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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">ZyzdWXbWwLmYTWhJ7fGzGMF</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2013000800001</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(13)10000100001</article-id>
      <article-id pub-id-type="doi">10.5935/abc.2013S002</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Diretrizes</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Diretriz em Cardiologia do Esporte e do Exerc&#237;cio da Sociedade Brasileira de Cardiologia e da Sociedade Brasileira de Medicina do Esporte</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>N&#243;brega</surname>
            <given-names>Antonio Cl&#225;udio Lucas da</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Herdy</surname>
            <given-names>Artur Haddad</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Sellera</surname>
            <given-names>Carlos Alberto Cyrillo</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Baptista</surname>
            <given-names>Claudio Apar&#237;cio Silva</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Ara&#250;jo</surname>
            <given-names>Claudio Gil Soares de</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Moreira</surname>
            <given-names>Dalmo Antonio Ribeiro</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Kopiler</surname>
            <given-names>Daniel Arkader</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Santos</surname>
            <given-names>Daniel Fernando Pellegrino dos</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Cruz Filho</surname>
            <given-names>Fernando Eug&#234;nio dos Santos</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Dioguardi</surname>
            <given-names>Giuseppe Sebastiano</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Fonseca</surname>
            <given-names>Gustavo Paz Esteves Ferreira</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Pinto</surname>
            <given-names>Ibraim Masciarelli Francisco</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Assef</surname>
            <given-names>Jorge Eduardo</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Lazzoli</surname>
            <given-names>Jos&#233; Kawazoe</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Matos</surname>
            <given-names>Luciana Diniz Nagem Janot de</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Emed</surname>
            <given-names>Luiz Gustavo Marin</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Mastrocola</surname>
            <given-names>Luiz Eduardo</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Leit&#227;o</surname>
            <given-names>Marcelo Bichels</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Silva</surname>
            <given-names>Odwaldo Barbosa e</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Francisco</surname>
            <given-names>Ricardo Contesini</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Stein</surname>
            <given-names>Ricardo</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Serra</surname>
            <given-names>Salvador Manoel</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Borges</surname>
            <given-names>Serafim Ferreira</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Timerman</surname>
            <given-names>S&#233;rgio</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Vertematti</surname>
            <given-names>Silvana</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Carvalho</surname>
            <given-names>Tales de</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Garcia</surname>
            <given-names>Thiago Ghorayeb</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Gimenes</surname>
            <given-names>Vera M&#225;rcia Lopes</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Chalela</surname>
            <given-names>William Azem</given-names>
          </name>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <addr-line>
          <named-content content-type="state"/>
        </addr-line>
        <institution content-type="orgname">Sociedade Brasileira de Cardiologia</institution>
        <country country="BR">Brazil</country>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>01</month>
        <year>2013</year>
      </pub-date>
      <volume>100</volume>
      <issue>1 suppl 2</issue>
      <fpage>1</fpage>
      <lpage>41</lpage>
      <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>
      <pub-date publication-format="electronic" date-type="pub">
        <day>04</day>
        <month>04</month>
        <year>2013</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <p>
      <bold>DIRETRIZES</bold>
    </p>
    <p>
      <bold>Diretriz em Cardiologia do Esporte e do Exerc&#237;cio da Sociedade Brasileira de Cardiologia e da Sociedade Brasileira de Medicina do Esporte</bold>
    </p>
    <p>
      <bold>Antonio Cl&#225;udio Lucas da N&#243;brega; Artur Haddad Herdy; Carlos Alberto Cyrillo Sellera; Claudio Apar&#237;cio Silva Baptista; Claudio Gil Soares de Ara&#250;jo; Dalmo Antonio Ribeiro Moreira; Daniel Arkader Kopiler; Daniel Fernando Pellegrino dos Santos; Fernando Eug&#234;nio dos Santos Cruz Filho; Giuseppe Sebastiano Dioguardi; Gustavo Paz Esteves Ferreira Fonseca; Ibraim Masciarelli Francisco Pinto; Jorge Eduardo Assef; Jos&#233; Kawazoe Lazzoli; Luciana Diniz Nagem Janot de Matos; Luiz Gustavo Marin Emed; Luiz Eduardo Mastrocola; Marcelo Bichels Leit&#227;o; Odwaldo Barbosa e Silva; Ricardo Contesini Francisco; Ricardo Stein; Salvador Manoel Serra; Serafim Ferreira Borges; S&#233;rgio Timerman; Silvana Vertematti; Tales de Carvalho; Thiago Ghorayeb Garcia; Vera M&#225;rcia Lopes Gimenes; William Azem Chalela</bold>
    </p>
    <p>
      <xref ref-type="corresp" rid="end">Correspond&#234;ncia</xref>
    </p>
    <p>
      <xref ref-type="undefined" rid="con01">Clique para ampliar</xref>
    </p>
    <p content-type="asset">
      <undefined id="con01">
        <inline-graphic xlink:href="https://minio.scielo.br/documentstore/1678-4170/ZyzdWXbWwLmYTWhJ7fGzGMF/ea2064c354aef026a006da00df2826aab6889993.jpg"/>
      </undefined>
    </p>
    <p>
      <xref ref-type="undefined" rid="def01">Clique para ampliar</xref>
    </p>
    <p content-type="asset">
      <undefined id="def01">
        <inline-graphic xlink:href="https://minio.scielo.br/documentstore/1678-4170/ZyzdWXbWwLmYTWhJ7fGzGMF/6406b3ad42250bb1bcf60d71a30067827365ee88.jpg"/>
      </undefined>
    </p>
    <p>
      <bold>Apresenta&#231;&#227;o</bold>
    </p>
    <p>No ano de 1986 em Belo Horizonte durante o XLII Congresso Brasileiro de Cardiologia foi formalizada, com a coleta de assinaturas de s&#243;cios, a cria&#231;&#227;o do Grupo de Estudos em Cardiologia do Esporte, no in&#237;cio diretamente ligado &#224; diretoria da SBC e depois integrante do DERC. </p>
    <p>A concretiza&#231;&#227;o cient&#237;fica dessa verdadeira &#225;rea de atua&#231;&#227;o da cardiologia brasileira, foi conclu&#237;da com a primeira Diretriz em Cardiologia do Esporte. No mesmo ritmo das Sociedades de Cardiologia e de Medicina do Esporte de todo o mundo, sem d&#250;vida, ir&#225; aumentar a massa cr&#237;tica dos estudiosos e interessados que atuam no esporte e no exerc&#237;cio f&#237;sico dos profissionais e da popula&#231;&#227;o. O interesse, at&#233; governamental, da preven&#231;&#227;o das cardiopatias come&#231;a pela dissemina&#231;&#227;o da atividade f&#237;sica para todos. A explos&#227;o de praticantes das mais diferentes modalidades esportivas e por todas as idades &#233; a atual realidade.</p>
    <p>A necessidade de termos uma base de consultas compat&#237;vel com nossos h&#225;bitos e costumes se concretizou nesse texto. Os participantes s&#227;o cardiologistas e m&#233;dicos do esporte, o que facilitou a integra&#231;&#227;o necess&#225;ria e um legado, a diretriz, muito bem elaborada feita com as dificuldades de ser a primeira, para ser otimizada e modificada periodicamente. A Cardiologia do Esporte por ser uma &#225;rea nova da cardiologia &#233; baseada em experi&#234;ncia, mas que procura criar suas evid&#234;ncias em n&#237;vel mundial. </p>
    <p>Cada vez mais novas modalidades com intensidades e dificuldades esportivas crescentes s&#227;o "inventadas" e imediatamente incorporadas nas academias, milhares de novos praticantes das longas corridas de rua nos procuram para avalia&#231;&#245;es e questionamentos t&#233;cnicos, tudo isso obrigam o m&#233;dico a se manter atualizado para maior seguran&#231;a aos esportistas. deve ficar claro que n&#227;o existe risco zero, mesmo com todo o aparato especializado de emerg&#234;ncia e conhecimento adquirido. </p>
    <p>O fundamental que est&#225; descrito nessa Diretriz, que foi aprofundada em muitos aspectos das cardiopatias para facilitar o leitor. Dificuldades e falta de evidencias mais consistentes em determinadas situa&#231;&#245;es clinicas ainda v&#227;o persistir, mas solu&#231;&#245;es mais pertinentes est&#227;o presentes em todo texto. Tamb&#233;m foi buscado um pareamento com as outras Diretrizes da SBC. </p>
    <p>Esta Diretriz procurou abordar a avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o e recomenda&#231;&#245;es para preven&#231;&#227;o de eventos fatais e n&#227;o fatais nos atletas, nos esportistas em geral e nos paratletas</p>
    <p>Ao finalizarmos queremos lembrar que, pela primeira vez numa Diretriz da Sociedade Brasileira de Cardiologia foi inclu&#237;do um cap&#237;tulo para indiv&#237;duos portadores de necessidades especiais, os festejados PARATLETAS.</p>
    <p>Um fraterno abra&#231;o de parab&#233;ns e de agradecimento aos colaboradores. Aos colegas que a ir&#227;o utilizar esperamos que possa ser &#250;til para o bom exerc&#237;cio da Medicina.</p>
    <p>
      <bold>Nabil Ghorayeb</bold>
    </p>
    <p>
      <bold>1. Introdu&#231;&#227;o</bold>
