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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">k7YRCS6wps7xrfFR7tfSphK</article-id>
      <article-id pub-id-type="other">00015</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2010001400015</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(10)09500415</article-id>
      <article-id pub-id-type="doi">10.1590/S0066-782X2010005000112</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Artigos Originais</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Cardiomiopatia chag&#225;sica: progn&#243;stico no perfil cl&#237;nico-hemodin&#226;mico C</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Cardoso</surname>
            <given-names>Juliano</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Novaes</surname>
            <given-names>Milena</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Ochiai</surname>
            <given-names>Marcelo</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Regina</surname>
            <given-names>Kelly</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Morgado</surname>
            <given-names>Paulo</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Munhoz</surname>
            <given-names>Robinson</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Brancalh&#227;o</surname>
            <given-names>Euler</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Lima</surname>
            <given-names>Marcelo</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Barretto</surname>
            <given-names>Antonio Carlos Pereira</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">S&#227;o Paulo</named-content>
        </addr-line>
        <institution content-type="orgname">Universidade de S&#227;o Paulo</institution>
        <institution content-type="orgdiv1">InCor Hospital de Cotox&#243; </institution>
        <country country="BR">Brazil</country>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>10</month>
        <year>2010</year>
      </pub-date>
      <volume>95</volume>
      <issue>4</issue>
      <fpage>518</fpage>
      <lpage>523</lpage>
      <history>
        <date date-type="received">
          <day>03</day>
          <month>11</month>
          <year>2009</year>
        </date>
        <date date-type="rev-recd">
          <day>10</day>
          <month>03</month>
          <year>2010</year>
        </date>
        <date date-type="accepted">
          <day>08</day>
          <month>04</month>
          <year>2010</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: Os pacientes com insufici&#234;ncia card&#237;aca (IC) que s&#227;o internados apresentando m&#225; perfus&#227;o e congest&#227;o (perfil cl&#237;nico-hemodin&#226;mico C) constituem o grupo que evolui com pior progn&#243;stico na IC descompensada. Entretanto, h&#225; pouca informa&#231;&#227;o na literatura se a etiologia da cardiopatia influencia na evolu&#231;&#227;o dos pacientes na fase avan&#231;ada. OBJETIVO: Avaliar a evolu&#231;&#227;o dos pacientes que se internaram com perfil cl&#237;nico-hemodin&#226;mico C e verificar o papel da etiologia nesta fase. M&#201;TODOS: Um estudo de coorte foi realizado incluindo pacientes com fra&#231;&#227;o de eje&#231;&#227;o do ventr&#237;culo esquerdo (FEVE) &lt; 45,0%, classe funcional IV e interna&#231;&#227;o hospitalar apresentando perfil cl&#237;nico-hemodin&#226;mico C. O grupo foi dividido em pacientes portadores de cardiomiopatia chag&#225;sica (Ch) e n&#227;o chag&#225;sica (NCh). Para an&#225;lise estat&#237;stica foram utilizados os testes t de Student, exato de Fisher, qui-quadrado e o programa SPSS. O significante de p &lt; 0,05 foi considerado. RESULTADOS: Cem pacientes, com idade m&#233;dia de 57,6 &#177; 15,1 anos e FEVE m&#233;dia de 23,8 &#177; 8,5%, foram inclu&#237;dos. Dentre os pacientes estudados, 33,0% eram chag&#225;sicos e, na compara&#231;&#227;o com os NCh, apresentaram menor press&#227;o arterial sist&#243;lica (Ch 89,3 &#177; 17,1 mmHg versus NCh 98,8 &#177; 21,7 mmHg; p = 0,03) e menor idade m&#233;dia - Ch 52,9 &#177; 14,5 anos versus NCh 59,8 &#177; 14,9 anos; p = 0,03). Durante o acompanhamento de 25 meses, a mortalidade foi de 66,7% nos Ch e de 37,3% nos NCh (p = 0,019). A etiologia chag&#225;sica foi um marcador independente de mau progn&#243;stico na an&#225;lise multivariada com raz&#227;o de risco de 2,75 (IC 95,0%; 1,35 - 5,63). CONCLUS&#195;O: Nos pacientes com IC avan&#231;ada, a etiologia chag&#225;sica &#233; um importante preditor de pior progn&#243;stico.</p>
      </abstract>
      <kwd-group xml:lang="pt" kwd-group-type="author-generated">
        <kwd>Insufici&#234;ncia card&#237;aca</kwd>
        <kwd>progn&#243;stico</kwd>
        <kwd>reperfus&#227;o</kwd>
        <kwd>cardiomiopatia chag&#225;sica</kwd>
      </kwd-group>
      <pub-date publication-format="electronic" date-type="pub">
        <day>27</day>
        <month>08</month>
        <year>2010</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <p>ARTIGO ORIGINAL </p>
    <p> INSUFICI&#202;NCIA CARD&#205;ACA </p>
    <p>
      <bold>Cardiomiopatia chag&#225;sica: progn&#243;stico no perfil cl&#237;nico-hemodin&#226;mico C</bold>
    </p>
    <p>
      <bold>Juliano Cardoso; Milena Novaes; Marcelo Ochiai; Kelly Regina; Paulo Morgado; Robinson Munhoz; Euler Brancalh&#227;o; Marcelo Lima; Antonio Carlos Pereira Barretto</bold>
    </p>
    <p>InCor - Hospital de Cotox&#243; - HCFMUSP, S&#227;o Paulo, SP - Brasil</p>
    <p>
      <xref ref-type="corresp" rid="correspbaixo">Correspond&#234;ncia</xref>
    </p>
    <p>
      <bold>RESUMO</bold>
    </p>
    <p><bold>FUNDAMENTO:</bold> Os pacientes com insufici&#234;ncia card&#237;aca (IC) que s&#227;o internados apresentando m&#225; perfus&#227;o e congest&#227;o (perfil cl&#237;nico-hemodin&#226;mico C) constituem o grupo que evolui com pior progn&#243;stico na IC descompensada. Entretanto, h&#225; pouca informa&#231;&#227;o na literatura se a etiologia da cardiopatia influencia na evolu&#231;&#227;o dos pacientes na fase avan&#231;ada. </p>
    <p><bold>OBJETIVO:</bold> Avaliar a evolu&#231;&#227;o dos pacientes que se internaram com perfil cl&#237;nico-hemodin&#226;mico C e verificar o papel da etiologia nesta fase. </p>
    <p><bold>M&#201;TODOS:</bold> Um estudo de coorte foi realizado incluindo pacientes com fra&#231;&#227;o de eje&#231;&#227;o do ventr&#237;culo esquerdo (FEVE) &lt; 45,0%, classe funcional IV e interna&#231;&#227;o hospitalar apresentando perfil cl&#237;nico-hemodin&#226;mico C. O grupo foi dividido em pacientes portadores de cardiomiopatia chag&#225;sica (Ch) e n&#227;o chag&#225;sica (NCh). Para an&#225;lise estat&#237;stica foram utilizados os testes <italic>t</italic> de <italic>Student</italic>, exato de Fisher, qui-quadrado e o programa SPSS. O significante de p &lt; 0,05 foi considerado. </p>
    <p><bold>RESULTADOS:</bold> Cem pacientes, com idade m&#233;dia de 57,6 &#177; 15,1 anos e FEVE m&#233;dia de 23,8 &#177; 8,5%, foram inclu&#237;dos. Dentre os pacientes estudados, 33,0% eram chag&#225;sicos e, na compara&#231;&#227;o com os NCh, apresentaram menor press&#227;o arterial sist&#243;lica (Ch 89,3 &#177; 17,1 mmHg <italic>versus</italic> NCh 98,8 &#177; 21,7 mmHg; p = 0,03) e menor idade m&#233;dia - Ch 52,9 &#177; 14,5 anos <italic>versus</italic> NCh 59,8 &#177; 14,9 anos; p = 0,03). Durante o acompanhamento de 25 meses, a mortalidade foi de 66,7% nos Ch e de 37,3% nos NCh (p = 0,019). A etiologia chag&#225;sica foi um marcador independente de mau progn&#243;stico na an&#225;lise multivariada com raz&#227;o de risco de 2,75 (IC 95,0%; 1,35 - 5,63). </p>
    <p><bold>CONCLUS&#195;O:</bold> Nos pacientes com IC avan&#231;ada, a etiologia chag&#225;sica &#233; um importante preditor de pior progn&#243;stico. (Arq Bras Cardiol. 2010; [online]. ahead print, PP.0-0)</p>
    <p><bold>Palavras-chave:</bold> Insufici&#234;ncia card&#237;aca/complica&#231;&#245;es, progn&#243;stico, reperfus&#227;o, cardiomiopatia chag&#225;sica.</p>
    <p>
      <bold>Introdu&#231;&#227;o</bold>
    </p>
    <p>O avan&#231;o da medicina vem aprimorando o conhecimento sobre a insufici&#234;ncia card&#237;aca (IC), possibilitando o desenvolvimento de novos m&#233;todos diagn&#243;sticos, a determina&#231;&#227;o de fatores progn&#243;sticos e a institui&#231;&#227;o de tratamentos mais efetivos que melhoram sua evolu&#231;&#227;o. No entanto, a IC continua sendo uma doen&#231;a prevalente e com progn&#243;stico reservado, principalmente nas fases avan&#231;adas da doen&#231;a.</p>
    <p>Em tal contexto, &#233; importante identificar as caracter&#237;sticas cl&#237;nicas e laboratoriais dos pacientes com IC descompensada, que permitam determinar aqueles com tend&#234;ncia ao pior progn&#243;stico. Isto possibilita adotar medidas espec&#237;ficas e adequadas no tratamento desse grupo para melhorar a qualidade de vida e aumentar a sobrevida.</p>
    <p>Ao longo do tempo, alguns crit&#233;rios foram identificados e relacionados ao pior progn&#243;stico, dentre eles a classe funcional IV (NYHA), a hiponatremia, hipotens&#227;o arterial, insufici&#234;ncia renal, a ativa&#231;&#227;o exacerbada do sistema neuro-hormonal, o BNP elevado e o perfil cl&#237;nico-hemodin&#226;mico C<sup>1-9</sup>.</p>
