      </contrib-group>
      <aff id="aff1001">
        <label>1</label>
        <country country="BR">Brasil</country>
        <institution content-type="original">Instituto do Cora&#231;&#227;o do Hospital das Cl&#237;nicas da Universidade de S&#227;o Paulo, S&#227;o Paulo, SP - Brasil</institution>
      </aff>
      <aff id="aff2001">
        <label>2</label>
        <country country="BR">Brasil</country>
        <institution content-type="original">Faculdade de Medicina - Universidade Federal Fluminense, Niter&#243;i, RJ - Brasil</institution>
      </aff>
      <aff id="aff3001">
        <label>3</label>
        <country country="BR">Brasil</country>
        <institution content-type="original">Cl&#237;nica de Insufici&#234;ncia Card&#237;aca e Cardiomiopatias - Hospital Universit&#225;rio Pedro Ernesto - Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ - Brasil</institution>
      </aff>
      <aff id="aff4001">
        <label>4</label>
        <country country="BR">Brasil</country>
        <institution content-type="original">Faculdade de Medicina da Universidade de S&#227;o Paulo - Servi&#231;o de Preven&#231;&#227;o e Reabilita&#231;&#227;o do Instituto do Cora&#231;&#227;o, S&#227;o Paulo, SP - Brasil</institution>
      </aff>
      <aff id="aff5001">
        <label>5</label>
        <country country="BR">Brasil</country>
        <institution content-type="original">Grupo de Insufici&#234;ncia Card&#237;aca Avan&#231;ada do Servi&#231;o de Cardiologia do Hospital de Cl&#237;nicas de Porto Alegre, Porto Alegre, RS - Brasil</institution>
      </aff>
      <aff id="aff6001">
        <label>6</label>
        <country country="BR">Brasil</country>
        <institution content-type="original">Faculdade de Medicina da Universidade Federal do Rio Grande do Sul, Porto Alegre, RS - Brasil</institution>
      </aff>
      <author-notes>
        <corresp id="c01001"><bold>Mailing Address: Mucio Tavares de Oliveira Jr.</bold> &#8226; Instituto do Cora&#231;&#227;o &#8211; HC-FMUSP - Hospital Dia e Centro de Infus&#227;o Dr. Eneas Aguiar, 44. Postal Code 05403900, S&#227;o Paulo, SP &#8211; Brazil E-mail: mucio@incor.usp.br</corresp>
        <fn fn-type="con">
          <p>Author contributions</p>
          <p>Writing of the manuscript and Critical revision of the manuscript for intellectual content: Oliveira Jr MT, Villacorta H, Bittencourt MI, Barretto ACP, Mesquita ET, Rohde LE.</p>
        </fn>
        <fn fn-type="conflict">
          <p>Potential Conflict of Interest</p>
          <p>No potential conflict of interest relevant to this article was reported.</p>
        </fn>
      </author-notes>
      <kwd-group xml:lang="en">
        <kwd>Biomarkers</kwd>
        <kwd>Genetic Assessment</kwd>
        <kwd>Omecamtiv Mecarbil</kwd>
        <kwd>Mavacamten</kwd>
        <kwd>Telemedicine</kwd>
        <kwd>Imunization</kwd>
        <kwd>Vaccins</kwd>
        <kwd>Danon</kwd>
        <kwd>Fabry</kwd>
        <kwd>Amiloidosis</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <sec sec-type="intro">
        <title>Introduction</title>
        <p>The <italic>Heart Failure Summit Brazil 2020</italic> addressed new perspectives for assessment, diagnosis, risk stratification, and management of heart failure (HF), which may soon be available for widespread use in the clinic. These strategies involve the use of novel biomarkers, genetic assessment, potential new therapeutic targets, and personalized medicine.</p>
        <sec>
          <title>Novel Biomarkers</title>
          <p>Among novel biomarkers, two&#8212;both related to the process of fibrosis&#8212;are worthy of note. Galectin-3 (Gal-3) is expressed in various tissues and cells, including the myocardium. In the heart, Gal-3 activates quiescent fibroblasts, transforming them into myofibroblasts that alter the extracellular matrix to produce fibrosis; research has shown it is a predictor of remodeling in HF. In addition to being a marker of risk, Gal-3 appears to play an active role in the fibrosis process, and may thus constitute a potential therapeutic target.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> Soluble ST2 is another marker of fibrosis in HF, providing additional information as an adjunct to natriuretic peptides and troponins.<sup><xref ref-type="bibr" rid="B2">2</xref></sup> More recently, growth differentiation factor-15 (GDF-15) has been shown to be a predictor of events in HF.<sup><xref ref-type="bibr" rid="B3">3</xref></sup></p>
          <p>Although these biomarkers are promising, there is still no conclusive evidence from large studies that they add information to conventional.</p>
        </sec>
        <sec>
          <title>Genetic Assessment</title>