    </p>
    <p>A avalia&#231;&#227;o cl&#237;nica pr&#233;-participa&#231;&#227;o (APP) para atividades f&#237;sico-esportivas deve ser entendida como uma avalia&#231;&#227;o m&#233;dica sistem&#225;tica, uniformizada, capaz de abranger a ampla popula&#231;&#227;o de esportistas e atletas antes de sua libera&#231;&#227;o para treinamento f&#237;sico. Tem como proposta identificar, ou pelo menos aumentar, a suspeita de doen&#231;as cardiovasculares que sejam incompat&#237;veis com a realiza&#231;&#227;o de atividades f&#237;sicas visando a rendimento.</p>
    <p>O objetivo principal desta avalia&#231;&#227;o, realizada previamente ao in&#237;cio da atividade f&#237;sica e periodicamente com sua manuten&#231;&#227;o, &#233; a preven&#231;&#227;o do desenvolvimento de doen&#231;as do aparelho cardiovascular (DCV) e da morte s&#250;bita por meio da proibi&#231;&#227;o tempor&#225;ria ou definitiva da realiza&#231;&#227;o de atividades f&#237;sicas ou do tratamento de condi&#231;&#245;es que possam ser potencialmente fatais e desencadeadas pelo exerc&#237;cio f&#237;sico. Tanto a American Heart Association, como a Sociedade Europeia de Cardiologia e a Sociedade Brasileira de Medicina do Esporte<sup>1-3</sup> s&#227;o concordantes em recomendar a APP para todos os atletas profissionais. Tamb&#233;m encontra indica&#231;&#227;o para a correta prescri&#231;&#227;o de exerc&#237;cios em esportistas n&#227;o profissionais, mas que realizam atividades em alta intensidade.</p>
    <p>Atualmente, a principal discuss&#227;o na aplica&#231;&#227;o da APP s&#227;o os custos envolvidos nessa avalia&#231;&#227;o. Devido &#224; baixa preval&#234;ncia de condi&#231;&#245;es capazes de desencadear morte s&#250;bita durante atividades esportivas e a grande popula&#231;&#227;o de praticantes existentes no pa&#237;s, muito tem se debatido sobre qual seria o modelo de avalia&#231;&#227;o com melhor custo-benef&#237;cio. Enquanto algumas sociedades como a American Heart Association defendem a simples aplica&#231;&#227;o de um question&#225;rio e exame f&#237;sico, acreditando que o custo financeiro e psicol&#243;gico atrelado a resultados falsos positivos na realiza&#231;&#227;o de exames complementares n&#227;o justificariam os benef&#237;cios que poderiam ser encontrados, outras, como a Sociedade Europeia de Cardiologia, refor&#231;am a utiliza&#231;&#227;o de m&#233;todos diagn&#243;sticos complementares, pois sua realiza&#231;&#227;o tem capacidade de modificar a incid&#234;ncia de morte s&#250;bita na popula&#231;&#227;o de atletas<sup>3-7</sup>. Apesar de n&#227;o dispormos de trabalhos randomizados comparando os dois modelos de avalia&#231;&#227;o sugerimos, assim como a Sociedade Brasileira de Medicina do Esporte, que a APP deva ser associada a m&#233;todos complementares para atletas profissionais, considerando ser plenamente justificada sua indica&#231;&#227;o na tentativa de garantir a integridade do atleta e todo o custo envolvido na sua forma&#231;&#227;o. Outro aspecto pol&#234;mico refere-se &#224; APP em crian&#231;as, sobre a qual at&#233; o momento n&#227;o existe consenso sobre protocolos a serem seguidos<sup>6,8,9</sup>.</p>
    <p>Esses aspectos ser&#227;o abordados neste documento, que visa a estabelecer as normas para a APP em nosso pa&#237;s. Didaticamente e tamb&#233;m pelas diferen&#231;as relacionadas &#224; fisiologia, epidemiologia e aspectos cl&#237;nicos, optamos por dividir em tr&#234;s grupos os indiv&#237;duos a serem avaliados: um formado por esportistas, outro por atletas profissionais e um terceiro contemplando crian&#231;as e adolescentes e ainda para-atletas ou atletas portadores de necessidades especiais. Uma zona de interse&#231;&#227;o entre eles sempre existir&#225;, quando considerados v&#225;rios aspectos do exerc&#237;cio, como intensidade, frequ&#234;ncia, volume de treinamento, etc. O bom senso da pr&#225;tica m&#233;dica e a experi&#234;ncia individual do m&#233;dico avaliador ser&#227;o fundamentais na escolha do caminho a trilhar para a realiza&#231;&#227;o da APP nesses casos.</p>
    <p>
      <bold>2. Grupo esportista</bold>
    </p>
    <p>Caracterizado por indiv&#237;duos adultos que praticam atividades f&#237;sicas e esportivas de maneira regular, de moderada a alta intensidade, competindo eventualmente, por&#233;m sem v&#237;nculo profissional com o esporte.</p>
    <p>
      <bold>2.1. Anamnese e exame cl&#237;nico</bold>
    </p>
    <p>O ideal &#233; que todo indiv&#237;duo candidato &#224; pr&#225;tica de exerc&#237;cios ou esportes em n&#237;vel moderado / elevado de intensidade, seja submetido, obrigatoriamente, a um exame m&#233;dico que permita a detec&#231;&#227;o de fatores de risco, sinais e sintomas sugestivos de doen&#231;as cardiovasculares, pulmonares, metab&#243;licas ou do aparelho locomotor<sup>1,10,11</sup>. As t&#233;cnicas cl&#225;ssicas de anamnese cl&#237;nica devem ser empregadas, com alguns diferenciais, notadamente privilegiando aspectos relacionados ao exerc&#237;cio e &#224; hist&#243;ria de doen&#231;as familiares ou eventos cardiovasculares relacionados &#224; pr&#225;tica de esportes.</p>
    <p>Durante a anamnese pode-se aplicar sistematicamente o Question&#225;rio de Prontid&#227;o para Atividade F&#237;sica (PAR-Q), desenvolvido no Canad&#225; aliado a questionamentos b&#225;sicos aplicados por um m&#233;dico (<xref ref-type="table" rid="tab1">Tabela 1</xref>). Devemos ficar atentos a casos de morte s&#250;bita ou cardiopatias cong&#234;nitas na fam&#237;lia; hist&#243;ria familiar para anemia falciforme ou outras hemoglobinopatias; proced&#234;ncia de &#225;reas end&#234;micas para doen&#231;a de Chagas ou regi&#245;es nas quais haja maior preval&#234;ncia de doen&#231;as cong&#234;nitas, como descendentes de imigrantes da regi&#227;o do V&#234;neto, na It&#225;lia, onde h&#225; especial preval&#234;ncia de casos de displasia arritmog&#234;nica do ventr&#237;culo direito<sup>3-12,13</sup>. Deve-se ter especial cuidado na obten&#231;&#227;o de informa&#231;&#245;es que possam levar ao esclarecimento do uso de drogas l&#237;citas ou il&#237;citas que possam ser consideradas como doping, mesmo que de forma involunt&#225;ria, ou que sejam prejudiciais &#224; sa&#250;de ou possam causar morte s&#250;bita<sup>13,14</sup>. </p>
    <table-wrap id="tab1">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt01.jpg"/></table-wrap>
    <p>Entre os sintomas, devem chamar nossa aten&#231;&#227;o as palpita&#231;&#245;es, s&#237;ncope, dor precordial ou desconforto tor&#225;cico; dispneia aos esfor&#231;os; tontura/lipotimia; astenia; ou qualquer outro sintoma desencadeado pelo exerc&#237;cio. &#201; necess&#225;rio ter uma sensibilidade apurada para saber avaliar se os sintomas citados acima podem ser indicativos de algum estado patol&#243;gico ou se s&#227;o meramente a consequ&#234;ncia de um treino mais intenso ou uma competi&#231;&#227;o. Quanto &#224; s&#237;ncope no atleta, &#233; necess&#225;ria uma investiga&#231;&#227;o detalhada, pois, at&#233; prova em contr&#225;rio, deve ser encarada como um epis&#243;dio de morte s&#250;bita abortada espontaneamente<sup>14</sup>.</p>
    <p>No exame f&#237;sico, merecem destaque algumas condi&#231;&#245;es cl&#237;nicas como: anemia; altera&#231;&#245;es posturais; focos infecciosos (dent&#225;rios, p.ex.); doen&#231;as sist&#234;micas ou infecciosas graves; asma br&#244;nquica, obesidade, diabetes <italic>mellitus</italic>; hipertens&#227;o arterial sist&#234;mica; altera&#231;&#245;es da ausculta pulmonar e cardiovascular; e situa&#231;&#245;es especiais como a gravidez.</p>
    <p>Deve-se privilegiar a procura de sinais caracter&#237;sticos e relacionados com a possibilidade de uma doen&#231;a cardiovascular como: a presen&#231;a de sopro card&#237;aco, terceira ou quarta bulhas, estalidos valvares, altera&#231;&#245;es na palpa&#231;&#227;o dos pulsos de membros superiores e inferiores, caracter&#237;sticas f&#237;sicas de s&#237;ndrome de Marfan, al&#233;m da aferi&#231;&#227;o adequada da press&#227;o arterial (nos dois bra&#231;os na primeira avalia&#231;&#227;o)<sup>15,16</sup>.</p>
    <p>Ainda no exame f&#237;sico, deve-se caracterizar o grau de eventual encurtamento musculotendinoso, principalmente de alguns grupos musculares: isquiotibiais, quadr&#237;ceps, iliopsoas, panturrilhas, adutores da coxa, trato iliotibial, musculatura do dorso e ombros, pois a sua devida orienta&#231;&#227;o terap&#234;utica pode auxiliar na preven&#231;&#227;o e tratamento de les&#245;es musculares, melhorando o desempenho desportivo.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: I</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: C</bold>
    </p>
    <p>
      <bold>2.2. Exames complementares (n&#227;o-cardiovasculares)</bold>
    </p>
    <p>Entre os exames laboratoriais de rotina visando &#224; sa&#250;de, destacamos: hemograma completo, glicemia de jejum, ureia e creatinina, lipidograma completo, &#225;cido &#250;rico, hepatograma (TGO, TGP, gama-GT, bilirrubinas, TAP/INR), exame de urina, exame parasitol&#243;gico de fezes. </p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: I</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: B</bold>
    </p>
    <p>Em indiv&#237;duos sujeitos a praticar exerc&#237;cios ou competir em altitudes superiores a 2.000m, &#233; importante a realiza&#231;&#227;o de eletroforese de hemoglobina, para descartar a possibilidade de hemoglobinopatias (p.ex., anemia falciforme). Em nosso meio, principalmente naqueles com epidemiologia compat&#237;vel, a sorologia para doen&#231;a de Chagas est&#225; recomendada<sup>6,7</sup> (IA). A telerradiografia de t&#243;rax em PA (posteroanterior) e perfil esquerdo deve ser solicitada de rotina, pelo baixo custo e por fornecer informa&#231;&#245;es relevantes sobre doen&#231;as cardiovasculares, doen&#231;as pulmonares e doen&#231;as do arcabou&#231;o tor&#225;cico.</p>
    <p>