    <p>No perfil cl&#237;nico-hemodin&#226;mico proposto por Stevenson<sup>10</sup>, utiliza-se dois par&#226;metros cl&#237;nicos para estratificar os pacientes: congest&#227;o e perfus&#227;o. A congest&#227;o &#233; diagnosticada quando o paciente apresenta os seguintes sinais no exame f&#237;sico: estase de jugular, estertores pulmonares, edema sacral, edema de membros inferiores e hepatomegalia. O diagn&#243;stico de m&#225; perfus&#227;o &#233; feito quando os seguintes sinais est&#227;o presentes: press&#227;o arterial sist&#243;lica sintom&#225;tica menor do que 90 mmHg, m&#225; perfus&#227;o de extremidades, altera&#231;&#227;o do n&#237;vel de consci&#234;ncia e insufici&#234;ncia pr&#233;-renal. Quando o paciente apresenta sinais de congest&#227;o, denomina-se que ele encontra-se com o "padr&#227;o congesto", e na sua aus&#234;ncia de "padr&#227;o seco". Com rela&#231;&#227;o &#224; perfus&#227;o, denominamos quente, se bem perfundido, e frio, se mal perfundido. Seguindo esses crit&#233;rios, podemos encontrar 4 perfis cl&#237;nico-hemodin&#226;micos: perfil A (quente e seco), perfil B (quente e congesto), perfil L (frio e seco) e perfil C (frio e congesto).</p>
    <p>A utiliza&#231;&#227;o dessa classifica&#231;&#227;o cl&#237;nico-hemodin&#226;mica permite orientar a terapia medicamentosa fundamentada no perfil de cada doente e tamb&#233;m permite prognosticar a evolu&#231;&#227;o. Em estudo publicado em 2003, Stevenson e colegas demonstraram que os pacientes com perfil C foram os que tiveram a pior evolu&#231;&#227;o dentre os pacientes que se internaram com IC descompensada<sup>11-13</sup>.</p>
    <p>Estudos brasileiros t&#234;m identificado a cardiomiopatia chag&#225;sica, doen&#231;a muito prevalente em nosso pa&#237;s, como associada a um pior progn&#243;stico, quando comparada &#224;s outras etiologias<sup>14-15</sup>.Em um estudo anterior de nosso grupo, verificamos que os pacientes chag&#225;sicos tiveram pior evolu&#231;&#227;o em compara&#231;&#227;o aos de outras etiologias, no entanto, neste estudo, foram inclu&#237;dos pacientes com a fun&#231;&#227;o ventricular preservada e n&#227;o houve sele&#231;&#227;o quanto ao perfil cl&#237;nico-hemodin&#226;mico<sup>16</sup>. Tamb&#233;m devemos considerar que nos estudos feitos por Stevenson e cols.<sup>11</sup>, com avalia&#231;&#227;o do perfil cl&#237;nico, n&#227;o foram inclu&#237;dos pacientes com cardiomiopatia chag&#225;sica.</p>
    <p>Neste artigo, procuramos preencher tal lacuna no conhecimento, verificando se h&#225; rela&#231;&#227;o entre a etiologia e o progn&#243;stico nos pacientes com perfil cl&#237;nico-hemodin&#226;mico mais grave (tipo C).</p>
    <p>Neste estudo, inclu&#237;mos os pacientes que se internaram com insufici&#234;ncia card&#237;aca com disfun&#231;&#227;o sist&#243;lica descompensada, em classe funcional IV(NYHA) e perfil cl&#237;nico-hemodin&#226;mico C, e procuramos verificar se a evolu&#231;&#227;o dos chag&#225;sicos seria diferente dos pacientes com IC de outras etiologias.</p>
    <p>
      <bold>Material e m&#233;todos</bold>
    </p>
    <p>Este &#233; um estudo do tipo coorte, no qual foram inclu&#237;dos consecutivamente os pacientes que se internaram com IC congestiva descompensada, provenientes do pronto-socorro do Instituto do Cora&#231;&#227;o - HCFMUSP e internados no Hospital Auxiliar de Cotox&#243;. Foram selecionados os pacientes com idade acima de 18 anos, com fra&#231;&#227;o de eje&#231;&#227;o do ventr&#237;culo esquerdo menor do que 45,0% e em perfil C (frio e congesto).</p>
    <p>Na interna&#231;&#227;o, os pacientes foram submetidos &#224; anamnese, &#224; exame f&#237;sico e &#224; coleta de sangue para dosagem s&#233;rica de s&#243;dio, pot&#225;ssio, urueia, creatinina, BNP, hemograma completo e sorologia para doen&#231;a de Chagas.</p>
    <p>Todos os pacientes foram classificados de acordo com o perfil cl&#237;nico-hemodin&#226;mico de Stevenson e selecionamos apenas os que apresentavam sinais de baixo d&#233;bito e congest&#227;o. Os crit&#233;rios adotados para caracteriza&#231;&#227;o do baixo d&#233;bito foram a presen&#231;a de pelo menos dois dos seguintes sinais ou sintomas: PAS (press&#227;o arterial sist&#243;lica) menor do que 90 mmHg sintom&#225;tica, m&#225; perfus&#227;o em extremidades (enchimento capilar lentificado), altera&#231;&#227;o do n&#237;vel de consci&#234;ncia ou insufici&#234;ncia pr&#233;-renal. Na caracteriza&#231;&#227;o da presen&#231;a de congest&#227;o, sendo tamb&#233;m necess&#225;ria a presen&#231;a de pelos menos dois deles, utilizamos os seguintes crit&#233;rios: estase jugular, estertores pulmonares, edema em regi&#227;o sacral, edema de membros inferiores ou hepatomegalia. Tal avalia&#231;&#227;o foi realizada simultaneamente por dois m&#233;dicos especialistas em insufici&#234;ncia card&#237;aca respons&#225;veis pelo estudo.</p>
    <p>Para identifica&#231;&#227;o da etiologia da insufici&#234;ncia card&#237;aca, utilizamos os seguintes crit&#233;rios:</p>
    <p>1) <italic>Isqu&#234;mica -</italic> &#193;rea inativa no eletrocardiograma, hist&#243;ria de revasculariza&#231;&#227;o do mioc&#225;rdio ou obstru&#231;&#227;o coron&#225;ria demonstrada por cineangiocoronariografia;</p>
    <p>2) <italic>Chag&#225;sica -</italic> Foi solicitada sorologia pelo m&#233;todo de ELISA e imunofluoresc&#234;ncia indireta;</p>
    <p>3) <italic>Hipertensiva -</italic> Hist&#243;ria de hipertens&#227;o arterial sist&#234;mica afastando outras causas para cardiomiopatia ;</p>
    <p>4) <italic>Valvopatia -</italic> Altera&#231;&#227;o valvar prim&#225;ria precedendo &#224; cardiomiopatia e afastando outras causas;</p>
    <p>5) <italic>Alco&#243;lica -</italic> Pacientes que relataram ingest&#227;o de bebida alco&#243;lica em grande quantidade, por mais de 10 anos e excluindo outras causas;</p>
    <p>6) <italic>Idiop&#225;tica -</italic> Quando foi afastada qualquer outra causa para cardiomiopatia .</p>
    <p>Para an&#225;lise estat&#237;stica foram utilizados os testes <italic>t</italic> de <italic>Student</italic>, exato de Fisher, qui-quadrado e o programa SPSS. O significante p &lt; 0,05 foi considerado. As curvas de sobreviv&#234;ncia foram feitas com o modelo de Kaplan-Meier<sup>17 </sup>e comparadas pelo m&#233;todo de <italic>log rank</italic>. A raz&#227;o de risco (IC 95,0%) foi calculada pela regress&#227;o de Cox.</p>
    <p>
      <bold>Resultados</bold>
    </p>
    <p>No per&#237;odo de jul/2006-out/2007, no Hospital Auxiliar de Cotox&#243;, foram internados 153 pacientes com IC descompensada e disfun&#231;&#227;o sist&#243;lica, sendo que 100 pacientes (65,0%) apresentaram o perfil C (congest&#227;o e m&#225; perfus&#227;o presentes), 34 pacientes (22,0%) com perfil cl&#237;nico B (congest&#227;o presente e boa perfus&#227;o) e 19 pacientes (12,4%) com perfil L (aus&#234;ncia de congest&#227;o e m&#225; perfus&#227;o presente), conforme mostrado na <xref ref-type="fig" rid="aop10810fig01">Figura 1</xref>. Apenas os pacientes com perfil C foram inclu&#237;dos no estudo e o acompanhamento foi feito por at&#233; 25 meses.</p>
    <p content-type="asset">
      <fig id="aop10810fig01">
        <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gf01.jpg"/></fig>
    </p>
    <p>Na <xref ref-type="table" rid="tab1">Tabela 1</xref>, apresentamos as principais caracter&#237;sticas dos pacientes internados com perfil C, grupo onde 68,0% eram do sexo masculino e 33,0% tinham rea&#231;&#245;es sorol&#243;gicas positivas para doen&#231;a de Chagas. A maioria dos pacientes necessitou da prescri&#231;&#227;o de um inotr&#243;pico para compensa&#231;&#227;o (89,0% dos pacientes).</p>
    <table-wrap id="tab1">
      <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gt01.jpg"/></table-wrap>
    <p>Na <xref ref-type="table" rid="tab2">Tabela 2</xref>, apresentamos as principais caracter&#237;sticas da popula&#231;&#227;o chag&#225;sica (Ch) e da n&#227;o chag&#225;sica (NCh). Constatou-se que os chag&#225;sicos eram mais jovens (52,9 &#177; 4, 5 anos <italic>versus</italic> 59,8 &#177; 14,9; p = 0,03), tinham a fra&#231;&#227;o de eje&#231;&#227;o m&#233;dia do ventr&#237;culo esquerdo (FEVE) menor (20,8 &#177; 7,9% <italic>versus</italic> 25,2 &#177; 8,4%; p = 0,01), a press&#227;o arterial sist&#243;lica m&#233;dia mais baixa 89,3 &#177; 17,1 mmHg <italic>versus</italic> 98,8 &#177; 21,7 mmHg; p = 0,03). O tempo de interna&#231;&#227;o foi semelhante nos dois grupos: Ch 31,6 &#177; 21,3 dias e NCh 27,1 &#177; 18,5 dias; p = 0,3.</p>
    <table-wrap id="tab2">
      <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gt02.jpg"/></table-wrap>
    <p>
      <bold>Dados sobre a mortalidade</bold>
    </p>
    <p>Durante o seguimento da popula&#231;&#227;o estudada, a mortalidade hospitalar foi de 11,0% e a mortalidade ao longo do acompanhamento todo foi de 47,0%. Quando comparamos o grupo de chag&#225;sicos com os n&#227;o chag&#225;sicos, observamos que a mortalidade dos chag&#225;sicos foi maior (Ch 66,7% <italic>versus</italic> NCh 37,3%; p = 0,019) (<xref ref-type="fig" rid="aop10810fig02">Figura 2</xref>).</p>
    <p content-type="asset">
      <fig id="aop10810fig02">
        <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gf02.jpg"/></fig>
    </p>