          <p>Advances in genetics are improving our understanding of the various hereditary heart diseases, especially cardiomyopathies, which are frequent causes of HF. Diseases such as dilated cardiomyopathy and hypertrophic cardiomyopathy have been impacted by such research;<sup><xref ref-type="bibr" rid="B4">4</xref></sup> new evidence has clarified certain etiopathogenetic aspects. One example is the finding that truncating variants of the titin gene account for up to a quarter of all dilated cardiomyopathies. Advances in genetics have also changed the approach to initial assessment of arrhythmogenic cardiomyopathy, the topic of a recently published consensus statement.<sup><xref ref-type="bibr" rid="B5">5</xref></sup> Once associated exclusively with right ventricular cardiomyopathy caused by mutations in desmosomal protein genes, we now know that this umbrella term covers a wide spectrum of genetic, systemic, and inflammatory conditions. The advent of next-generation sequencing has increased the sensitivity of genetic tests, which allows for early diagnosis with an interventional perspective. However, not all clinicians are aware of the applicability of this tool, nor of the pitfalls that arise with its incorporation into practice. There is a clear need for more efficient ways of using genetics, especially in family counseling, to achieve more safe and sustainable outcomes in the management of these patients and their families.</p>
        </sec>
        <sec>
          <title>New Therapeutic Targets</title>
          <p>Two new drugs targeting myosin have yielded promising results in phase 1 and 2 trials for the treatment of HF and hypertrophic cardiomyopathy.</p>
          <sec>
            <title>Omecamtiv Mecarbil</title>
            <p>This is a selective myosin activator and is thus believed to address the core abnormality of ventricular dysfunction, improving compromised ventricular contraction in cases of HF with reduced ejection fraction. Its mechanism of action is distinct from that of current treatments, which counteract elevated neurohormonal stimulation. Mechanistic trials, such as ATOMIC-AHF (Acute Treatment with Omecamtiv Mecarbil to Increase Contractility in Acute Heart Failure) and COSMIC-HF (Chronic Oral Study of Myosin Activation to Increase Contractility in Heart Failure), have shown that this drug improves contractility, improving ejection fraction, stroke volume, and cardiac output, in addition to other parameters suggestive of improved cardiac function. Studies have shown that omecamtiv mecarbil promotes a reduction in NT-proBNP levels. Elevation of troponin levels, with no clinical repercussions, has also been reported. Nevertheless, the ATOMIC-AHF study of patients with acute HF did not observe a reduction in dyspnea in patients treated with the drug. A study, GALACTIC-HF (Registrational Study With Omecamtiv Mecarbil/AMG 423 to Treat Chronic Heart Failure With Reduced Ejection Fraction) fail to demonstrate long-term survival benefit, and showed only a 5% reduction for first HF hospitalization.<sup><xref ref-type="bibr" rid="B6">6</xref></sup> Further studies in acute HF patients and patients with terminal HF are necessary to stablish the usefulness of this drug.</p>
          </sec>
          <sec>
            <title>Mavacamten</title>
            <p>Mavacamten is a cardiac myosin-specific inhibitor. Studies have shown that it enhances physical performance in patients with obstructive hypertrophic cardiomyopathy, with improved oxygen consumption.<sup><xref ref-type="bibr" rid="B7">7</xref></sup> Its administration was associated with a reduction in NT-proBNP and troponin levels, suggesting reductions in stress in the myocardial wall, ventricular obstruction, and ejection fraction. In the MAVERICK study, adverse events were frequent and a not-insignificant percentage of patients experienced excessive decline in ejection fraction, which was however reversible upon discontinuation. Proper dose adjustment appears to be essential, and the ejection fraction response has been proposed as a guide. Again, survival studies are needed to ensure that mavacamten is safe and to better understand the reductions in contractility and ejection fraction that appear to follow its use.</p>
          </sec>
        </sec>
      </sec>
      <sec>
        <title>Telemedicine</title>