      <bold>2.2.1. Eletrocardiograma</bold>
    </p>
    <p>
      <italic>2.2.1.1. Introdu&#231;&#227;o </italic>
    </p>
    <p>&#201; sabido que existem controv&#233;rsias na abordagem em grupos de atletas mais jovens; a diretriz americana (AHA/ACC/ACSM) n&#227;o contempla a inclus&#227;o do ECG, mas o protocolo italiano, j&#225; seguido pela Sociedade Europeia de Cardiologia (ESC), justifica e recomenda sua realiza&#231;&#227;o. </p>
    <p>Em rela&#231;&#227;o aos indiv&#237;duos classificados como m&#225;ster e idosos, o ECG de repouso &#233; mandat&#243;rio; some-se a isso, a ampla disponibilidade e o baixo custo do m&#233;todo. Nessa idade j&#225; existe uma maior preval&#234;ncia de doen&#231;as cardiovasculares, sendo a principal delas a doen&#231;a arterial coron&#225;ria. Essa indica&#231;&#227;o aplica-se mesmo a indiv&#237;duos assintom&#225;ticos e/ou sem conhecimento de patologia cardiovascular pr&#233;via.</p>
    <p>
      <italic>2.2.1.2. M&#233;todo</italic>
    </p>
    <p>O ECG convencional de 12 deriva&#231;&#245;es deve ser realizado com o indiv&#237;duo em posi&#231;&#227;o supina, registrado em velocidade de 25 mm/s e obtido com no m&#237;nimo 24 horas ap&#243;s a &#250;ltima atividade esportiva. Repouso pr&#233;vio de ao menos 5 minutos &#233; mandat&#243;rio<sup>17,18</sup>.</p>
    <p>
      <italic>2.2.1.3 An&#225;lise</italic>
    </p>
    <p>O exame dever&#225; ser avaliado por profissional m&#233;dico, cardiologista e com experi&#234;ncia na &#225;rea desportiva, para que n&#227;o sejam confundidas altera&#231;&#245;es fisiol&#243;gicas do cora&#231;&#227;o de atleta com eventuais cardiopatias.</p>
    <p>
      <italic>2.2.1.4. Altera&#231;&#245;es</italic>
    </p>
    <p>O ECG de 12 deriva&#231;&#245;es tem limitado valor diagn&#243;stico para detec&#231;&#227;o de doen&#231;a arterial coron&#225;ria em popula&#231;&#227;o de indiv&#237;duos assintom&#225;ticos, principalmente pelas varia&#231;&#245;es dos padr&#245;es eletrocardiogr&#225;ficos associadas ao treinamento f&#237;sico<sup>17</sup>. Tem sua maior utilidade quando realizado como parte de uma avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o, quando poder&#225; identificar altera&#231;&#245;es n&#227;o esperadas, como infarto do mioc&#225;rdio pr&#233;vio (em faixas et&#225;rias mais elevadas), arritmias, dist&#250;rbios de condu&#231;&#227;o, entre outras.</p>
    <p>Pode tamb&#233;m auxiliar no diagn&#243;stico de doen&#231;as menos prevalentes, como MCH, s&#237;ndrome do QT-longo, s&#237;ndrome do QT-curto, s&#237;ndrome de Brugada, s&#237;ndrome de WPW e pr&#233;-excita&#231;&#227;o, al&#233;m de displasia arritmog&#234;nica do VD.</p>
    <p>O ECG de 12 deriva&#231;&#245;es pode auxiliar ainda na avalia&#231;&#227;o diagn&#243;stica de valvopatias a&#243;rtica e mitral, batimentos ect&#243;picos (extrassistoles supraventriculares e ventriculares), bradi e taquiarritmias, outras arritmias ventriculares e supraventriculares, dist&#250;rbios do sistema de condu&#231;&#227;o (BRE, BRD, BAV de graus vari&#225;veis). Pode ainda detectar altera&#231;&#245;es do segmento ST, como repolariza&#231;&#227;o precoce, depress&#227;o ou eleva&#231;&#227;o do segmento ST, invers&#227;o de onda T em deriva&#231;&#245;es precordiais e/ou perif&#233;ricas, aumento de voltagem das ondas R/S sugestivas de HVE<sup>2,19</sup>.</p>
    <p>Podem existir varia&#231;&#245;es na preval&#234;ncia das altera&#231;&#245;es eletrocardiogr&#225;ficas, sendo maior no sexo masculino que no feminino; em rela&#231;&#227;o &#224; idade, na popula&#231;&#227;o de m&#225;sters ou idosos, encontramos maior frequ&#234;ncia de ondas T invertidas em deriva&#231;&#245;es precordiais e/ou perif&#233;ricas, ondas R/S aumentadas sugerindo HVE e dist&#250;rbios na condu&#231;&#227;o do estimulo. </p>
    <p>Tamb&#233;m s&#227;o estatisticamente significativas as varia&#231;&#245;es encontradas no eletrocardiograma convencional de 12 deriva&#231;&#245;es em rela&#231;&#227;o ao tipo de esporte praticado e na depend&#234;ncia da faixa et&#225;ria avaliada na <xref ref-type="table" rid="tab2">tabela 2</xref>.</p>
    <table-wrap id="tab2">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt02.jpg"/></table-wrap>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: I</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>
      <bold>2.2.2. Teste ergom&#233;trico</bold>
    </p>
    <p>O teste ergom&#233;trico (TE) pode ser indicado na avalia&#231;&#227;o inicial de um esportista na identifica&#231;&#227;o precoce de doen&#231;a cardiovascular, assim como contribuir na an&#225;lise do progn&#243;stico em assintom&#225;ticos ou quando houver refer&#234;ncia a algum sintoma potencialmente indicativo desta condi&#231;&#227;o. Sua indica&#231;&#227;o tamb&#233;m se imp&#245;e com objetivo de avalia&#231;&#227;o da aptid&#227;o cardiorrespirat&#243;ria na evolu&#231;&#227;o do treinamento em determinadas modalidades esportivas, notadamente as com predomin&#226;ncia do componente aer&#243;bico<sup>21-23</sup>.</p>
    <p>A sobrecarga cardiovascular imposta pelo estresse da atividade f&#237;sica, realizada como lazer, durante a pr&#225;tica de algum esporte ou na competi&#231;&#227;o, exige uma grande demanda metab&#243;lica e hemodin&#226;mica perif&#233;rica. Para atend&#234;-la, ocorre aumento progressivo do consumo de oxig&#234;nio pelo mioc&#225;rdico com o objetivo de possibilitar a eleva&#231;&#227;o do d&#233;bito card&#237;aco. A identifica&#231;&#227;o de eventuais limita&#231;&#245;es ao atendimento a essa demanda crescente por oxig&#234;nio pelo m&#250;sculo card&#237;aco poder&#225; ser avaliada por meio do TE.</p>
    <p>Embora idealmente o TE deva ser sempre indicado na APP, na condi&#231;&#227;o espec&#237;fica de atividades de lazer de leve e moderada intensidades, indiv&#237;duos assintom&#225;ticos e sem fatores de risco cardiovascular podem ser liberados sem a necessidade do exame. Nas demais condi&#231;&#245;es, o TE ser&#225; sempre recomendado<sup>24</sup>.</p>
    <p>No adulto at&#233; 65 anos a doen&#231;a arterial coronariana &#233; a principal respons&#225;vel pela mortalidade e a indica&#231;&#227;o do TE para esses indiv&#237;duos visa, predominantemente, a identifica&#231;&#227;o de isquemia mioc&#225;rdica, refletindo prov&#225;vel doen&#231;a coronariana (DAC). Tamb&#233;m naqueles assintom&#225;ticos e mesmo nos com DAC conhecida, a indica&#231;&#227;o do TE se apoia na necessidade de uma prescri&#231;&#227;o adequada da atividade f&#237;sica.</p>
    <p>A presen&#231;a de altera&#231;&#245;es no eletrocardiograma de repouso, frequentemente decorrentes de hipertrofia ventricular esquerda fisiol&#243;gica do atleta, reduz o poder diagn&#243;stico, no aspecto eletrocardiogr&#225;fico, de isquemia mioc&#225;rdica no TE. A an&#225;lise simult&#226;nea de outras vari&#225;veis do TE contribuem na avalia&#231;&#227;o<sup>25,26</sup>.</p>
    <p>A avalia&#231;&#227;o da resposta da press&#227;o arterial no TE possibilita a ado&#231;&#227;o de medidas preventivas e terap&#234;uticas precoces, al&#233;m de contribuir para a correta prescri&#231;&#227;o do exerc&#237;cio.</p>
    <p>A refer&#234;ncia de palpita&#231;&#227;o durante a atividade f&#237;sica dever&#225; ser investigada por meio do TE com o objetivo de reproduzir, sob monitora&#231;&#227;o, a queixa do paciente. O diagn&#243;stico de arritmia card&#237;aca poder&#225;, ent&#227;o, ser realizado, sendo o tratamento adequado orientado.</p>
    <p>
      <italic>2.2.2.1. Vari&#225;veis a serem avaliadas no teste ergom&#233;trico</italic>
    </p>
    <p>2.2.2.1.1. <underline>Capacidade de exerc&#237;cio</underline></p>
    <p>A fraca capacidade de exerc&#237;cio expressa mau progn&#243;stico. A sua identifica&#231;&#227;o merecer&#225; investiga&#231;&#227;o quanto ao motivo da sua exist&#234;ncia<sup>27,28</sup>.</p>
    <p>2.2.2.1.2. <underline>Dor tor&#225;cica</underline></p>
    <p>Reproduzir por meio do TE a queixa de dor ou desconforto tor&#225;cico durante o exerc&#237;cio possibilitar&#225; o prov&#225;vel diagn&#243;stico de isquemia mioc&#225;rdica por doen&#231;a coronariana, com consequente prosseguimento da investiga&#231;&#227;o e afastamento das atividades f&#237;sicas. Quando durante o TE se identificarem caracter&#237;sticas absolutamente n&#227;o isqu&#234;micas da dor e esta for indicada pelo atleta como semelhante &#224;quela que motivou o TE e inexistir altera&#231;&#227;o em alguma vari&#225;vel do teste, a probabilidade de doen&#231;a coronariana torna-se insignificante, podendo o atleta ser liberado para a competi&#231;&#227;o<sup>29</sup>.</p>
    <p>2.2.2.1.3. <underline>Segmento ST-T</underline></p>
    <p>
      <bold>Desnivelamento de ST </bold>
    </p>
    <p>Infradesnivelamento ou supradesnivelamento do segmento ST em ascens&#227;o lenta, horizontal ou descendente, pode caracterizar DCV, em especial a DAC, principalmente quando ocorrer concomitantemente a refer&#234;ncia de dor tor&#225;cica ou outra manifesta&#231;&#227;o que contribui com o diagn&#243;stico de isquemia mioc&#225;rdica<sup>30</sup>.</p>
    <p>Nos atletas assintom&#225;ticos, quando ocorrerem altera&#231;&#245;es de ST durante o TE, mesmo que n&#227;o sejam acompanhadas de dor tor&#225;cica ou que ocorram em elevado duplo produto e em alta capacidade de exerc&#237;cio, associadas a arritmias card&#237;acas frequentes, justifica-se o afastamento tempor&#225;rio ou n&#227;o in&#237;cio das atividades f&#237;sicas e o prosseguimento na investiga&#231;&#227;o de doen&#231;a cardiovascular. </p>
    <p>Esse enfoque pode ser embasado pela maior exig&#234;ncia cardiovascular e o maior risco de eventos cardiovasculares, inclusive morte s&#250;bita, durante o exerc&#237;cio ou durante a pr&#225;tica esportiva, notadamente acima dos 35 anos e quando um ou mais fatores de risco para DAC estiverem presentes. </p>
    <p>A an&#225;lise do segmento ST dever&#225; considerar:</p>
    <disp-quote>