    <p>Na <xref ref-type="table" rid="tab3">Tabela 3</xref>, apresentamos as principais caracter&#237;sticas dos pacientes que morreram e a dos que permaneceram vivos durante o estudo. Os pacientes que morreram eram mais velhos, tinham a fra&#231;&#227;o de eje&#231;&#227;o mais reduzida, a fun&#231;&#227;o renal mais deteriorada na admiss&#227;o e n&#237;veis de BNP plasm&#225;tico mais elevados.</p>
    <table-wrap id="tab3">
      <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gt03.jpg"/></table-wrap>
    <p>Na an&#225;lise multivariada, identificamos apenas dois marcadores independentes de mau progn&#243;stico: etiologia chag&#225;sica - raz&#227;o de risco de 2,75 (IC 95%, 1,35 - 5,63) e idade - raz&#227;o de risco de 1,045 (IC 95%, 1,02 - 1,07). A fra&#231;&#227;o de eje&#231;&#227;o n&#227;o foi o marcador de pior progn&#243;stico na an&#225;lise multivariada.</p>
    <p>
      <bold>Discuss&#227;o</bold>
    </p>
    <p>Entre os pacientes que foram internados com IC e disfun&#231;&#227;o sist&#243;lica descompensados, aqueles com perfil C (frio e congesto) constituem um grupo mais grave, que apresenta hipotens&#227;o acentuada com maior frequ&#234;ncia, BNP elevado, fun&#231;&#227;o renal deteriorada, hiponatremia e necessidade de suporte inotr&#243;pico positivo para compensa&#231;&#227;o. Esse grupo tem um progn&#243;stico reservado e geralmente necessita de um tempo de interna&#231;&#227;o mais prolongado para a compensa&#231;&#227;o cl&#237;nica.</p>
    <p>A utiliza&#231;&#227;o da classifica&#231;&#227;o cl&#237;nico-hemodin&#226;mica no paciente descompensado vem se mostrando muito &#250;til para orientar o tratamento nessa fase. O paciente que apresenta congest&#227;o sem sinais de m&#225; perfus&#227;o (perfil B) deve ser tratado com diur&#233;tico e vasodilatadores para controlar a hipervolemia e a resist&#234;ncia vascular perif&#233;rica. O paciente que apresenta congest&#227;o associada &#224; m&#225; perfus&#227;o necessita, al&#233;m do tratamento da hipervolemia com diur&#233;ticos, tamb&#233;m de medicamentos que controlem o baixo d&#233;bito card&#237;aco, como os inotr&#243;picos e os vasodilatadores.</p>
    <p>Os estudos que empregaram o perfil cl&#237;nico-hemodin&#226;mico em hospital geral mostraram que o perfil B (quente e congesto) &#233; o mais comum entre os pacientes que se internam com IC descompensada, sendo descrito em cerca de 50,0% dos pacientes hospitalizados para compensa&#231;&#227;o. O perfil C (frio e congesto) &#233; o segundo em frequ&#234;ncia, sendo descrito em cerca de 20,0% dos pacientes, seguido do perfil L (frio e seco), em 3,5%<sup>11-13</sup>. Em nosso servi&#231;o, um centro de refer&#234;ncia no tratamento da insufici&#234;ncia card&#237;aca, os n&#250;meros s&#227;o substancialmente diferentes, sendo o perfil C o mais frequente identificado e que atinge, aproximadamente, 65,0% dos doentes internados.</p>
    <p>Nessa popula&#231;&#227;o, onde estudamos a mortalidade hospitalar (11,0%) e a do seguimento (47,0%), ambos os desfechos foram elevados. Em trabalho anterior do nosso grupo, j&#225; hav&#237;amos documentado que a mortalidade dos pacientes que s&#227;o tratados em nosso hospital &#233; alta e maior do que a descrita em registros e muitas coortes<sup>18</sup>. Essa maior mortalidade decorre, provavelmente, da maior intensidade das manifesta&#231;&#245;es cl&#237;nicas e da gravidade da cardiopatia dos pacientes que procuram e s&#227;o internados em um hospital terci&#225;rio. No estudo anterior<sup>18</sup>, a mortalidade dos pacientes hospitalizados entre os anos de 2005-2006 foi de 8,8%, &#237;ndice que &#233; maior do que o descrito no Registro ADHERE<sup>9</sup> (4,0%). Entretanto, quando estratificamos os pacientes conforme a gravidade, pudemos verificar que em nosso hospital 75,6% internaram-se com PA sist&#243;lica abaixo de 115 mmHg contra 18,5% no Registro ADHERE. Comparando a evolu&#231;&#227;o dos pacientes mais graves no Registro ADHERE, a mortalidade foi de 20,9 % e a nossa 16,9%, mostrando n&#227;o haver diferen&#231;a expressiva quando se compara pacientes de gravidade semelhante. A mortalidade de 11,0% deste estudo atual, mais alta do que a do estudo de 2005/2006, tamb&#233;m deve estar relacionada &#224; sele&#231;&#227;o dos pacientes, uma vez que para o estudo atual selecionamos somente os pacientes com perfil mais grave (perfil C).</p>
    <p>A cardiomiopatia pela doen&#231;a de Chagas continua sendo uma afec&#231;&#227;o ainda muito prevalente no Brasil, inclusive em S&#227;o Paulo. O comprometimento do m&#250;sculo card&#237;aco nessa doen&#231;a &#233; complexo, envolvendo respostas auto-imunes, comprometimento do mioc&#225;rdio, do sistema nervoso aut&#244;nomo e um intenso processo inflamat&#243;rio. Quando se compara a evolu&#231;&#227;o dos pacientes com cardiomiopatia chag&#225;sica com a de outras etiologias, constata-se que o progn&#243;stico dos chag&#225;sicos em casos sintom&#225;ticos &#233; pior.</p>
    <p>Rassi Jr e cols.<sup>19</sup>, numa popula&#231;&#227;o predominantemente ambulatorial, identificaram alguns preditores de mortalidade em pacientes com cardiomiopatia chag&#225;sica: classe funcional III e IV (NYHA), evid&#234;ncia de cardiomegalia na radiografia de t&#243;rax, disfun&#231;&#227;o ventricular esquerda pelo ecocardiograma, evid&#234;ncia de taquicardia ventricular n&#227;o sustentada ao Holter, baixa voltagem do QRS no eletrocardiograma e sexo masculino. Nesse estudo de Rassi Jr e cols., apenas 10,4% dos pacientes apresentavam classe funcional III e IV, dado que caracteriza que esta popula&#231;&#227;o era constitu&#237;da por pacientes com cardiopatia menos grave do que a inclu&#237;da em nosso trabalho. Em outro estudo, Freitas e cols.<sup>14</sup> tamb&#233;m relacionaram a etiologia chag&#225;sica com pior progn&#243;stico, mas, para esta avalia&#231;&#227;o, foram usados pacientes ambulatoriais, que tamb&#233;m apresentam um perfil cl&#237;nico menos grave.</p>
    <p>No estudo de Stevenson e cols., foi observado uma mortalidade de aproximadamente 40% no primeiro ano de seguimento para os pacientes com perfil C. Em nosso estudo, a mortalidade dos pacientes n&#227;o chag&#225;sicos foi semelhante ao encontrado por Stevenson, mas a dos chag&#225;sicos foi maior, com cerca de 60,0% dos pacientes morrendo no primeiro ano de seguimento. Apesar dos pacientes chag&#225;sicos terem pior progn&#243;stico, eles apresentaram n&#237;veis de ureia e creatinina melhores que os n&#227;o chag&#225;sicos. Um fato que pode colaborar para esta fun&#231;&#227;o renal melhor &#233; a idade dos pacientes chag&#225;sicos, que eram significativamente mais jovens que os NCh.</p>
    <p>Na &#250;ltima d&#233;cada, estamos observando o aumento do n&#250;mero de publica&#231;&#245;es sobre IC descompensada, o que melhora o entendimento nesta fase mais cr&#237;tica da doen&#231;a. Na diretriz brasileira sobre IC aguda, publicada em 2009<sup>20</sup>, os seguintes marcadores cl&#237;nicos e hemodin&#226;micos s&#227;o destacados como de pior progn&#243;stico: baixo d&#233;bito card&#237;aco, congest&#227;o refrat&#225;ria, insufici&#234;ncia renal, terceira bulha persistente e hipotens&#227;o arterial. Com rela&#231;&#227;o &#224; etiologia, a diretriz cita que a etiologia &#233; um prov&#225;vel fator de mau progn&#243;stico, mas n&#227;o existem evid&#234;ncias mais consistentes<sup>20</sup>.</p>
    <p>Revisando a literatura, constatamos que at&#233; o momento nenhum estudo comparou especificamente a evolu&#231;&#227;o dos pacientes chag&#225;sicos e n&#227;o chag&#225;sicos com IC avan&#231;ada, e que, no momento da interna&#231;&#227;o, apresentavam o perfil C. Este estudo preencheu esta lacuna e revelou que a etiologia chag&#225;sica &#233; fator independente de pior progn&#243;stico tamb&#233;m na fase mais avan&#231;ada da insufici&#234;ncia card&#237;aca com disfun&#231;&#227;o sist&#243;lica.</p>
    <p>Os nossos dados indicam que todos os pacientes com IC avan&#231;ada merecem um tratamento agressivo, uma vez que a IC &#233; uma doen&#231;a com caracter&#237;sticas malignas e que o tratamento moderno pode modificar esta evolu&#231;&#227;o. Entretanto, devemos lembrar que o grupo de pacientes chag&#225;sicos tem um progn&#243;stico ainda pior. Apesar do avan&#231;o da medicina nessa &#225;rea, o paciente com cardiomiopatia chag&#225;sica continua sendo um grande desafio na pr&#225;tica cl&#237;nica di&#225;ria.</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="correspbaixo" fn-type="corresp">
        <label>
          <bold>Correspond&#234;ncia:</bold>
        </label>
        <p> Juliano Novaes Cardoso </p>
        <p> Rua Joaquin Ferreira, 147/161 bloco Perdizes - &#193;gua Branca </p>
        <p> 05033-080 - S&#227;o Paulo, SP - Brasil </p>
        <p> E-mail: </p>
        <p><email xlink:href="julianonc@cardiol.br">julianonc@cardiol.br</email>, </p>
        <p>
          <email xlink:href="juliano.cardoso@incor.usp.br">juliano.cardoso@incor.usp.br</email>
        </p>
      </fn>
    </p>
    <p>Artigo recebido em 03/11/09; revisado recebido em 10/03/10; aceito em 08/04/10</p>
    <p>Full texts in English - <ext-link ext-link-type="uri" xlink:href="http://www.arquivosonline.com.br">http://www.arquivosonline.com.br</ext-link></p>