        <p>Telemedicine is a broad platform of unique strategies with varied complexities that have emerged in the medical field as a promising tool to improve the treatment adherence of patients with chronic diseases and reduce health inequalities. Unfortunately, implementation of telemedicine has been erratic in Latin America and in many parts of the world, due to logistical difficulties in establishing the necessary technological support structures in a manner that is efficient and feasible for most patients. In addition, several telemonitoring strategies have been tested in HF, with inconsistent results. The lack of conclusive effectiveness may be explained by differences in the content and intensity of each intervention and by the heterogeneous nature of the patient populations included in different studies. Most studies that demonstrated beneficial effects of telemedicine strategies in HF have involved unstable and vulnerable patients with a history of recent hospitalization. It also seems essential that specific strategies be adapted to each health setting, considering social, economic, cognitive, and cultural aspects. An analysis of 15 systematic reviews on the effectiveness of these strategies for patients with HF suggests that home telemonitoring interventions reduce the relative risk of all-cause mortality and HF-related hospitalization compared to usual care. Risk reductions in all-cause mortality and hospitalization appeared to be greater in patients who were recently discharged (&#8804; 28 days) in the setting of acute decompensation after a recent exacerbation of HF.<sup><xref ref-type="bibr" rid="B8">8</xref></sup></p>
      </sec>
      <sec>
        <title>New Therapies in Heart Failure with Preserved Ejection Fraction (HFPEF)</title>
        <p>Among promising therapies for HFpEF, those that have drawn the most attention and interest are the sodium-glucose cotransporter inhibitors (SGLT2i), such as empagliflozin (evaluated in the EMPEROR-Preserved [Empagliflozin outcome trial in patients with chronic heart failure with preserved ejection fraction] and EMBRACE-HF [Empagliflozin impact on hemodynamics in patients with heart failure] trials), dapagliflozin (evaluated in PRESERVED-HF [Dapagliflozin in preserved ejection fraction heart failure]), and ertugliflozin (ERADICATE-HF [Ertugliflozin trial in diabetes with preserved or reduced and reduced fraction mechanistic evaluation in heart failure]). Other drugs are also at the investigational stage, such as TRC4186 (an inhibitor of advanced glycation end products), trimetazidine, praliciguat and vericiguat (soluble guanylate cyclase stimulants), neladenoson (a partial adenosine A1 receptor agonist), and pirfenidone (an antifibrotic agent), as is an invasive procedure (creation of an atrial septal defect to relieve high pressure in the left atrium).</p>
      </sec>
      <sec>
        <title>Immunizations in HF</title>
        <p>Until recently, there was no data on the impact of influenza on outcomes in patients with HF,<sup><xref ref-type="bibr" rid="B9">9</xref></sup> but a population-based study has since demonstrated a relationship between influenza season and higher incidence of hospitalization for HF, which coincided in four consecutive periods. In a subanalysis of the PARADIGM (Prospective comparison of ARNI with ACEI to determine impact on global mortality and morbidity) trial, the 21% of participants who had received the influenza vaccine were found to have a 19% lower overall mortality after propensity matching. In a Danish cohort study of 134,048 patients with HF, one or more vaccinations between 2003 and 2015 were also associated with an 18% reduction in overall mortality and all-cause mortality; more than three vaccinations resulted in a 28% reduction in overall mortality and a 29% reduction in cardiovascular mortality.<sup><xref ref-type="bibr" rid="B10">10</xref></sup> A database study of 6,435 patients with HF, 695 of whom were vaccinated before or during the winter of 2017&#8211;2018, showed a 22% reduction in overall mortality and a 17% reduction in cardiovascular death or hospitalization due to HF. The benefit of vaccination on overall mortality was greatest in patients over age 70 years, with a &gt;25% reduction.<sup><xref ref-type="bibr" rid="B11">11</xref></sup> There are no studies on the impact of pneumococcal vaccination. Several prospective studies are at the enrollment stage.</p>
      </sec>
      <sec>
        <title>Personalized HF Management</title>
        <p>The promise of personalized medicine in HF management is progressively becoming reality and a new field in its own right, supported by cardiac imaging, genomics, and data sciences. In 2015, the U.S. government launched the Precision Medicine Initiative, a major challenge and research effort designed to support research initiatives for chronic diseases aimed at incorporating the precision medicine paradigm. This effort has led to significant advances at several academic centers. HFpEF is currently one of the greatest challenges in clinical practice due to the absence of drugs capable of reducing morbidity and mortality. Accordingly, a new outlook for HFpEF research has arisen which relies on bioinformatics techniques and identification of phenotypic networks, seeking to identify patterns that may be associated with different prognoses and, possibly, present differential responses to pharmacotherapy.<sup><xref ref-type="bibr" rid="B12">12</xref></sup></p>