      <p>&#149; A caracter&#237;stica morfol&#243;gica, sendo descendente mais grave do que horizontal e esta mais grave que ascendente lenta<sup>31,32</sup>.</p>
      <p>&#149; A precocidade do seu aparecimento durante o esfor&#231;o e a persist&#234;ncia dessas altera&#231;&#245;es tardiamente na fase de recupera&#231;&#227;o, condi&#231;&#245;es indicativas de maior risco e gravidade<sup>33,34</sup>.</p>
      <p>&#149; A rela&#231;&#227;o da varia&#231;&#227;o da depress&#227;o do segmento ST em rela&#231;&#227;o &#224; varia&#231;&#227;o da frequ&#234;ncia card&#237;aca [(delta ST em mm x 100) / delta FC]. Considera-se potencialmente isqu&#234;mico quando igual ou maior a 1,6<sup>35,36</sup>.</p>
      <p>&#149; A depress&#227;o de ST quando maior do que 10% em rela&#231;&#227;o &#224; amplitude da onda R imediatamente anterior. Esse ajuste da avalia&#231;&#227;o do segmento ST merece ser considerado principalmente por conta da presen&#231;a habitual de altas ondas R, expressando hipertrofia ventricular esquerda, fisiologicamente presente nos atletas<sup>37</sup>.</p>
    </disp-quote>
    <p>Ainda em rela&#231;&#227;o &#224; fase de repolariza&#231;&#227;o ventricular devemos atentar para o fato de que, quando partindo de um ECG em repouso alterado, a normaliza&#231;&#227;o dessas altera&#231;&#245;es durante o exerc&#237;cio tem significado importante de benignidade e bom progn&#243;stico. Diferentemente, altera&#231;&#245;es que n&#227;o normalizam ou pioram com a eleva&#231;&#227;o da FC e do duplo produto muito frequentemente sinalizam para a presen&#231;a de coronariopatia ou miocardiopatia subjacente<sup>38-40</sup>.</p>
    <p>
      <bold>Despolariza&#231;&#227;o ventricular </bold>
    </p>
    <p>Durante o esfor&#231;o, na presen&#231;a de depress&#227;o do segmento ST, um aumento da amplitude da onda R e, simultaneamente, redu&#231;&#227;o ou manuten&#231;&#227;o da amplitude da onda Q em deriva&#231;&#245;es laterais (V4, V5, CM5, V6), aumentam o poder diagn&#243;stico para isquemia mioc&#225;rdica<sup>41,42</sup>.</p>
    <p>
      <italic>2.2.2.2. Press&#227;o arterial sist&#234;mica</italic>
    </p>
    <p>Valores excessivamente elevados da press&#227;o arterial durante o teste ergom&#233;trico permitem inferir que durante a pr&#225;tica de exerc&#237;cio e de esporte, de modo semelhante, a press&#227;o arterial dever&#225; estar muito elevada. Esportes que necessitem de um maior componente est&#225;tico possivelmente cursar&#227;o com press&#227;o arterial, sist&#243;lica e diast&#243;lica, ainda mais altas.</p>
    <p>A investiga&#231;&#227;o laboratorial e o tratamento da hipertens&#227;o arterial dever&#227;o se iniciar em seguida, devendo-se interromper temporariamente as atividades esportivas at&#233; o seu melhor controle<sup>43</sup>. Por outro lado, queda progressiva da press&#227;o arterial sist&#243;lica durante o TE, principalmente quando se alcan&#231;am valores da press&#227;o arterial sist&#243;lica inferiores ao pr&#233;-esfor&#231;o, merecer&#225; prosseguimento na investiga&#231;&#227;o da presen&#231;a de doen&#231;a card&#237;aca. </p>
    <p>
      <italic>2.2.2.3. Frequ&#234;ncia card&#237;aca</italic>
    </p>
    <p>A incompet&#234;ncia cronotr&#243;pica indica mau progn&#243;stico e tem sido associada a disfun&#231;&#227;o endotelial, altera&#231;&#227;o na modula&#231;&#227;o auton&#244;mica, valores elevados nos marcadores de inflama&#231;&#227;o e doen&#231;a coronariana. </p>
    <p>A inadequada resposta da frequ&#234;ncia card&#237;aca pode ser considerada por meio da incapacidade de alcan&#231;ar 85% da m&#225;xima frequ&#234;ncia card&#237;aca estimada. A equa&#231;&#227;o 208 (idade x 0,70) pode ser utilizada na previs&#227;o da frequ&#234;ncia card&#237;aca m&#225;xima. O &#237;ndice cronotr&#243;pico inferior a 80% &#233; outro m&#233;todo para identificar incompet&#234;ncia cronotr&#243;pica, possuindo valor progn&#243;stico. Ele &#233; obtido por meio da raz&#227;o [(Reserva de FC obtida/Reserva de FC estimada) x 100]<sup>44</sup>.</p>
    <p>A redu&#231;&#227;o da frequ&#234;ncia card&#237;aca no primeiro minuto da recupera&#231;&#227;o em rela&#231;&#227;o &#224; frequ&#234;ncia card&#237;aca do pico do esfor&#231;o possibilita inferir a modula&#231;&#227;o vagal card&#237;aca. Essa observa&#231;&#227;o foi inicialmente identificada em atletas comparativamente a pacientes com insufici&#234;ncia card&#237;aca<sup>45,46</sup>. Redu&#231;&#245;es iguais ou inferiores a 12 batimentos por minuto t&#234;m sido associadas a maior incid&#234;ncia de mortalidade<sup>47</sup>.</p>
    <p>
      <italic>2.2.2.4. Arritmias card&#237;acas</italic>
    </p>
    <p>Arritmias card&#237;acas com menor grau de complexidade, como extrass&#237;stoles ventriculares eventuais ao TE, frequentemente expressam aumento da modula&#231;&#227;o auton&#244;mica simp&#225;tica imposta pelo exerc&#237;cio graduado. Isoladamente, tais condi&#231;&#245;es, sem a presen&#231;a de outras altera&#231;&#245;es, n&#227;o justificam maior limita&#231;&#227;o &#224;s atividades f&#237;sicas nos indiv&#237;duos assintom&#225;ticos.</p>
    <p>Nos indiv&#237;duos sintom&#225;ticos ou nos assintom&#225;ticos que desenvolvam arritmias ventriculares complexas, como taquicardia ventricular, sustentada ou n&#227;o, merecer&#227;o investiga&#231;&#227;o previamente &#224; libera&#231;&#227;o para as atividades f&#237;sicas.</p>
    <p>Presen&#231;a de sete ou mais extrass&#237;stoles ventriculares exclusivamente na fase de recupera&#231;&#227;o, ou na recupera&#231;&#227;o e no esfor&#231;o, expressam um risco potencialmente maior de eventos cardiovasculares futuros<sup>48</sup>.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o e n&#237;vel de evid&#234;ncia</bold>
    </p>
    <p>Atividade f&#237;sica como lazer, de intensidade leve ou moderada, em indiv&#237;duo assintom&#225;tico e sem fator de risco cardiovascular: realizar teste ergom&#233;trico ao iniciar programa de atividade f&#237;sica. </p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: IIa</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>Atividade f&#237;sica como lazer, de intensidade leve ou moderada, em indiv&#237;duo assintom&#225;tico e sem fator de risco cardiovascular: realizar teste ergom&#233;trico ao iniciar programa de atividade f&#237;sica.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: III</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: C</bold>
    </p>
    <p>Atividade de lazer de alta intensidade, esporte e competi&#231;&#227;o: realizar teste ergom&#233;trico ao iniciar o programa de atividade f&#237;sica.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: IIa</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>
      <bold>A qualquer momento:</bold>
    </p>
    <p>Refer&#234;ncia a dor ou desconforto tor&#225;cico, in&#237;cio de cansa&#231;o ou dispneia de causa indefinida, palpita&#231;&#227;o, identifica&#231;&#227;o de arritmias previamente inexistentes, pr&#233;-s&#237;ncope ou s&#237;ncope relacionadas a exerc&#237;cio ou eleva&#231;&#227;o da press&#227;o arterial em repouso, com ou sem comprometimento em &#243;rg&#227;o-alvo: realizar teste ergom&#233;trico.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: I</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p><bold>Observa&#231;&#227;o:</bold> a solicita&#231;&#227;o de teste ergom&#233;trico estar&#225; na depend&#234;ncia da avalia&#231;&#227;o cl&#237;nica inicial e poder&#225; ser contra-indicada ou eventualmente antecedida ou sucedida de outros exames complementares, quando necess&#225;rio.</p>
    <p>
      <bold>2.2.3. Ecocardiograma com <italic>doppler</italic></bold>
    </p>
    <p>Deve ser reservado para os casos com hist&#243;ria cl&#237;nica/familiar ou achado de exame f&#237;sico suspeito de cardiopatia, bem como para os casos de eletrocardiograma de repouso com crit&#233;rios positivos para uma cardiomiopatia (<xref ref-type="table" rid="tab3">Tabela 3</xref>)<sup>49</sup>. Tamb&#233;m nos casos conhecidos de cardiopatias cong&#234;nitas, em especial as de baixa complexidade, em que a pr&#225;tica de atividades f&#237;sicas e mesmo esportivas de alto rendimento n&#227;o est&#227;o contra-indiciadas, a realiza&#231;&#227;o peri&#243;dica do ecocardiograma auxilia na avalia&#231;&#227;o evolutiva e no correto manejo da condi&#231;&#227;o em quest&#227;o. Vale ressaltar a import&#226;ncia do ecocardiograma com <italic>doppler</italic> associado a esfor&#231;o f&#237;sico em situa&#231;&#245;es em que a verifica&#231;&#227;o da fun&#231;&#227;o card&#237;aca durante o exerc&#237;cio pode auxiliar no diagn&#243;stico e conduta<sup>50</sup>.</p>
    <table-wrap id="tab3">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt03.jpg"/></table-wrap>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: IIa</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: B</bold>
    </p>
    <p>Com rela&#231;&#227;o aos atletas com idade superior a 35 anos, deve-se aplicar o protocolo padr&#227;o associado a question&#225;rio para avalia&#231;&#227;o espec&#237;fica de doen&#231;a arterial coron&#225;ria. Em homens &gt;40 anos e mulheres &gt;55 anos deve-se considerar a realiza&#231;&#227;o de teste funcional com exerc&#237;cio e nos indiv&#237;duos com mais de 2 fatores de risco para doen&#231;a arterial coron&#225;ria (al&#233;m do sexo e idade)<sup>51,52</sup>.</p>
    <p>Em caso de positividade na avalia&#231;&#227;o inicial para doen&#231;a arterial coron&#225;ria deve-se aprofundar a investiga&#231;&#227;o com exames mais acurados, podendo-se utilizar ecocardiograma de repouso, ecocardiografia com estresse ou cintilografia tomogr&#225;fica do mioc&#225;rdio, avaliando cada caso individualmente.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: IIa</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: B</bold>
    </p>
    <p>
      <bold>2.2.4. Outros exames complementares</bold>
    </p>