  </body>
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  <sub-article article-type="translation" id="TRes" xml:lang="es">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Art&#237;culos Originales</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="es">Cardiomiopat&#237;a chag&#225;sica: pron&#243;stico en el perfil cl&#237;nico-hemodin&#225;mico C</article-title>
      </title-group>
      <abstract xml:lang="es">
        <p>FUNDAMENTO: Los pacientes con insuficiencia card&#237;aca (IC) que son internados presentando mala perfusi&#243;n y congesti&#243;n (perfil cl&#237;nico-hemodin&#225;mico C) constituyen el grupo que evoluciona con peor pron&#243;stico en la IC descompensada. Mientras tanto, hay poca informaci&#243;n en la literatura sobre si la etiolog&#237;a de la cardiopat&#237;a influencia en la evoluci&#243;n de los pacientes en la fase avanzada. OBJETIVO: Evaluar la evoluci&#243;n de los pacientes que se internaron con perfil cl&#237;nico-hemodin&#225;mico C y verificar el papel de la etiolog&#237;a en esta fase. M&#201;TODOS: Un estudio de cohorte fue realizado incluyendo pacientes con fracci&#243;n de eyecci&#243;n del ventr&#237;culo izquierdo (FEVI) &lt; 45,0%, clase funcional IV e internaci&#243;n hospitalaria presentando perfil cl&#237;nico-hemodin&#225;mico C. El grupo fue dividido en pacientes portadores de cardiomiopat&#237;a chag&#225;sica (Ch) y no chag&#225;sica (NCh). Para an&#225;lisis estad&#237;stico fueron utilizados los test t de Student, exacto de Fisher, qui-cuadrado y el programa SPSS. El significante de p &lt; 0,05 fue considerado. RESULTADOS: Cien pacientes, con edad media de 57,6 &#177; 15,1 a&#241;os y FEVI media de 23,8 &#177; 8,5%, fueron incluidos. Entre los pacientes estudiados, 33,0% eran chag&#225;sicos y, en la comparaci&#243;n con los NCh, presentaron menor presi&#243;n arterial sist&#243;lica (Ch 89,3 &#177; 17,1 mmHg versus NCh 98,8 &#177; 21,7 mmHg; p = 0,03) y menor edad media - Ch 52,9 &#177; 14,5 a&#241;os versus NCh 59,8 &#177; 14,9 a&#241;os; p = 0,03). Durante el control de 25 meses, la mortalidad fue de 66,7% en los Ch y de 37,3% en los NCh (p = 0,019). La etiolog&#237;a chag&#225;sica fue un marcador independiente de mal pron&#243;stico en el an&#225;lisis multivariado con raz&#243;n de riesgo de 2,75 (IC 95,0%; 1,35 - 5,63). CONCLUSI&#211;N: En los pacientes con IC avanzada, la etiolog&#237;a chag&#225;sica es un importante predictor de peor pron&#243;stico.</p>
      </abstract>
      <kwd-group xml:lang="es">
        <kwd>Insuficiencia card&#237;aca</kwd>
        <kwd>pron&#243;stico</kwd>
        <kwd>reperfusi&#243;n</kwd>
        <kwd>cardiomiopat&#237;a chag&#225;sica</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>
        <bold>ART&#205;CULO ORIGINAL</bold>
      </p>
      <p>
        <fn id="top-body2">
          <label>
            <bold>Cardiomiopat&#237;a chag&#225;sica: pron&#243;stico en el perfil cl&#237;nico-hemodin&#225;mico C</bold>
          </label>
          <p>
            <bold>Juliano Cardoso; Milena Novaes; Marcelo Ochiai; Kelly Regina; Paulo Morgado; Robinson Munhoz; Euler Brancalh&#227;o; Marcelo Lima; Antonio Carlos Pereira Barretto</bold>
          </p>
        </fn>
      </p>
      <p>InCor - Hospital de Cotox&#243; - HCFMUSP, S&#227;o Paulo, SP - Brasil</p>
      <p>Correspondencia</p>
      <p>
        <bold>RESUMEN</bold>
      </p>
      <p><bold>FUNDAMENTO:</bold> Los pacientes con insuficiencia card&#237;aca (IC) que son internados presentando mala perfusi&#243;n y congesti&#243;n (perfil cl&#237;nico-hemodin&#225;mico C) constituyen el grupo que evoluciona con peor pron&#243;stico en la IC descompensada. Mientras tanto, hay poca informaci&#243;n en la literatura sobre si la etiolog&#237;a de la cardiopat&#237;a influencia en la evoluci&#243;n de los pacientes en la fase avanzada.</p>
      <p><bold>OBJETIVO:</bold> Evaluar la evoluci&#243;n de los pacientes que se internaron con perfil cl&#237;nico-hemodin&#225;mico C y verificar el papel de la etiolog&#237;a en esta fase.</p>
      <p><bold>M&#201;TODOS:</bold> Un estudio de cohorte fue realizado incluyendo pacientes con fracci&#243;n de eyecci&#243;n del ventr&#237;culo izquierdo (FEVI) &lt; 45,0%, clase funcional IV e internaci&#243;n hospitalaria presentando perfil cl&#237;nico-hemodin&#225;mico C. El grupo fue dividido en pacientes portadores de cardiomiopat&#237;a chag&#225;sica (Ch) y no chag&#225;sica (NCh). Para an&#225;lisis estad&#237;stico fueron utilizados los test t de Student, exacto de Fisher, qui-cuadrado y el programa SPSS. El significante de p &lt; 0,05 fue considerado.</p>
      <p><bold>RESULTADOS:</bold> Cien pacientes, con edad media de 57,6 &#177; 15,1 a&#241;os y FEVI media de 23,8 &#177; 8,5%, fueron incluidos. Entre los pacientes estudiados, 33,0% eran chag&#225;sicos y, en la comparaci&#243;n con los NCh, presentaron menor presi&#243;n arterial sist&#243;lica (Ch 89,3 &#177; 17,1 mmHg <italic>versus</italic> NCh 98,8 &#177; 21,7 mmHg; p = 0,03) y menor edad media - Ch 52,9 &#177; 14,5 a&#241;os <italic>versus</italic> NCh 59,8 &#177; 14,9 a&#241;os; p = 0,03). Durante el control de 25 meses, la mortalidad fue de 66,7% en los Ch y de 37,3% en los NCh (p = 0,019). La etiolog&#237;a chag&#225;sica fue un marcador independiente de mal pron&#243;stico en el an&#225;lisis multivariado con raz&#243;n de riesgo de 2,75 (IC 95,0%; 1,35 - 5,63).</p>
      <p><bold>CONCLUSI&#211;N:</bold> En los pacientes con IC avanzada, la etiolog&#237;a chag&#225;sica es un importante predictor de peor pron&#243;stico.</p>
      <p><bold>Palabras clave:</bold> Insuficiencia card&#237;aca/complicaciones, pron&#243;stico, reperfusi&#243;n, cardiomiopat&#237;a chag&#225;sica.</p>
      <p>
        <bold>Introducci&#243;n</bold>
      </p>
      <p>El avance de la medicina viene mejorando el conocimiento sobre la insuficiencia card&#237;aca (IC), posibilitando el desarrollo de nuevos m&#233;todos diagn&#243;sticos, la determinaci&#243;n de factores pron&#243;sticos y la instituci&#243;n de tratamientos m&#225;s efectivos que mejoran su evoluci&#243;n. Mientras tanto, la IC contin&#250;a siendo una enfermedad prevalente y con pron&#243;stico reservado, principalmente en las fases avanzadas de la enfermedad.</p>
      <p>En tal contexto, es importante identificar las caracter&#237;sticas cl&#237;nicas y de laboratorio de los pacientes con IC descompensada, que permitan determinar aquellos con tendencia al peor pron&#243;stico. Esto posibilita adoptar medidas espec&#237;ficas y adecuadas en el tratamiento de ese grupo para mejorar la calidad de vida y aumentar la sobrevida.</p>
      <p>A lo largo del tiempo, algunos criterios fueron identificados y relacionados al peor pron&#243;stico, entre ellos la clase funcional IV (NYHA), la hiponatremia, hipotensi&#243;n arterial, insuficiencia renal, la activaci&#243;n exacerbada del sistema neuro-hormonal, el BNP elevado y el perfil cl&#237;nico-hemodin&#225;mico C<sup>1-9</sup>.</p>
      <p>En el perfil cl&#237;nico-hemodin&#225;mico propuesto por Stevenson<sup>10</sup>, se utilizan dos par&#225;metros cl&#237;nicos para estratificar los pacientes: congesti&#243;n y perfusi&#243;n. La congesti&#243;n es diagnosticada cuando el paciente presenta los siguientes se&#241;ales en el examen f&#237;sico: estasis de yugular, estertores pulmonares, edema sacro, edema de miembros inferiores y hepatomegalia. El diagn&#243;stico de mala perfusi&#243;n es hecho cuando las siguientes se&#241;ales est&#225;n presentes: presi&#243;n arterial sist&#243;lica sintom&#225;tica menor que 90 mmHg, mala perfusi&#243;n de extremidades, alteraci&#243;n del nivel de conciencia e insuficiencia prerrenal. Cuando el paciente presenta se&#241;ales de congesti&#243;n, denom&#237;nase que se encuentra con el "est&#225;ndar congestionado", y en su ausencia de "est&#225;ndar seco". Con relaci&#243;n a la perfusi&#243;n, la denominamos caliente, si est&#225; bien perfundido, y fr&#237;o, si est&#225; mal perfundido. Siguiendo esos criterios, podemos encontrar 4 perfiles cl&#237;nico-hemodin&#225;micos: perfil A (caliente y seco), perfil B (caliente y congestionado), perfil L (fr&#237;o y seco) y perfil C (fr&#237;o y congestionado).</p>
      <p>La utilizaci&#243;n de esa clasificaci&#243;n cl&#237;nico-hemodin&#225;mica permite orientar la terapia medicamentosa fundamentada en el perfil de cada enfermo y tambi&#233;n permite pronosticar la evoluci&#243;n. En estudio publicado en 2003, Stevenson y colegas demostraron que los pacientes con perfil C fueron los que tuvieron la peor evoluci&#243;n entre los pacientes que se internaron con IC descompensada<sup>11-13</sup>.</p>
      <p>Estudios brasile&#241;os han identificado la cardiomiopat&#237;a chag&#225;sica, enfermedad muy prevalente en nuestro pa&#237;s, como asociada a un peor pron&#243;stico, cuando es comparada a las otras etiolog&#237;as<sup>14-15</sup>. En un estudio anterior de nuestro grupo, verificamos que los pacientes chag&#225;sicos tuvieron peor evoluci&#243;n en comparaci&#243;n a los de otras etiolog&#237;as, mientras tanto, en este estudio, fueron incluidos pacientes con la funci&#243;n ventricular preservada y no hubo selecci&#243;n en cuanto al perfil cl&#237;nico-hemodin&#225;mico<sup>16</sup>. Tambi&#233;n debemos considerar que en los estudios hechos por Stevenson et al<sup>11</sup>, con evaluaci&#243;n del perfil cl&#237;nico, no fueron incluidos pacientes con cardiomiopat&#237;a chag&#225;sica.</p>