        <p>Leveraging bioinformatics and data science techniques has enabled successful prediction of the clinical course of hereditary cardiomyopathies such as Danon disease and Fabry disease.<sup><xref ref-type="bibr" rid="B13">13</xref></sup> Great strides have been made in hypertrophic cardiomyopathy with the possibility of characterizing phenocopies&#8212;conditions that mimic the morphological presentation of hypertrophic cardiomyopathy, such as Fabry disease, cardiac amyloidosis, Pompe disease, Danon disease, etc. Genetic manipulation techniques, such as clustered regularly interspersed short palindromic repeats (CRISPR)-based gene editing, have potential for future utility in the treatment of monogenic diseases, and are already being tested in animal models.</p>
        <p>For diagnosis of cardiac amyloidosis and characterization of its main subtypes through a combination of molecular imaging, biomarkers, and genetic testing have been used.<sup><xref ref-type="bibr" rid="B14">14</xref></sup> Serum measurement of immunoglobulin light chain and immunofixation in blood and urine, technetium pyrophosphate myocardial perfusion scanning, a multimodal approach of advanced Doppler echocardiography techniques such as speckle tracking, and cardiac magnetic resonance, all in combination with genetic tests. This approach has successfully replaced adipose tissue and/or endomyocardial biopsy for the accurate diagnosis of transthyretin-mediated cardiac amyloidosis (ATTR-CM). New drugs with disease-modifying capacity, such as the transthyretin stabilizer tafamidis and the small interfering RNA molecule patisiran, are examples of the increasingly personalized approach to management of cardiac amyloidosis. A recent case report of regression and normalization of technetium pyrophosphate myocardial perfusion scan findings in a patient with ATTR-CM treated with these new drugs is representative of this new and future paradigm.<sup><xref ref-type="bibr" rid="B15">15</xref></sup></p>
      </sec>
      <sec>
        <title>List of participants of the Heart Failure Summit Brazil 2020 / Heart Failure Department - Brazilian Society of Cardiology</title>
        <p>Aguinaldo Freitas Junior, Andr&#233;ia Biolo, Antonio Carlos Pereira Barretto, Ant&#244;nio Lagoeiro Jorge, Bruno Biselli, Carlos Eduardo Montenegro, Denilson Campos de Albuquerque, Dirceu Rodrigues de Almeida, Edimar Alcides Bocchi, Edval Gomes dos Santos J&#250;nior, Est&#234;v&#227;o Lanna Figueiredo, Evandro Tinoco Mesquita, Fabiana G. Marcondes-Braga, F&#225;bio Fernandes, Fabio Serra Silveira, Felix Jos&#233; Alvarez Ramires, Fernando Atik, Fernando Bacal, Fl&#225;vio de Souza Brito, Germano Emilio Concei&#231;&#227;o Souza, Gustavo Calado de Aguiar Ribeiro, Humberto Villacorta Jr., Jefferson Luis Vieira, Jo&#227;o David de Souza Neto, Jo&#227;o Manoel Rossi Neto, Jos&#233; Albuquerque de Figueiredo Neto, L&#237;dia Ana Zytynski Moura, Livia Adams Goldraich, Lu&#237;s Beck-da- Silva, Lu&#237;s Eduardo Paim Rohde, Luiz Claudio Danzmann, Manoel Fernandes Canesin, Marcelo Bittencourt, Marcelo Westerlund Montera, Marcely Gimenes Bonatto, Marcus Vinicius Sim&#245;es, Maria da Consola&#231;&#227;o Vieira Moreira, Miguel Morita Fernandes da Silva, Monica Samuel Avila, Mucio Tavares de Oliveira Junior, Nadine Clausell, Odilson Marcos Silvestre, Otavio Rizzi Coelho Filho, Pedro Vellosa Schwartzmann, Reinaldo Bulgarelli Bestetti, Ricardo Mourilhe Rocha, Sabrina Bernadez Pereira, Salvador Rassi, Sandrigo Mangini, Silvia Marinho Martins, Silvia Moreira Ayub Ferreira, Victor Sarli Issa.</p>
      </sec>
    </body>
    <back>
      <fn-group>
        <fn fn-type="other">
          <p>Research letter related to Heart Failure Summit Brazil 2020 / Heart Failure Department - Brazilian Society of Cardiology</p>
        </fn>
        <fn fn-type="other">
          <p>Study Association</p>
          <p>This study is not associated with any thesis or dissertation work.</p>
        </fn>
      </fn-group>
      <fn-group>
        <fn fn-type="supported-by">
          <p><bold>Sources of Funding</bold> .There were no external funding sources for this study.</p>
        </fn>
      </fn-group>
    </back>
  </sub-article>
</article>