    <p>A utiliza&#231;&#227;o de outras ferramentas diagn&#243;sticas, sejam m&#233;todos laboratoriais, gr&#225;ficos, de imagem, invasivos ou n&#227;o, devem obedecer a crit&#233;rios cl&#237;nicos e evid&#234;ncias cient&#237;ficas j&#225; estabelecidas na literatura, em fun&#231;&#227;o dos achados no decorrer da APP.</p>
    <p>Detalhes espec&#237;ficos sobre a indica&#231;&#227;o e interpreta&#231;&#227;o desses exames complementares ser&#227;o encontrados no t&#243;pico sobre preven&#231;&#227;o de morte s&#250;bita e eventos cardiovasculares na atividade f&#237;sica e esportiva dessa diretriz.</p>
    <p>
      <bold>3. Grupo atletas</bold>
    </p>
    <p>Caracterizado por indiv&#237;duos que praticam atividades f&#237;sicas e esportivas de maneira regular e profissional, competindo sistematicamente, com v&#237;nculo profissional com o esporte por meio de clubes e/ou patrocinadores de qualquer natureza. Esse grupo trabalha sempre na busca de supera&#231;&#227;o de limites e recordes, submetendo-se frequentemente a cargas de treinamento de alt&#237;ssima intensidade, que os colocam invariavelmente sob estresse f&#237;sico e ps&#237;quico intenso, com consequ&#234;ncias frequentemente danosas.</p>
    <p>
      <bold>3.1. Anamnese e exame f&#237;sico</bold>
    </p>
    <p>A avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o (APP) de atletas exige uma estrat&#233;gia exequ&#237;vel em termos econ&#244;micos, em especial em um pa&#237;s em desenvolvimento como o Brasil, de dimens&#227;o continental, muito habitado e de grande diversidade econ&#244;mica e social. A abordagem cardiol&#243;gica merece aten&#231;&#227;o especial, tendo em vista ser a eventualidade da morte s&#250;bita dependente principalmente de causas cardiovasculares. Nesse contexto, torna-se fundamental uma correta anamnese e exame f&#237;sico<sup>53,54</sup>.</p>
    <p>Deve ser considerado na anamnese, contribuindo para uma correta interpreta&#231;&#227;o do exame f&#237;sico, que as adapta&#231;&#245;es card&#237;acas ao exerc&#237;cio f&#237;sico s&#227;o dependentes de sua frequ&#234;ncia, quantidade e intensidade, variando em decorr&#234;ncia das distintas solicita&#231;&#245;es observadas nas diversas modalidades desportivas, diferentes sistemas de treinamento e, tamb&#233;m, de acordo com respostas individuais55. Esse &#250;ltimo aspecto torna poss&#237;vel a exist&#234;ncia de diferentes caracter&#237;sticas card&#237;acas em indiv&#237;duos submetidos a atividades f&#237;sicas semelhantes. Portanto, existem modifica&#231;&#245;es de FC e de PAS que dependem da atividade f&#237;sica habitual e, tamb&#233;m, de caracter&#237;sticas pr&#243;prias de cada indiv&#237;duo. Vale ressaltar que as modifica&#231;&#245;es que comp&#245;em a s&#237;ndrome do cora&#231;&#227;o de atleta devem, a princ&#237;pio, ser consideradas como adapta&#231;&#245;es fisiol&#243;gicas e normais ao exerc&#237;cio f&#237;sico, sendo transit&#243;rias e sem repercuss&#245;es negativas para a sa&#250;de<sup>56,57</sup>.</p>
    <p>Exames laboratoriais, a princ&#237;pio, n&#227;o s&#227;o necess&#225;rios, devendo a sua solicita&#231;&#227;o decorrer dos dados cl&#237;nicos obtidos, com &#234;nfase nos aspectos cardiocirculat&#243;rios. Os exames laboratoriais listados na primeira parte deste documento (grupo esportistas) devem ser considerados tamb&#233;m no grupo dos atletas.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: I</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>
      <bold>3.1.1. Considera&#231;&#245;es sobre a s&#237;ndrome do excesso de treinamento (SET)</bold>
    </p>
    <p>Muitas vezes a magnitude e as repercuss&#245;es cl&#237;nicas das modifica&#231;&#245;es cardiovasculares e de outros sistemas configuram um problema de sa&#250;de, como deve ser considerada a s&#237;ndrome de excesso de treinamento. Por se tratar de um quadro de dif&#237;cil reconhecimento e depender essencialmente da an&#225;lise cl&#237;nica para a suspei&#231;&#227;o da sua presen&#231;a, optamos por incluir aqui sua descri&#231;&#227;o e as recomenda&#231;&#245;es para seu manejo. Na confirma&#231;&#227;o diagn&#243;stica, o laborat&#243;rio tem papel por vezes fundamental.</p>
    <p> Existem dois tipos de excesso de treinamento: o simp&#225;tico, ou do tipo Basedow, e o parassimp&#225;tico, ou do tipo Addison. </p>
    <p>A SET do tipo parassimp&#225;tico &#233; mais comum em atletas veteranos. Nem sempre &#233; acompanhada de queda do rendimento desportivo. Muitas vezes, manifesta-se somente por certo estado de letargia, consequ&#234;ncia do grande predom&#237;nio vagal. As respostas reflexas simp&#225;ticas est&#227;o inibidas, o que pode levar &#224; ocorr&#234;ncia de hipotens&#227;o ortost&#225;tica, tontura, epis&#243;dios de lipotimia e Stokes-Adams em situa&#231;&#245;es da vida cotidiana. </p>
    <p>A SET do tipo simp&#225;tico, que &#233; a mais comum, costuma ocasionar queda de rendimento f&#237;sico, irritabilidade, ins&#244;nia, falta de apetite, sudorese profusa, taquicardia persistente e outras taquiarritmias, retorno lento &#224; frequ&#234;ncia card&#237;aca basal ap&#243;s o esfor&#231;o f&#237;sico e hipertens&#227;o arterial. Pode significar um processo catab&#243;lico acentuado, com emagrecimento por perda de massa muscular e, at&#233; mesmo, osteoporose e fraturas de estresse. Podem ocorrer altera&#231;&#245;es laboratoriais, com aumento de excre&#231;&#227;o de nitrog&#234;nio urin&#225;rio, redu&#231;&#227;o de horm&#244;nios anabolizantes, como testosterona e horm&#244;nio do crescimento, e deple&#231;&#227;o dos fatores de defesa, com menor resist&#234;ncia imunol&#243;gica. Configurando o processo catab&#243;lico, a redu&#231;&#227;o de horm&#244;nios anab&#243;licos se acompanha de aumento de horm&#244;nios catab&#243;licos, como o cortisol. Assim, a rela&#231;&#227;o cortisol s&#233;rico/testosterona s&#233;rica costuma apresentar valores acima do normal. A queda de rendimento e os sintomas relacionados exigem uma imediata redu&#231;&#227;o da carga ou, at&#233; mesmo, um per&#237;odo de descanso prolongado, com interrup&#231;&#227;o dos exerc&#237;cios f&#237;sicos. O tempo de recupera&#231;&#227;o &#233; bem variado, exigindo monitora&#231;&#227;o que indique a ocasi&#227;o mais prop&#237;cia de retomada das atividades. </p>
    <p>
      <bold>3.2. Eletrocardiograma</bold>
    </p>
    <p>A pr&#225;tica esportiva promove altera&#231;&#245;es morfofuncionais no cora&#231;&#227;o relacionadas a tempo e intensidade do treinamento, que s&#227;o demonstr&#225;veis ao ECG de repouso, como sobrecarga ventricular, dist&#250;rbios do ritmo e da condu&#231;&#227;o atrioventricular, estas impostas pela exacerba&#231;&#227;o vagal do exerc&#237;cio. Anormalidades que colocam o atleta em risco durante a pr&#225;tica esportiva podem ser detectadas, representando a express&#227;o de uma doen&#231;a card&#237;aca subjacente. Quando o ECG de um atleta &#233; analisado, o principal objetivo &#233; distinguir entre os padr&#245;es fisiol&#243;gicos e aqueles que exigem a&#231;&#227;o e/ou testes adicionais para excluir (ou confirmar) a suspeita de uma doen&#231;a cardiovascular subjacente levando a risco aumentado de morte s&#250;bita no esporte<sup>58</sup>.</p>
    <p>Erros na diferencia&#231;&#227;o entre o fisiol&#243;gico e o patol&#243;gico podem ter graves consequ&#234;ncias. Atletas podem ser desnecessariamente desqualificados de competi&#231;&#245;es por mudan&#231;as no ECG que se inserem no intervalo normal para atletas. Por outro lado, podem ser submetidos a exames desnecess&#225;rios, elevando de sobremaneira os custos da avalia&#231;&#227;o. Isso &#233; de particular relev&#226;ncia para o profissional, pois a desqualifica&#231;&#227;o do competidor gera importantes transtornos psicol&#243;gicos e, eventualmente, financeiros. Alternativamente, sinais de doen&#231;as cardiovasculares potencialmente fatais podem ser erroneamente interpretados como variantes do normal no ECG de um atleta. </p>
    <p>As peculiaridades do eletrocardiograma de repouso de atletas implicam que a interpreta&#231;&#227;o do exame deve ser realizada por m&#233;dicos cardiologistas com experi&#234;ncia na &#225;rea de fisiologia do exerc&#237;cio ou m&#233;dicos do esporte com treinamento na &#225;rea de cardiologia</p>
    <p>Dados atualmente dispon&#237;veis permitem uma defini&#231;&#227;o da utilidade e do custo-benef&#237;cio do uso do ECG na avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o<sup>59,60</sup>. A Sociedade Brasileira de Cardiologia o recomenda em toda consulta inicial de cardiologia. A Sociedade Europeia de Cardiologia e o Comit&#234; Ol&#237;mpico Internacional, a FIFA, indicam a realiza&#231;&#227;o em todos aqueles que queiram ingressar em um programa de exerc&#237;cios f&#237;sicos de lazer ou competitivo<sup>61</sup>. A American Heart Association n&#227;o o indica como obrigat&#243;rio na avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o para a pr&#225;tica de exerc&#237;cios ou esportes<sup>62</sup>. No Brasil, em muitas institui&#231;&#245;es onde s&#227;o avaliados atletas, sua realiza&#231;&#227;o &#233; obrigat&#243;ria. </p>
    <p>
      <bold>3.2.1. Altera&#231;&#245;es consideradas fisiol&#243;gicas X sugestivas de cardiopatias</bold>
    </p>
    <p>Os esfor&#231;os concentram-se na melhor compreens&#227;o de bases para a interpreta&#231;&#227;o, definindo crit&#233;rios de ECG para a diferencia&#231;&#227;o entre o cora&#231;&#227;o de atleta e reais doen&#231;as card&#237;acas. Mais estudos s&#227;o necess&#225;rios para testar a acur&#225;cia, utilidade e custo-efic&#225;cia do ECG apresenta varia&#231;&#245;es de crit&#233;rios em rela&#231;&#227;o ao sexo, idade, etnia e diferentes n&#237;veis de forma&#231;&#227;o e/ou tipo de esporte<sup>63,64</sup>. As altera&#231;&#245;es no ECG do atleta podem ser divididas em dois grupos: comuns e/ou relacionadas com o treinamento esportivo (grupo1) ou pouco frequentes e/ou sugestivas de cardiopatias (grupo2),conforme listadas na <xref ref-type="table" rid="tab4">tabela 4</xref>.</p>