      <p>En este art&#237;culo, procuramos llenar tal laguna del conocimiento, verificando si hay relaci&#243;n entre la etiolog&#237;a y el pron&#243;stico en los pacientes con perfil cl&#237;nico-hemodin&#225;mico m&#225;s grave (tipo C).</p>
      <p>En este estudio, incluimos los pacientes que se internaron con insuficiencia card&#237;aca con disfunci&#243;n sist&#243;lica descompensada, en clase funcional IV(NYHA) y perfil cl&#237;nico-hemodin&#225;mico C, y procuramos verificar si la evoluci&#243;n de los chag&#225;sicos ser&#237;a diferente de los pacientes con IC de otras etiolog&#237;as.</p>
      <p>
        <bold>Material y m&#233;todos</bold>
      </p>
      <p>Este es un estudio del tipo cohorte, en el cual fueron incluidos consecutivamente los pacientes que se internaron con IC congestiva descompensada, provenientes del Pronto-Socorro del Instituto do Cora&#231;&#227;o - HCFMUSP e internados en el Hospital Auxiliar de Cotox&#243;. Fueron seleccionados los pacientes con edad encima de 18 a&#241;os, con fracci&#243;n de eyecci&#243;n del ventr&#237;culo izquierdo menor que 45,0% y en perfil C (fr&#237;o y congestionado).</p>
      <p>En la internaci&#243;n, los pacientes fueron sometidos a anamnesis, a examen f&#237;sico y a recolecci&#243;n de sangre para dosaje s&#233;rica de sodio, potasio, urea, creatinina, BNP, hemograma completo y serolog&#237;a para enfermedad de Chagas.</p>
      <p>Todos los pacientes fueron clasificados de acuerdo con el perfil cl&#237;nico-hemodin&#225;mico de Stevenson y seleccionamos apenas los que presentaban se&#241;ales de bajo d&#233;bito y congesti&#243;n. Los criterios adoptados para caracterizaci&#243;n del bajo d&#233;bito fueron la presencia de por lo menos dos de las siguientes se&#241;ales o s&#237;ntomas: PAS (presi&#243;n arterial sist&#243;lica) menor que 90 mmHg sintom&#225;tica, mala perfusi&#243;n en extremidades (llenado capilar lentificado), alteraci&#243;n del nivel de conciencia o insuficiencia prerrenal. En la caracterizaci&#243;n de la presencia de congesti&#243;n, siendo tambi&#233;n necesaria la presencia de por lo menos dos de ellos, utilizamos los siguientes criterios: estasis yugular, estertores pulmonares, edema en regi&#243;n sacra, edema de miembros inferiores o hepatomegalia. Tal evaluaci&#243;n fue realizada simult&#225;neamente por dos m&#233;dicos especialistas en insuficiencia card&#237;aca responsables por el estudio.</p>
      <p>Para identificaci&#243;n de la etiolog&#237;a de la insuficiencia card&#237;aca, utilizamos los siguientes criterios:</p>
      <p>1) Isqu&#233;mica: &#193;rea inactiva en el electrocardiograma, historia de revascularizaci&#243;n del miocardio o obstrucci&#243;n coronaria demostrada por cineangiocoronariograf&#237;a;</p>
      <p>2) Chag&#225;sica: Fue solicitada serolog&#237;a por el m&#233;todo de ELISA e inmunofluorescencia indirecta;</p>
      <p>3) Hipertensiva: Historia de hipertensi&#243;n arterial sist&#233;mica descartando otras causas para cardiomiopat&#237;a ;</p>
      <p>4) Valvulopat&#237;a: Alteraci&#243;n valvar primaria precediendo a la cardiomiopat&#237;a y apartando otras causas;</p>
      <p>5) Alcoh&#243;lica: Pacientes que relataron ingesti&#243;n de bebida alcoh&#243;lica en gran cantidad, por m&#225;s de 10 a&#241;os y excluyendo otras causas;</p>
      <p>6) Idiop&#225;tica: Cuando fue descartada cualquier otra causa para cardiomiopat&#237;a.</p>
      <p>Para an&#225;lisis estad&#237;stico fueron utilizados los test <italic>t</italic> de <italic>Student</italic>, exacto de Fisher, qui-cuadrado y el programa SPSS. El significante p &lt; 0,05 fue considerado. Las curvas de supervivencia fueron hechas con el modelo de Kaplan-Meier<sup>17</sup> y comparadas por el m&#233;todo de log rank. La raz&#243;n de riesgo (IC 95,0%) fue calculada por la regresi&#243;n de Cox.</p>
      <p>
        <bold>Resultados</bold>
      </p>
      <p>En el per&#237;odo de jul/2006-oct/2007, en el Hospital Auxiliar de Cotox&#243;, fueron internados 153 pacientes con IC descompensada y disfunci&#243;n sist&#243;lica, siendo que 100 pacientes (65,0%) presentaron el perfil C (congesti&#243;n y mala perfusi&#243;n presentes), 34 pacientes (22,0%) con perfil cl&#237;nico B (congesti&#243;n presente y buena perfusi&#243;n) y 19 pacientes (12,4%) con perfil L (ausencia de congesti&#243;n y mala perfusi&#243;n presente), seg&#250;n mostrado en la <xref ref-type="fig" rid="f1-body2">Figura 1</xref>. Apenas los pacientes con perfil C fueron incluidos en el estudio y el control fue hecho por hasta 25 meses.</p>
      <fig id="f1-body2">
        <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gf01-es.jpg"/></fig>
      <p>En la <xref ref-type="table" rid="t1-body2">Tabla 1</xref>, presentamos las principales caracter&#237;sticas de los pacientes internados con perfil C, grupo donde 68,0% eran del sexo masculino y 33,0% ten&#237;an reacciones serol&#243;gicas positivas para enfermedad de Chagas. La mayor&#237;a de los pacientes necesit&#243; la prescripci&#243;n de un inotr&#243;pico para compensaci&#243;n (89,0% de los pacientes).</p>
      <table-wrap id="t1-body2">
        <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gt01-es.jpg"/></table-wrap>
      <p>En la <xref ref-type="table" rid="t2-body2">Tabla 2</xref>, presentamos las principales caracter&#237;sticas de la poblaci&#243;n chag&#225;sica (Ch) y de la no chag&#225;sica (NCh). Se constat&#243; que los chag&#225;sicos eran m&#225;s j&#243;venes (52,9 &#177; 4,5 a&#241;os <italic>versus</italic> 59,8 &#177; 14,9; p = 0,03), ten&#237;an la fracci&#243;n de eyecci&#243;n media del ventr&#237;culo izquierdo (FEVI) menor (20,8 &#177; 7,9% <italic>versus</italic> 25,2 &#177; 8,4%; p = 0,01), la presi&#243;n arterial sist&#243;lica media m&#225;s baja 89,3 &#177; 17,1 mmHg <italic>versus</italic> 98,8 &#177; 21,7 mmHg; p = 0,03). El tiempo de internaci&#243;n fue semejante en los dos grupos: Ch 31,6 &#177; 21,3 d&#237;as y NCh 27,1 &#177; 18,5 d&#237;as; p = 0,3.</p>
      <table-wrap id="t2-body2">
        <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gt02-es.jpg"/></table-wrap>
      <p>
        <bold>Datos sobre la mortalidad</bold>
      </p>
      <p>Durante el control de la poblaci&#243;n estudiada, la mortalidad hospitalaria fue de 11,0% y la mortalidad a lo largo de todo el control fue de 47,0%. Cuando comparamos el grupo de chag&#225;sicos con los no chag&#225;sicos, observamos que la mortalidad de los chag&#225;sicos fue mayor (Ch 66,7% <italic>versus</italic> NCh 37,3%; p = 0,019) (<xref ref-type="fig" rid="f2-body2">Figura 2</xref>).</p>
      <fig id="f2-body2">
        <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gf02-es.jpg"/></fig>
      <p>En la <xref ref-type="table" rid="t3-body2">Tabla 3</xref>, presentamos las principales caracter&#237;sticas de los pacientes que murieron y la de los que permanecieron vivos durante el estudio. Los pacientes que murieron eran mayores, ten&#237;an la fracci&#243;n de eyecci&#243;n m&#225;s reducida, la funci&#243;n renal m&#225;s deteriorada en la admisi&#243;n y niveles de BNP plasm&#225;tico m&#225;s elevados.</p>
      <table-wrap id="t3-body2">
        <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gt03-es.jpg"/></table-wrap>
      <p>En el an&#225;lisis multivariado, identificamos apenas dos marcadores independientes de mal pron&#243;stico: etiolog&#237;a chag&#225;sica - raz&#243;n de riesgo de 2,75 (IC 95%, 1,35 - 5,63) y edad - raz&#243;n de riesgo de 1,045 (IC 95%, 1,02 - 1,07). La fracci&#243;n de eyecci&#243;n no fue el marcador de peor pron&#243;stico en el an&#225;lisis multivariado.</p>
      <p>
        <bold>Discusi&#243;n</bold>
      </p>
      <p>Entre los pacientes que fueron internados con IC y disfunci&#243;n sist&#243;lica descompensados, aquellos con perfil C (fr&#237;o y congestionado) constituyen un grupo m&#225;s grave, que presenta hipotensi&#243;n acentuada con mayor frecuencia, BNP elevado, funci&#243;n renal deteriorada, hiponatremia y necesidad de soporte inotr&#243;pico positivo para compensaci&#243;n. Ese grupo tiene un pron&#243;stico reservado y generalmente necesita de un tiempo de internaci&#243;n m&#225;s prolongado para la compensaci&#243;n cl&#237;nica.</p>
      <p>La utilizaci&#243;n de la clasificaci&#243;n cl&#237;nico-hemodin&#225;mica en el paciente descompensado viene mostr&#225;ndose muy &#250;til para orientar el tratamiento en esa fase. El paciente que presenta congesti&#243;n sin se&#241;ales de mala perfusi&#243;n (perfil B) debe ser tratado con diur&#233;tico y vasodilatadores para controlar la hipervolemia y la resistencia vascular perif&#233;rica. El paciente que presenta congesti&#243;n asociada a mala perfusi&#243;n necesita, adem&#225;s del tratamiento de la hipervolemia con diur&#233;ticos, tambi&#233;n de medicamentos que controlen el bajo d&#233;bito card&#237;aco, como los inotr&#243;picos y los vasodilatadores.</p>
      <p>Los estudios que emplearon el perfil cl&#237;nico-hemodin&#225;mico en hospital general mostraron que el perfil B (caliente y congestionado) es el m&#225;s com&#250;n entre los pacientes que se internan con IC descompensada, siendo descripto en cerca de 50,0% de los pacientes hospitalizados para compensaci&#243;n. El perfil C (fr&#237;o y congestionado) es el segundo en frecuencia, siendo descripto en cerca de 20,0% de los pacientes, seguido del perfil L (fr&#237;o y seco), en 3,5%<sup>11-13</sup>. En nuestro servicio, un centro de referencia en el tratamiento de la insuficiencia card&#237;aca, los n&#250;meros son sustancialmente diferentes, siendo el perfil C el m&#225;s frecuentemente identificado y que alcanza, aproximadamente, al 65,0% de los enfermos internados.</p>
      <p>En esa poblaci&#243;n, donde estudiamos la mortalidad intrahospitalaria (11,0%) y la de control (47,0%), ambos desenlaces fueron elevados. En trabajo anterior de nuestro grupo, ya hab&#237;amos documentado que la mortalidad de los pacientes que son tratados en nuestro hospital es alta y mayor que la descripta en registros y muchas cohortes<sup>18</sup>. Esa mayor mortalidad proviene, probablemente, de la mayor intensidad de las manifestaciones cl&#237;nicas y de la gravedad de la cardiopat&#237;a de los pacientes que buscan y son internados en un hospital terciario. En el estudio anterior<sup>18</sup>, la mortalidad de los pacientes hospitalizados entre los a&#241;os 2005-2006 fue de 8,8%, &#237;ndice que es mayor que el descripto en el Registro ADHERE<sup>9</sup> (4,0%). Mientras tanto, cuando estratificamos los pacientes seg&#250;n la gravedad, pudimos verificar que en nuestro hospital 75,6% se internaron con PA sist&#243;lica abajo de 115 mmHg contra 18,5% en el Registro ADHERE. Comparando la evoluci&#243;n de los pacientes m&#225;s graves en el Registro ADHERE, la mortalidad fue de 20,9 % y la nuestra 16,9%, mostrando no haber diferencia significativa cuando se compara pacientes de gravedad semejante. La mortalidad de 11,0% de este estudio actual, m&#225;s alta que la del estudio de 2005/2006, tambi&#233;n debe estar relacionada a la selecci&#243;n de los pacientes, una vez que para el estudio actual seleccionamos solamente los pacientes con perfil m&#225;s grave (perfil C).</p>
      <p>La cardiomiopat&#237;a por la enfermedad de Chagas contin&#250;a siendo una afecci&#243;n aun muy prevalente en el Brasil, inclusive en S&#227;o Paulo. El compromiso del m&#250;sculo card&#237;aco en esa enfermedad es complejo, envolviendo respuestas autoinmunes, compromiso del miocardio, del sistema nervioso aut&#243;nomo y un intenso proceso inflamatorio. Cuando se compara la evoluci&#243;n de los pacientes con cardiomiopat&#237;a chag&#225;sica con la de otras etiolog&#237;as, se constata que el pron&#243;stico de los chag&#225;sicos en casos sintom&#225;ticos es peor.</p>
      <p>Rassi Jr et al<sup>19</sup>, en una poblaci&#243;n predominantemente ambulatoria, identificaron algunos predictores de mortalidad en pacientes con cardiomiopat&#237;a chag&#225;sica: clase funcional III y IV (NYHA), evidencia de cardiomegalia en la radiograf&#237;a de t&#243;rax, disfunci&#243;n ventricular izquierda por el ecocardiograma, evidencia de taquicardia ventricular no sustentada al Holter, bajo voltaje del QRS en el electrocardiograma y sexo masculino. En ese estudio de Rassi Jr et al, apenas 10,4% de los pacientes presentaban clase funcional III y IV, dato que caracteriza que esta poblaci&#243;n era constituida por pacientes con cardiopat&#237;a menos grave que la incluida en nuestro trabajo. En otro estudio, Freitas et al<sup>14</sup> tambi&#233;n relacionaron la etiolog&#237;a chag&#225;sica con peor pron&#243;stico, pero, para esta evaluaci&#243;n, fueron usados pacientes ambulatorios, que tambi&#233;n presentan un perfil cl&#237;nico menos grave.</p>
      <p>En el estudio de Stevenson et al, fue observada una mortalidad de aproximadamente 40% en el primer a&#241;o de control para los pacientes con perfil C. En nuestro estudio, la mortalidad de los pacientes no chag&#225;sicos fue semejante al encontrado por Stevenson, pero la de los chag&#225;sicos fue mayor, con cerca de 60,0% de los pacientes muriendo en el primer a&#241;o de control. A pesar de que los pacientes chag&#225;sicos ten&#237;an peor pron&#243;stico, presentaron niveles de urea y creatinina mejores que los no chag&#225;sicos. Un hecho que puede colaborar para esta funci&#243;n renal mejor, es la edad de los pacientes chag&#225;sicos, que eran significativamente m&#225;s j&#243;venes que los NCh.</p>
      <p>En la &#250;ltima d&#233;cada, estamos observando el aumento del n&#250;mero de publicaciones sobre IC descompensada, lo que mejora el entendimiento en esta fase m&#225;s cr&#237;tica de la enfermedad. En la directriz brasile&#241;a sobre IC aguda, publicada en 2009<sup>20</sup>, los siguientes marcadores cl&#237;nicos y hemodin&#225;micos son destacados como de peor pron&#243;stico: bajo d&#233;bito card&#237;aco, congesti&#243;n refractaria, insuficiencia renal, tercer ruido persistente e hipotensi&#243;n arterial. Con relaci&#243;n a la etiolog&#237;a, la directriz cita que la etiolog&#237;a es un probable factor de mal pron&#243;stico, pero no existen evidencias m&#225;s consistentes<sup>20</sup>.</p>
      <p>Revisando la literatura, constatamos que hasta el momento ning&#250;n estudio compar&#243; espec&#237;ficamente la evoluci&#243;n de los pacientes chag&#225;sicos y no chag&#225;sicos con IC avanzada, y que, en el momento de la internaci&#243;n, presentaban el perfil C. Este estudio llen&#243; esta laguna y revel&#243; que la etiolog&#237;a chag&#225;sica es factor independiente de peor pron&#243;stico tambi&#233;n en la fase m&#225;s avanzada de la insuficiencia card&#237;aca con disfunci&#243;n sist&#243;lica.</p>
      <p>Nuestros datos indican que todos los pacientes con IC avanzada merecen un tratamiento agresivo, una vez que la IC es una enfermedad con caracter&#237;sticas malignas y que el tratamiento moderno puede modificar esta evoluci&#243;n. Mientras tanto, debemos recordar que el grupo de pacientes chag&#225;sicos tiene un pron&#243;stico aun peor. A pesar del avance de la medicina en esa &#225;rea, el paciente con cardiomiopat&#237;a chag&#225;sica contin&#250;a siendo un gran desaf&#237;o en la pr&#225;ctica cl&#237;nica diaria.</p>
      <p>
        <bold>Potencial Conflicto de Intereses</bold>
      </p>
      <p>Declaro no haber conflicto de intereses pertinentes.</p>
      <p>
        <bold>Fuentes de Financiamiento</bold>
      </p>
      <p>EL presente estudio no tuvo fuentes de financiamiento externas.</p>
      <p>
        <bold>Vinculaci&#243;n Acad&#233;mica</bold>
      </p>
      <p>No hay vinculaci&#243;n de este estudio a programas de post-grado.</p>
      <p>
        <bold>Referencias</bold>
      </p>
    </body>
  </sub-article>
  <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">Chagas cardiomyopathy: prognosis in clinical and hemodynamic profile C</article-title>
      </title-group>
      <abstract xml:lang="en">
        <p>BACKGROUND: Patients with heart failure (HF) who are admitted showing poor perfusion and congestion (clinical-hemodynamic profile C) are the group that evolves with the worst prognosis in decompensated heart failure. However, there is little information in literature on the etiology of cardiopathy influences the outcome of patients in advanced stage. OBJECTIVE: To assess the outcome of patients admitted with clinical and hemodynamic profile C and verify the role of the etiology in this phase. METHODS: A cohort study was performed including patients with left ventricle ejection fraction (LVEF) &lt; 45.0%, functional class IV and hospitalization presenting clinical-hemodynamic profile C. The group was divided into patients with chagasic (Ch) and non chagasic (NCh) cardiomyopathy. Statistical analysis used Student t test, Fisher exact test, chi-square and SPSS tests. The significance of p &lt; 0.05 was considered. RESULTS: One hundred patients, with mean age 57.6 &#177; 15.1 years and mean LVEF of 23.8 &#177; 8.5%, were included. Among the patients studied, 33.0% were chagasic and, in comparison with NCh, had lower systolic blood pressure (Ch 89.3 &#177; 17.1 mmHg versus NCh 98.8 &#177; 21.7 mmHg, p = 0.03 ) and lowest average age - Ch 52.9 &#177; 14.5 years versus NCh 59.8 &#177; 14.9 years, p = 0.03). During follow-up of 25 months, mortality was 66.7% for Ch and 37.3% in NCh (p = 0.019). The Chagas disease etiology was an independent marker of poor prognosis in multivariate analysis with risk ratio of 2.75 (HF 95.0%, from 1.35 to 5.63). CONCLUSION: In patients with advanced HF, Chagas disease is an important predictor of the worst prognosis.</p>
      </abstract>
      <kwd-group xml:lang="en">
        <kwd>Heart failure</kwd>
        <kwd>reperfusion</kwd>
        <kwd>prognostic</kwd>
        <kwd>Chagas cardiomyopathy</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>
        <bold>ORIGINAL ARTICLE</bold>
      </p>
      <p>
        <fn id="correspcima-body3" fn-type="corresp">
          <label>
            <bold>Chagas cardiomyopathy: prognosis in clinical and hemodynamic profile C</bold>
          </label>
          <p>