    <table-wrap id="tab4">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt04.jpg"/></table-wrap>
    <p>Atletas frequentemente (at&#233; 80%) mostram altera&#231;&#245;es eletrocardiogr&#225;ficas tais como bradicardia/arritmia sinusal (13-69%), bloqueio atrioventricular de primeiro grau (35%), repolariza&#231;&#227;o precoce (50-80%), resultantes de adapta&#231;&#245;es fisiol&#243;gicas decorrentes do aumento do t&#244;nus vagal. Tamb&#233;m podem apresentar crit&#233;rios de voltagem (ou seja, baseados apenas em medidas de amplitude do QRS) para hipertrofia fisiol&#243;gica do ventr&#237;culo esquerdo que reflete o remodelamento dessa cavidade, por&#233;m sem a presen&#231;a concomitante de ondas Q patol&#243;gicas, desvio de eixo el&#233;trico, sobrecarga atrial e altera&#231;&#245;es da repolariza&#231;&#227;o<sup>65,66</sup>.</p>
    <p>Essas mudan&#231;as fisiol&#243;gicas no ECG devem ser claramente separadas de padr&#245;es sugestivos de cardiopatias reconhecidos por altera&#231;&#245;es de repolariza&#231;&#227;o, ondas Q patol&#243;gicas, desvio do eixo el&#233;trico, defeitos de condu&#231;&#227;o intraventricular, pr&#233;-excita&#231;&#227;o, intervalo QT curto/longo e Brugada. Esses achados s&#227;o raros (5%), mas podem ser a express&#227;o de cardiomiopatias, heran&#231;as gen&#233;ticas e canalopatias, que predisp&#245;em a morte s&#250;bita<sup>67</sup>.</p>
    <p>Altera&#231;&#245;es por causa de adapta&#231;&#227;o card&#237;aca ao esfor&#231;o f&#237;sico (grupo 1) n&#227;o devem causar alarme e o atleta pode ser liberado para participar em esportes competitivos sem avalia&#231;&#227;o adicional, assim como devem prosseguir em investiga&#231;&#227;o os atletas com achados sugestivos de cardiopatias mesmo que assintom&#225;ticos, na aus&#234;ncia de hist&#243;ria familiar positiva ou de achados anormais ao exame f&#237;sico<sup>68-70</sup>.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: I</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>
      <bold>3.3. Teste ergom&#233;trico </bold>
    </p>
    <p>O teste ergom&#233;trico (TE) pode ser indicado na avalia&#231;&#227;o inicial de atletas em qualquer faixa et&#225;ria como parte da estrat&#233;gia de identifica&#231;&#227;o precoce de doen&#231;a cardiovascular, assim como contribuir na an&#225;lise do progn&#243;stico, em assintom&#225;ticos ou quando houver refer&#234;ncia a algum sintoma potencialmente indicativo desta condi&#231;&#227;o<sup>71,72</sup>.</p>
    <p>Sua solicita&#231;&#227;o estar&#225; na depend&#234;ncia da avalia&#231;&#227;o cl&#237;nica inicial e poder&#225; ser contra-indicada ou eventualmente antecedida ou sucedida de outros exames complementares, quando necess&#225;rios. </p>
    <p>As considera&#231;&#245;es feitas sobre o m&#233;todo no cap&#237;tulo dedicado aos esportistas s&#227;o plenamente aplic&#225;veis tamb&#233;m aos atletas profissionais. Sugerimos, portanto, a leitura do texto citado nesse documento.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: I</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>
      <bold>3.4. Teste cardiopulmonar</bold>
    </p>
    <p>De longa data, inclusive no Brasil, os atletas e indiv&#237;duos que participam de atividades f&#237;sicas de alto rendimento v&#234;m sendo submetidos ao teste cardiopulmonar de exerc&#237;cio m&#225;ximo (TCPE) objetivando avalia&#231;&#227;o do desempenho e prescri&#231;&#227;o do treinamento aer&#243;bico<sup>73</sup>. Conforme descrito na <xref ref-type="table" rid="tab5">tabela 5</xref>, o TCPE diferencia-se primariamente do teste de exerc&#237;cio convencional pela adi&#231;&#227;o de medidas e an&#225;lises dos gases expirados<sup>74,75</sup>. Consoante com seus objetivos prim&#225;rios, quando realizado em atletas aparentemente saud&#225;veis, muitas vezes, ao contr&#225;rio dos testes de exerc&#237;cio com objetivo de diagn&#243;stico cl&#237;nico, n&#227;o s&#227;o feitas medidas de press&#227;o arterial e at&#233; mesmo de eletrocardiograma, sendo a medida da frequ&#234;ncia card&#237;aca obtida nesses casos pelo uso de frequenc&#237;metros.</p>
    <table-wrap id="tab5">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt05.jpg"/></table-wrap>
    <p>Com a disponibilidade de algumas centenas de equipamentos em nosso meio (laborat&#243;rios, cl&#237;nicas, hospitais, clubes e centros desportivos) capazes de realizar essas medidas, na pr&#225;tica h&#225; pouco sentido em realizar a avalia&#231;&#227;o da condi&#231;&#227;o aer&#243;bica de atletas por meio de um teste de esfor&#231;o convencional, no qual h&#225; um erro de aproximadamente 20% quando s&#227;o realizadas estimativas baseadas em f&#243;rmulas desenvolvidas para protocolos cl&#237;nicos para esteiras ou cicloerg&#244;metros. Aparentemente consensual para os m&#233;dicos e profissionais da &#225;rea de educa&#231;&#227;o f&#237;sica que lidam com atletas, na impossibilidade da realiza&#231;&#227;o de um TCPE, a tend&#234;ncia &#233; optar por testes de campo como o de 2.400 m ou at&#233; mesmo o tradicional teste de Cooper em detrimento do teste de exerc&#237;cio convencional. </p>
    <p>No contexto cl&#237;nico da avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o de atletas e indiv&#237;duos que pretendem iniciar exerc&#237;cios aer&#243;bicos intensos, o TCPE apresenta muitas vantagens sobre o teste de exerc&#237;cio convencional, conforme &#233; ilustrado na <xref ref-type="table" rid="tab5">tabela 5</xref>, al&#233;m da mensura&#231;&#227;o objetiva e v&#225;lida da condi&#231;&#227;o aer&#243;bica ou VO2 m&#225;ximo. Em determinadas circunst&#226;ncias cl&#237;nicas e para determinados grupos diferenciados de atletas, como por exemplo, os atletas m&#225;steres ou aqueles indiv&#237;duos com enfermidades cardiovasculares e/ou pulmonares que est&#227;o envolvidos com competi&#231;&#227;o desportiva recreativa (ex. meias maratonas, maratonas, escaladas de alta montanha, provas de ciclismo de estrada, travessias aqu&#225;ticas, etc.) ou profissional, a inclus&#227;o do TCPE na sua avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o pode ser recomendada e at&#233; mesmo fundamental para a estratifica&#231;&#227;o do risco individual, em fun&#231;&#227;o das informa&#231;&#245;es agregadas pela medida e an&#225;lise de gases expirados. Nessas circunst&#226;ncias e sempre que poss&#237;vel, dever&#225; ser preferida a utiliza&#231;&#227;o do erg&#244;metro que mais se aproxima da atividade desportiva praticada. </p>
    <p>Com o crescente envolvimento de indiv&#237;duos de meia-idade em eventos desportivos de massa<sup>76</sup>, &#233; prov&#225;vel que o uso do TCPE seja para obter subs&#237;dios objetivos e v&#225;lidos que orientam mais cientificamente o treinamento ou para ter uma maior seguran&#231;a na caracteriza&#231;&#227;o de um baixo risco cl&#237;nico para eventos cardiovasculares desfavor&#225;veis, especialmente naqueles que possuem fatores de risco coronariano, ser&#225; cada vez mais comum em nosso meio. </p>
    <p>Dentre as v&#225;rias possibilidades de informa&#231;&#245;es cl&#237;nicas adicionais derivadas exclusivamente a partir de um TCPE no atleta ou indiv&#237;duo saud&#225;vel fisicamente ativo, destacam-se duas: a) identifica&#231;&#227;o mais precisa e objetiva do(s) fator(es) limitante(s) ao esfor&#231;o m&#225;ximo (cardiovascular, respirat&#243;rio e muscular ou metab&#243;lico) e b) avalia&#231;&#227;o do comportamento do volume sist&#243;lico, obtida pela an&#225;lise das curvas e dos valores m&#225;ximos do pulso de oxig&#234;nio (VO2/FC) e dos equivalentes ventilat&#243;rios (VE/VO2 e VE/VCO2) quando &#233; realizado um protocolo incremental e m&#225;ximo com pelo menos 8 a 10 minutos de dura&#231;&#227;o (mais comumente protocolo de rampa)<sup>77</sup>.</p>
    <p>Em muitos casos, especialmente considerando a elevada preval&#234;ncia relativa de anormalidades eletrocardiogr&#225;ficas de atletas masculinos com longos anos de treinamento predominantemente aer&#243;bico, comprometendo, pelo menos em parte, a especificidade e a sensibilidade diagn&#243;stica dos tra&#231;ados obtidos no esfor&#231;o, o comportamento das vari&#225;veis cardiopulmonares obtidas durante o TCPE pode contribuir para dirimir d&#250;vidas e estratificar apropriadamente o risco individual de um dado atleta. Em outras situa&#231;&#245;es, uma redu&#231;&#227;o da press&#227;o arterial sist&#243;lica nos &#250;ltimos minutos do TCPE em um atleta aparentemente saud&#225;vel, quando acompanhada de respostas ventilat&#243;rias normais, muito mais provavelmente reflete uma redu&#231;&#227;o acentuada da resist&#234;ncia vascular perif&#233;rica resultante de franca acidose metab&#243;lica com um d&#233;bito card&#237;aco preservado ou at&#233; mesmo crescente e n&#227;o de uma disfun&#231;&#227;o aguda do inotropismo/lusitropismo card&#237;aco decorrente de isquemia mioc&#225;rdica. </p>
    <p>O TCPE, j&#225; est&#225; incorporado na pr&#225;tica cardiol&#243;gica para a avalia&#231;&#227;o de pacientes com insufici&#234;ncia card&#237;aca<sup>56</sup> e para a identifica&#231;&#227;o da etiologia da dispneia de esfor&#231;o<sup>57</sup> e, mais recentemente, consideradado como capaz de identificar isquemia mioc&#225;rdica<sup>58</sup> ou respostas anormais ap&#243;s cirurgias card&#237;acas<sup>59</sup>.</p>
    <p>Em se tratando de atletas, &#233; o procedimento de escolha quando se deseja obter uma medida v&#225;lida e precisa da condi&#231;&#227;o aer&#243;bica e da determina&#231;&#227;o da frequ&#234;ncia card&#237;aca dos limiares para prescri&#231;&#227;o do exerc&#237;cio. </p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: I</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>Para a estratifica&#231;&#227;o mais precisa do fator limitante do exerc&#237;cio. </p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: II.a</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>Quando houver altera&#231;&#245;es do eletrocardiograma de repouso que possam interferir na sua interpreta&#231;&#227;o ao exerc&#237;cio ou respostas hemodin&#226;micas suspeitas.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: II.a</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: B</bold>