            <bold>Juliano Cardoso; Milena Novaes; Marcelo Ochiai; Kelly Regina; Paulo Morgado; Robinson Munhoz; Euler Brancalh&#227;o; Marcelo Lima; Antonio Carlos Pereira Barretto</bold>
          </p>
        </fn>
      </p>
      <p>InCor - Hospital de Cotox&#243; - HCFMUSP, S&#227;o Paulo, SP - Brazil</p>
      <p>Mailing address</p>
      <p>
        <bold>ABSTRACT</bold>
      </p>
      <p><bold>BACKGROUND:</bold> Patients with heart failure (HF) who are admitted showing poor perfusion and congestion (clinical-hemodynamic profile C) are the group that evolves with the worst prognosis in decompensated heart failure. However, there is little information in literature on the etiology of cardiopathy influences the outcome of patients in advanced stage.</p>
      <p><bold>OBJECTIVE:</bold> To assess the outcome of patients admitted with clinical and hemodynamic profile C and verify the role of the etiology in this phase.</p>
      <p><bold>METHODS:</bold> A cohort study was performed including patients with left ventricle ejection fraction (LVEF) &lt; 45.0%, functional class IV and hospitalization presenting clinical-hemodynamic profile C. The group was divided into patients with chagasic (Ch) and non chagasic (NCh) cardiomyopathy. Statistical analysis used Student t test, Fisher exact test, chi-square and SPSS tests. The significance of p &lt; 0.05 was considered.</p>
      <p><bold>RESULTS:</bold> One hundred patients, with mean age 57.6 &#177; 15.1 years and mean LVEF of 23.8 &#177; 8.5%, were included. Among the patients studied, 33.0% were chagasic and, in comparison with NCh, had lower systolic blood pressure (Ch 89.3 &#177; 17.1 mmHg <italic>versus</italic> NCh 98.8 &#177; 21.7 mmHg, p = 0.03) and lowest average age - Ch 52.9 &#177; 14.5 years <italic>versus</italic> NCh 59.8 &#177; 14.9 years, p = 0.03). During follow-up of 25 months, mortality was 66.7% for Ch and 37.3% in NCh (p = 0.019). The Chagas disease etiology was an independent marker of poor prognosis in multivariate analysis with risk ratio of 2.75 (HF 95.0%, from 1.35 to 5.63).</p>
      <p><bold>CONCLUSION:</bold> In patients with advanced HF, Chagas disease is an important predictor of the worst prognosis. (Arq Bras Cardiol. 2010; [online]. ahead print, PP.0-0)</p>
      <p><bold>Key words:</bold> Heart failure/complications; reperfusion; prognostic; Chagas cardiomyopathy.</p>
      <p>
        <bold>Introduction</bold>
      </p>
      <p>The advance of medicine has been improving the knowledge about heart failure (HF), enabling the development of new diagnostic methods, the determination of prognostic factors and the establishment of more effective treatments that enhance their development. However, HF is still a prevalent disease with a poor prognosis, especially in advanced stages of disease.</p>
      <p>In this context, it is important to identify the clinical and laboratory characteristics of patients with decompensated HF, to determine those with a tendency to the worst prognosis. This makes possible to adopt specific measures and appropriate treatment for this group to improve the quality of life and increase survival.</p>
      <p>Over time, some criteria were identified and related to poor prognosis, among them functional class IV (NYHA), hyponatremia, hypotension, renal failure, exacerbated activation of the neurohormonal system, high BNP and clinical hemodynamic C profile<sup>1-9</sup>.</p>
      <p>In clinical and hemodynamic profile proposed by Stevenson<sup>10</sup>, it is used two clinical parameters to stratify patients: congestion and perfusion. The congestion is diagnosed when the patient presents the following signs on physical examination: jugular stasis, pulmonary rales, sacral edema, lower limbs edema and hepatomegaly. The diagnosis of poor perfusion is done when the following signs are present: symptomatic systolic blood pressure lower than 90 mmHg, poor perfusion of the extremities, altered level of consciousness and pre-renal failure. When the patient shows signs of congestion, it is said that he/she is in "congested pattern" and it is not present, in "dry pattern". With respect to perfusion, it is hot, if well perfused and, it is cold, if poorly perfused. Following these criteria, we can find four clinical and hemodynamic profiles: profile A (hot and dry), profile B (hot and congested), profile L (dry and cold) and profile C (cold and congested).</p>
      <p>The use of clinical-hemodynamic classification helps orient the drug therapy based on the profile of each patient and also allows the prognosis of outcome. In a study published in 2003, Stevenson et al demonstrated that patients with profile C were those who had the poorest performance among patients admitted with decompensated HF<sup>11-13</sup>.</p>
      <p>Brazilian studies have identified the Chagas cardiomyopathy, a disease very prevalent in our country, as associated with the worst prognosis when compared to other etiologies<sup>14-15</sup>. In a previous study by our group, we found that chagasic patients have the worst outcomes compared to other etiologies, however, this study included patients with preserved ventricular function and no selection for the clinical-hemodynamic profile<sup>16</sup>. We must also consider that the studies made by Stevenson et al<sup>11</sup>, with evaluation of the clinical profile, were not included patients with Chagas cardiomyopathy.</p>
      <p>In this study, we tried to fill this knowledge gap, checking if there is any relationship between the etiology and prognosis in patients with the most severe clinical-hemodynamic profile (type C).</p>
      <p>In this study, we included patients admitted with heart failure with decompensated systolic dysfunction, functional class IV (NYHA) and clinical and hemodynamic profile C, and we assessed whether the evolution of Chagas disease patients would be different from patients with HF of other etiologies.</p>
      <p>
        <bold>Materials and methods</bold>
      </p>
      <p>This is a cohort study, which included the consecutive patients admitted with decompensated congestive heart failure, from the emergency room of the <italic>Instituto do Cora&#231;&#227;o </italic>- HCFMUSP and from <italic>Hospital Auxiliar de Cotox&#243;</italic>. Patients aged over 18 years, with an ejection fraction of left ventricle smaller than 45.0% and in profile C (cold and congested) were selected.</p>
      <p>At admission, patients underwent anamnesis, physical examination and blood collection for serum sodium dosage, potassium, urea, creatinine, BNP, complete blood count and serology for Chagas disease.</p>
      <p>All patients were classified according to clinical and hemodynamic profile of Stevenson and only those who showed signs of low output and congestion were selected. Criteria used for characterization of low output were the presence of at least two of the following signs or symptoms: symptomatic SBP (systolic blood pressure) less than 90 mmHg, poor perfusion in extremities (slowed capillary refill), altered level of consciousness or pre-renal failure. In characterizing the presence of congestion, and also requires the presence of at least two of them, use the following criteria: jugular stasis, pulmonary rales, edema in the sacral region, lower limbs edema or hepatomegaly. This evaluation was conducted simultaneously by two specialists in heart failure responsible for the study.</p>
      <p>To identify the etiology of heart failure, we used the following criteria:</p>
      <p>1) <italic>Ischemic -</italic> Inactive area on electrocardiogram, history of myocardial revascularization or coronary obstruction demonstrated by cineangiocoronariography;</p>
      <p>2) <italic>Chagasic -</italic> Serology was requested by ELISA method and indirect immunofluorescence;</p>
      <p>3) <italic>Hypertension -</italic> History of hypertension excluding other causes of cardiomyopathy;</p>
      <p>4) <italic>Valvopathy -</italic> Changing primary valvar before cardiomyopathy and excluding other causes;</p>
      <p>5) <italic>Alcohol -</italic> Patients who reported drinking alcohol in large quantities for more than 10 years and excluding other causes;</p>
      <p>6) <italic>Idiopathic -</italic> When any other cause for cardiomyopathy was excluded.</p>
      <p>The statistical analysis used Student t test, Fisher exact test, chi-square test and SPSS software. The significant p &lt; 0.05 was considered. The survival curves were made with the model of Kaplan-Meier<sup>17</sup> model and compared by the log rank method. The risk ratio (HF 95.0%) was calculated by Cox regression</p>
      <p>
        <bold>Results</bold>
      </p>
      <p>In Jul/2006-Oct/2007 period, at Hospital Auxiliar de Cotoxo, 153 patients were admitted with decompensated HF and systolic dysfunction, with 100 patients (65.0%) showed profile C (congestion and poor perfusion present) 34 patients (22.0%) with clinical profile B (this congestion and good perfusion) and 19 patients (12.4%) with profile L (absence of congestion and poor perfusion present), as shown in <xref ref-type="fig" rid="en_aop10810fig01-body3">Figure 1</xref>. Only patients with profile C were included in the study and followed up for up to 25 months.</p>
      <p content-type="asset">
        <fig id="en_aop10810fig01-body3">