    </p>
    <p>O seu uso rotineiro em crian&#231;as e adolescentes aparentemente saud&#225;veis, apenas com o objetivo de estratificar risco de morte s&#250;bita ao exerc&#237;cio n&#227;o parece ser especialmente &#250;til.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: II.b</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: B</bold>
    </p>
    <p>
      <bold>3.5. Ecocardiograma</bold>
    </p>
    <p>A avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o tem como objetivo a preven&#231;&#227;o de ocorr&#234;ncias que possam colocar em risco a integridade de indiv&#237;duos praticantes de atividades f&#237;sicas sejam elas recreativas ou competitivas, priorizando a identifica&#231;&#227;o de altera&#231;&#245;es cardiovasculares estruturais e/ou funcionais que podem aumentar o risco de morbidade e mortalidade durante essa pr&#225;tica<sup>40,60,61</sup>.</p>
    <p>A utiliza&#231;&#227;o de m&#233;todos complementares na avalia&#231;&#227;o cardiovascular rotineira &#233; controversa, tendo como aspecto de maior relev&#226;ncia, o custo/benef&#237;cio desta estrat&#233;gia<sup>39</sup>. Nesse cen&#225;rio, a ecocardiografia assume papel fundamental, pela possibilidade de diagnosticar as principais doen&#231;as implicadas em morte s&#250;bita em atletas (<xref ref-type="table" rid="tab6">Tabela 6</xref>) e, diferenciar altera&#231;&#245;es fisiol&#243;gicas do cora&#231;&#227;o de atleta da hipertrofia patol&#243;gica da cardiomiopatia hipertr&#243;fica, de forma in&#243;cua, r&#225;pida e com relativo baixo custo.</p>
    <table-wrap id="tab6">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt06.jpg"/></table-wrap>
    <p>A morte s&#250;bita em atletas jovens (12-35 anos) afeta, em sua maioria, indiv&#237;duos da ra&#231;a negra (&gt;50%) e do sexo masculino (1:9). No entanto, o risco de morte s&#250;bita independe do n&#237;vel de competi&#231;&#227;o (escolar, amador, profissional)<sup>63-65</sup>.</p>
    <p>
      <bold>3.6. Recomenda&#231;&#245;es</bold>
    </p>
    <p>Entidades reconhecidas internacionalmente como a Sociedade Europeia de Cardiologia (SEC), o Comit&#234; Ol&#237;mpico Internacional (COI) e a Sociedade Americana de Cardiologia (SAC) divergem quanto &#224; defini&#231;&#227;o de exames diagn&#243;sticos de triagem para o estabelecimento de protocolos de investiga&#231;&#227;o em sa&#250;de p&#250;blica<sup>66-68</sup>. A complexidade dessa quest&#227;o parece apoiar-se na relativa infrequ&#234;ncia de morte s&#250;bita em jovens atletas (entre 1:100.000 e 1:300.000 por ano), al&#233;m da discut&#237;vel efici&#234;ncia em prevenir sua ocorr&#234;ncia, sendo que esse evento invariavelmente provoca imensa como&#231;&#227;o e repercuss&#227;o na sociedade<sup>3,5</sup>.</p>
    <p>Considerando esse panorama, a Sociedade Europeia de Cardiologia (SEC) amparada pela consistente experi&#234;ncia italiana que acompanhou atletas por 25 anos, determina em seu programa de triagem para indiv&#237;duos entre 12-35 anos um exame inicial composto por hist&#243;ria familiar, exame f&#237;sico, ECG-12 deriva&#231;&#245;es sendo que exames adicionais somente ser&#227;o realizados com achados positivos durante avalia&#231;&#227;o inicial. (<xref ref-type="fig" rid="fig1">figura 1</xref>)<sup>17,69</sup>.</p>
    <fig id="fig1">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gf01.jpg"/></fig>
    <p>Essa estrat&#233;gia se mostrou efetiva em reduzir em quase 90% a incid&#234;ncia anual de morte s&#250;bita em atletas no nordeste italiano<sup>40</sup>.</p>
    <p>A utiliza&#231;&#227;o da ecocardiografia em programas populacionais em jovens atletas (12-35 anos) assintom&#225;ticos mostrou-se uma estrat&#233;gia de alto custo e n&#227;o h&#225; at&#233; o momento nenhum estudo populacional com acompanhamento adequado que comprove sua efic&#225;cia<sup>63-65</sup>.</p>
    <p>Com rela&#231;&#227;o aos atletas com idade superior a 35 anos, deve-se aplicar o protocolo padr&#227;o associado a question&#225;rio para avalia&#231;&#227;o espec&#237;fica de doen&#231;a arterial coron&#225;ria. Em homens &gt;40 anos e mulheres &gt; 55 anos deve-se considerar a realiza&#231;&#227;o de teste funcional com exerc&#237;cio e nos indiv&#237;duos com mais de dois fatores de risco para doen&#231;a arterial coron&#225;ria (al&#233;m do sexo e idade)<sup>1,70.</sup></p>
    <p>Em caso de positividade na avalia&#231;&#227;o inicial para doen&#231;a arterial coron&#225;ria deve-se aprofundar a investiga&#231;&#227;o com exames mais acurados, podendo-se utilizar o ecocardiograma de repouso ou ecocardiografia com estresse, avaliando cada caso individualmente<sup>40,41</sup>.</p>
    <p>Diversos estudos t&#234;m sugerido a introdu&#231;&#227;o de modalidades ecocardiogr&#225;ficas limitadas com exame restrito ao modo bidimensional sendo realizado em 5 minutos. Os resultados demonstram boa sensibilidade e especificidade para o diagn&#243;stico de diversas afec&#231;&#245;es relacionadas a morte s&#250;bita em atletas, principalmente a cardiomiopatia hipertr&#243;fica implicada em mais de 30% dos casos de morte s&#250;bita em atletas jovens<sup>71</sup>.</p>
    <p>As recomenda&#231;&#245;es da <xref ref-type="table" rid="tab7">tabela 7</xref> levam em considera&#231;&#227;o a formula&#231;&#227;o de estrat&#233;gia investigativa de triagem populacional para pol&#237;ticas de sa&#250;de p&#250;blica e podem n&#227;o ser adequadas para a tomada de decis&#227;o em casos singulares, baseando-se em resultado de estudos e registros populacionais alicer&#231;ados em programas de planejamento de custo.</p>
    <table-wrap id="tab7">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt07.jpg"/></table-wrap>
    <p>Atualmente, associa&#231;&#245;es e conselhos dirigentes de atletas profissionais possuem protocolos pr&#243;prios, visto a aprecia&#231;&#227;o de quest&#245;es legais e econ&#244;micas envolvidas ao aspecto profissional<sup>40</sup>.</p>
    <p>A avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o baseada em consulta cl&#237;nica inicial e ECG-12 deriva&#231;&#245;es permite a identifica&#231;&#227;o dos atletas sob maior risco de morte s&#250;bita entretanto, n&#227;o se mostrou como estrat&#233;gia de triagem definitiva nesse segmento. Outros m&#233;todos diagn&#243;sticos com maior acur&#225;cia devem ocupar maior espa&#231;o como exame de screening inicial no futuro<sup>72-74,78</sup>.</p>
    <p>No presente momento, a ecocardiografia representa modalidade diagn&#243;stica confirmat&#243;ria a ser realizada ap&#243;s suspei&#231;&#227;o durante avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o inicial. </p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: I</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>N&#227;o h&#225; evid&#234;ncia para sua utiliza&#231;&#227;o rotineira em programas de triagem populacional em indiv&#237;duos assintom&#225;ticos. </p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: III</bold>
    </p>
    <p>
      <bold>4. Grupo crian&#231;as e adolescentes</bold>
    </p>
    <p>Caracterizado por indiv&#237;duos que praticam atividades f&#237;sicas e esportivas de maneira muito vari&#225;vel, engajando-se na maioria das vezes em esportes recreativos mas que atingem n&#237;veis de moderada a alta intensidade, sendo t&#227;o competitivos como nos n&#237;veis atl&#233;ticos e, mesmo n&#227;o realizando treinamentos sistem&#225;ticos, em determinadas ocasi&#245;es superam at&#233; os de n&#237;veis atl&#233;ticos. Torna-se, portanto, imposs&#237;vel, em termos de intensidade e gastos energ&#233;ticos, uma diferencia&#231;&#227;o entre atletas e n&#227;o atletas. S&#227;o crian&#231;as e adolescentes que podem competir sistematicamente, por vezes j&#225; vinculadas profissionalmente com o esporte por meio de clubes e patrocinadores de qualquer natureza. Por vezes s&#227;o colocados sob estresse f&#237;sico e ps&#237;quico intenso, inclusive em algumas situa&#231;&#245;es pelo posicionamento question&#225;vel dos pais ou respons&#225;veis, que devem ser sempre orientados quantos aos riscos inerentes de tal pr&#225;tica nessa faixa et&#225;ria<sup>12,75</sup>.</p>
    <p>As causas de morte s&#250;bita mais frequentes relacionadas a atividades f&#237;sicas nessa faixa et&#225;ria<sup>3</sup> s&#227;o: cardiomiopatia hipertr&#243;fica, anomalia cong&#234;nita de art&#233;ria coron&#225;ria, displasia arritmog&#234;nica de ventr&#237;culo direito, altera&#231;&#245;es cardiol&#243;gicas da s&#237;ndrome de Marfan (ruptura de aorta), s&#237;ndrome de pr&#233;-excita&#231;&#227;o (WPW), s&#237;ndrome de Brugada, s&#237;ndrome do QT longo, repercuss&#245;es arr&#237;tmicas ou hemodin&#226;micas de cardiopatias cong&#234;nitas, miocardites, <italic>comottion cordis</italic>, doen&#231;a de Chagas, infec&#231;&#245;es e outras como dist&#250;rbio de condu&#231;&#227;o, altera&#231;&#245;es hidroeletrol&#237;ticas, anemia falciforme al&#233;m de causas indeterminadas. N&#227;o temos registros epidemiol&#243;gicos estat&#237;sticos no Brasil de mortes s&#250;bitas relacionadas a pr&#225;ticas esportivas nessa faixa et&#225;ria prendendo-se apenas &#224; publica&#231;&#227;o de relatos de casos. A ordem acima mencionada, portanto, &#233; seletiva, n&#227;o caracterizando sua preval&#234;ncia na popula&#231;&#227;o estudada.</p>