          <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gf01-en.jpg"/></fig>
      </p>
      <p><xref ref-type="table" rid="tab1-body3">Table 1</xref> shows the main characteristics of hospitalized patients with profile C, group where 68.0% were male and 33.0% had positive serological tests for Chagas disease. Most patients needed a prescription for inotropic compensation (89.0% of patients).</p>
      <table-wrap id="tab1-body3">
        <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gt01-en.jpg"/></table-wrap>
      <p><xref ref-type="table" rid="tab2-body3">Table 2</xref> shows the main characteristics of the Chagasic (Ch) and non chagasic (NCh) population. It was found that patients with Chagas' were younger (52.9 &#177; 14.5 years old <italic>versus</italic> 59.8 &#177; 14.9, p = 0.03) had a lower mean left ventricle ejection fraction (LVEF) (20.8 &#177; 7.9% <italic>versus</italic> 25.2% &#177; 8.4%, p = 0.01), average systolic blood pressure lower 89.3 &#177; 17.1 mmHg <italic>versus</italic> 98.8 &#177; 21.7 mmHg, p = 0.03). The hospitalization time was similar in both groups: Ch 31.6 &#177; 21.3 days and NCh 27.1 &#177; 18.5 days; p = 0,3.</p>
      <table-wrap id="tab2-body3">
        <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gt02-en.jpg"/></table-wrap>
      <p>
        <bold>Data on mortality</bold>
      </p>
      <p>During the follow-up of the studied population, the mortality rate was 11.0% and mortality during follow-up was around 47.0%. When comparing the group of chagasic patients with the non chagasic one, we found that mortality was higher in the chagasic one (Ch 66.7% versus NCh 37.3%, p = 0.019) (<xref ref-type="fig" rid="en_aop10810fig02-body3">Figure 2</xref>).</p>
      <p content-type="asset">
        <fig id="en_aop10810fig02-body3">
          <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gf02-en.jpg"/></fig>
      </p>
      <p><xref ref-type="table" rid="tab3-body3">Table 3</xref> presents the main characteristics of patients who died and those who remained alive during the study. Patients who died were older, had a lower ejection fraction, renal function more deteriorated in the admission and higher plasma BNP levels.</p>
      <table-wrap id="tab3-body3">
        <graphic xlink:href="1678-4170-abc-95-04-0518-00112-gt03-en.jpg"/></table-wrap>
      <p>In multivariate analysis, only two independent markers of poor prognosis were identified: chagasic etiology - risk ratio of 2.75 (HF 95%, 1.35 - 5.63) and Age - risk ratio was 1.045 (HF 95%, 1.02 - 1.07). The ejection fraction was not a marker of the worst prognosis in multivariate analysis.</p>
      <p>
        <bold>Discussion</bold>
      </p>
      <p>Among patients who were hospitalized with decompensated HF and systolic dysfunction, those with profile C (cold and congested) represent a more severe group, which has marked hypotension more frequently, high BNP, impaired renal function, hyponatremia and the need for positive inotropic support for compensation. This group has a poor prognosis and usually requires a hospital stay longer for clinical compensation.</p>
      <p>The use of clinical-hemodynamic classification in decompensated patient has been very useful to guide treatment in this phase. The patient who presents congestion without signs of poor perfusion (profile B) may be treated with diuretics and vasodilators to control hypervolemia and peripheral vascular resistance. The patient who presents congestion associated with poor perfusion needs, beyond the hypervolemia treatment with diuretics, drugs that also control the low cardiac output, such as inotropes and vasodilators.</p>
      <p>Studies that used the clinical and hemodynamic profile in a general hospital showed that the profile B (hot and congested) is the most common among patients who were hospitalized with decompensated HF, described in approximately 50.0% of patients hospitalized for compensation. Profile C (cold and congested) is second in frequency, being described in approximately 20.0% of patients, followed by profile L (cold and dry), 3.5%<sup>11-13</sup>. In our hospital, a referral center for the treatment of heart failure, the numbers are substantially different, being C the most frequently identified profile, in approximately 65.0% of hospitalized patients.</p>
      <p>In this population, in which we studied the hospital mortality (11.0%) and the follow-up (47.0%) one, both conditions were high. In previous work from our group, we had already documented that the mortality of patients who are treated in our hospital is high and larger than the one described in the records and many cohorts<sup>18</sup>. This increased mortality due, probably, to the increased intensity of clinical manifestations and severity of cardiopathy of the patients who seek for and are admitted to a tertiary hospital. In the previous study<sup>18</sup>, the mortality of patients hospitalized between the years 2005-2006 was 8.8%, a rate that is higher than that reported in the registry ADHERE<sup>9</sup> (4.0%). However, when we stratified the patients according to severity, we observed that in our hospital 75.6% were hospitalized with systolic BP below 115 mmHg compared to 18.5% in the ADHERE registry. Comparing the evolution of more severe patients in the ADHERE Registry, the mortality rate was 20.9% and our 16.9%, showing no significant difference when comparing patients of similar severity. The mortality rate of 11.0% of this current study, higher than the study of 2005/2006, may also be related to patient selection, since for the current study we selected only patients with more severe profile (profile C).</p>
      <p>Cardiomyopathy by Chagas disease remains a very prevalent disease in Brazil, including S&#227;o Paulo. The impairment of the cardiac muscle in this disease is complex, involving auto immune responses, myocardial impairment, autonomic nervous system impairment and an intense inflammatory process. When comparing the evolution of patients with Chagas cardiomyopathy with that of other etiologies, it appears that the prognosis of Chagas disease in symptomatic cases is worse.</p>
      <p>Rassi Jr et al<sup>19</sup>, in a predominantly outpatient population, identified some predictors of mortality in patients with Chagas cardiomyopathy: functional class III and IV (NYHA), evidence of cardiomegaly on chest radiography, left ventricular dysfunction by echocardiogram, evidence of non sustained ventricular tachycardia by Holter, low QRS voltage on electrocardiogram and male. In this study of Rassi Jr et al, only 10.4% of patients had functional class III and IV, data that characterizes that this population was consisted of patients with less severe cardiopathy than that included in our work. In another study, Freitas et al<sup>14</sup> also related to chagasic etiology with poor prognosis, but for this evaluation outpatients were used, which also have a less severe clinical profile.</p>
      <p>In the study by Stevenson et al, which examined the mortality of different profiles, chagasic etiology described mortality of about 40.0% in the first year of follow up for patients with profile C. In our study, the mortality of non chagasic patients was similar to that found by Stevenson, but that of chagasic patients was higher, about 60.0% of patients dying within the first year of follow-up. Although chagasic patients have had a worse prognosis, they presented better levels of creatinine and urea than the non chagasic. A fact that might contribute to better renal function is the age of chagasic patients, who were significantly younger than the NCh ones.</p>
      <p>In the last decade, we have been seeing an increase in the number of publications on decompensated HF, which improves the understanding in this most critical phase of the disease. In the Brazilian guideline on acute HF, published in 2009<sup>20</sup>, the following clinical and hemodynamic markers are highlighted as having the worst prognosis: low cardiac output refractory congestion, renal failure, persistent third heart sound, and arterial hypotension. Regarding etiology, the guidance mentions HF as a probable factor of poor prognosis, but without more consistent evidences<sup>20</sup>.</p>
      <p>Reviewing the literature, we found that so far no study has specifically compared the evolution of chagasic and non chagasic patients with advanced HF, and that at the time of admission, they presented profile C. This study filled this gap and showed that chagasic etiology is also an independent factor of poor prognosis in advanced stage of heart failure with systolic dysfunction.</p>
      <p>Our data indicate that all patients with advanced HF deserve aggressive treatment, since HF is a disease with malignant characteristics and that the modern treatment can modify this trend. However, we must remember that the group of chagasic patients has an even worse prognosis. Despite the advances in this area of medicine, the patient with Chagas cardiomyopathy remains a major challenge in clinical practice.</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>
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  </sub-article>
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