    <p>Atleta competitivo &#233; aquele que participa de um time organizado ou esporte individual que requer treinamento sistem&#225;tico e competi&#231;&#245;es regulares visando a um objetivo, seja ele pr&#234;mio ou excel&#234;ncia na modalidade. Em geral s&#227;o federados e/ou pertencentes a clubes esportivos. Nessa faixa et&#225;ria em especial, a diferencia&#231;&#227;o entre atletas e n&#227;o atletas "competitivos", como j&#225; comentado anteriormente, &#233; praticamente imposs&#237;vel.</p>
    <p>A avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o esportiva vem se desenvolvendo e se tornando cada vez mais formal, sendo uma atitude legal em alguns pa&#237;ses, como a It&#225;lia. Um consenso mundial j&#225; estabelecido &#233; o da realiza&#231;&#227;o de uma hist&#243;ria cl&#237;nica bem conduzida, focando principalmente sintomas e antecedentes pessoais assim como antecedentes familiares de cardiopatia, principalmente ocorr&#234;ncia de morte s&#250;bita precoce. A melhor estrat&#233;gia para realizar a APP nessa faixa et&#225;ria ainda &#233; um motivo de grande discuss&#227;o em v&#225;rios pa&#237;ses<sup>3,75</sup>. Tais dados podem ser muito bem obtidos por meio de question&#225;rios validados como da American Heart Association (AHA) e das Recomenda&#231;&#245;es para Morte S&#250;bita do Comit&#234; Ol&#237;mpico Internacional (Lausanne), adaptados na <xref ref-type="table" rid="tab1">tabela 1</xref>.</p>
    <p>
      <bold>4.1. Avalia&#231;&#227;o espec&#237;fica: est&#225;gios de Tanner l <sup>79,80</sup></bold>
    </p>
    <p>No processo de crescimento e desenvolvimento, temos a sequ&#234;ncia de eventos puberais que culminam com aparecimento de caracteres sexuais secund&#225;rios resultantes da matura&#231;&#227;o hormonal, sistematizada por Tanner e classificada em cinco etapas, levando em conta, no sexo feminino, o desenvolvimento mam&#225;rio e a distribui&#231;&#227;o e a quantidade de pelos pubianos e, no sexo masculino, os aspectos dos &#243;rg&#227;os genitais e tamb&#233;m a quantidade e distribui&#231;&#227;o de pelos pubianos. A avalia&#231;&#227;o desses par&#226;metros &#233; fundamental, pois o aumento de massa muscular, estatura, peso al&#233;m da especializa&#231;&#227;o motora est&#227;o relacionadas a ele. Apesar de haver uma const&#226;ncia na sequ&#234;ncia das etapas de Tanner, o tempo de passagem de um est&#225;gio para outro &#233; muito vari&#225;vel e, assim, a matura&#231;&#227;o sexual pode durar de 2 a 5 anos. </p>
    <p>O grande incremento do crescimento f&#237;sico que ocorre na puberdade, o conhecido estir&#227;o do crescimento, &#233; a fase da vida em que o indiv&#237;duo mais cresce. Geralmente, a acelera&#231;&#227;o do crescimento no sexo feminino ocorre no in&#237;cio da puberdade, entre os est&#225;gio 2 e 3, e sempre precede a menarca, que geralmente coincide com a fase de desacelera&#231;&#227;o do crescimento, e com o est&#225;gio 4. No masculino, usualmente a acelera&#231;&#227;o ocorre no est&#225;gio 3 e tem seu pico no est&#225;gio 4.</p>
    <p>Eletrocardiograma em repouso nesse grupo se acompanha da mesma controv&#233;rsia j&#225; descrita como exame rotineiro. Pelas diferen&#231;as regionais extremas do pa&#237;s<sup>79,81</sup> levando em conta as evid&#234;ncias cient&#237;ficas dispon&#237;veis, recomendamos o ECG como segue:</p>
    <p>Crian&#231;as e adolescentes saud&#225;veis assintom&#225;ticos e sem nenhum fato cl&#237;nico importante observado na avalia&#231;&#227;o m&#233;dica inicial com hist&#243;ria cl&#237;nica detalhada e exame f&#237;sico minucioso, atendendo aos questionamentos acima aqui mencionados.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: IIa</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: C</bold>
    </p>
    <p>Na APP em crian&#231;as e adolescentes de 5 a 18 anos em in&#237;cio de treinamento organizado e competitivo em escolas esportivas, academias e clubes.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: I</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>Em todas as crian&#231;as e adolescentes com alguma suspeita de cardiopatia de base, detectada com os dados obtidos durante a avalia&#231;&#227;o m&#233;dica.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: I</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>
      <bold>4.2. Exames laboratoriais</bold>
    </p>
    <p>Em rela&#231;&#227;o &#224; realiza&#231;&#227;o de exames laboratoriais, na faixa et&#225;ria em quest&#227;o assumem import&#226;ncia para controle de situa&#231;&#245;es frequentes nessa popula&#231;&#227;o como parasitoses, anemias, erros alimentares e at&#233; em alguns casos desnutri&#231;&#227;o. Consideramos os exames abaixo relacionados como pass&#237;veis de indica&#231;&#227;o, sempre na depend&#234;ncia da avalia&#231;&#227;o cl&#237;nica pr&#233;via<sup>76,77</sup>:</p>
    <p>Hemograma: an&#225;lise da hemoglobina, associada a anemias e leucopenia muito comum principalmente em jovens em treinamento, que pode acarretar aumento no risco de IVAS.</p>
    <p>Ferro e ferritina: ajuda no diagn&#243;stico de anemia ferropriva e tamb&#233;m serve para detectar s&#237;ndrome de excesso de treinamento, na qual encontramos baixos n&#237;veis de ferritina.</p>
    <p>S&#243;dio, pot&#225;ssio e cloro:detec&#231;&#227;o de dist&#250;rbios hidroeletrol&#237;ticos.</p>
    <p>Perfil lip&#237;dico e glicemia: atualmente devido a constantes erros alimentares das crian&#231;as e adolescentes, vem adquirindo import&#226;ncia principalmente na preven&#231;&#227;o prim&#225;ria da hipercolesterolemia na idade adulta.</p>
    <p>Sorologia de Chagas: ainda &#233; uma doen&#231;a end&#234;mica no Brasil e na Am&#233;rica do Sul, causa de miocardiopatia, frequentemente subdiagnosticada, principalmente em indiv&#237;duos de n&#237;vel socioecon&#244;mico mais baixo.</p>
    <p>Coprol&#243;gico: identifica&#231;&#227;o de parasitoses.</p>
    <p>Eletroforese de hemoglobina: avalia&#231;&#227;o de hemoglobinopatias como a anemia falciforme, importante na elegibilidade de indiv&#237;duos competitivos.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: II</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: C</bold>
    </p>
    <p>Nos casos selecionados com hist&#243;ria pessoal ou familiar de doen&#231;a card&#237;aca, altera&#231;&#245;es no exame f&#237;sico ou no eletrocardiograma, imp&#245;e-se uma avalia&#231;&#227;o cardiol&#243;gica mais aprofundada antes da libera&#231;&#227;o para atividade esportiva. Essa avalia&#231;&#227;o pode incluir a realiza&#231;&#227;o de ecocardiograma transtor&#225;cico, teste ergom&#233;trico m&#225;ximo e holter de 24 horas<sup>77</sup>. </p>
    <p>Em posicionamento oficial a Sociedade Brasileira de Medicina do Esporte recomenda que, do ponto de vista de sa&#250;de p&#250;blica, crian&#231;as e adolescentes podem participar de atividades f&#237;sicas recreacionais de baixa ou moderada intensidade sem a necessidade de um exame pr&#233;-participa&#231;&#227;o formal. Quando o objetivo for o esporte competitivo ou atividades f&#237;sicas de alta intensidade, o jovem necessita de uma avalia&#231;&#227;o m&#233;dica e funcional, incluindo composi&#231;&#227;o corporal e capacidade aer&#243;bia e anaer&#243;bia<sup>76</sup>. </p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: IIa</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: B</bold>
    </p>
    <p>A American Heart Association, em documento publicado em 2006 sobre o teste ergom&#233;trico em crian&#231;as e adolescentes, descreve entre as principais indica&#231;&#245;es nessa faixa et&#225;ria: 1- a avalia&#231;&#227;o espec&#237;fica de sintomas ou sinais induzidos ou agravados pelo exerc&#237;cio; 2- avaliar ou identificar resposta anormal ao exerc&#237;cio em crian&#231;as com doen&#231;as card&#237;acas, pulmonares ou em outros sistemas, incluindo a presen&#231;a de isquemia mioc&#225;rdica e arritmias; 3- avalia&#231;&#227;o da capacidade funcional para atividades recreacionais ou atl&#233;ticas<sup>77</sup>. </p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: IIa</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: B</bold>
    </p>
    <p>A <italic>36th Bethesda conference</italic> e as <italic>Recommendations for competitive sports participation in athletes with cardiovascular disease</italic> referem que a realiza&#231;&#227;o do teste ergom&#233;trico est&#225; indicada na avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o nos indiv&#237;duos com cardiopatias cong&#234;nitas, doen&#231;as valvares, miocardiopatias, hipertens&#227;o arterial, arritmias e outras condi&#231;&#245;es de doen&#231;a suspeita ou diagnosticada com o objetivo de avaliar a capacidade funcional, sintomas, arritmias e orientar a intensidade permitida para o exerc&#237;cio<sup>81</sup>.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: I</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>
      <bold>4.2.1. Ecocardiograma </bold>
    </p>
    <p>A ecocardiografia representa modalidade diagn&#243;stica confirmat&#243;ria a ser realizada ap&#243;s suspei&#231;&#227;o durante avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o inicial. Em crian&#231;as e adolescentes torna-se exame de extrema utilidade na presen&#231;a de anormalidades no exame f&#237;sico que levantem a suspeita de cardiopatia estrutural, em especial quando da ausculta de sopros card&#237;acos.</p>
    <p>Nos casos onde s&#227;o diagnosticadas altera&#231;&#245;es no ECG, sua realiza&#231;&#227;o passa a fazer parte do arsenal para o diagn&#243;stico diferencial de cardiopatias graves e com potencial para desencadear morte s&#250;bita durante a atividade f&#237;sica, como a cardiomiopatia hipertr&#243;fica e a displasia arritmog&#234;nica do VD<sup>1,12,79,80</sup>.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: I</bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>Em indiv&#237;duos assintom&#225;ticos n&#227;o existem, no presente momento, evid&#234;ncias que justifiquem sua utiliza&#231;&#227;o rotineira em programas de triagem populacional.</p>
    <p>
      <bold>Grau de recomenda&#231;&#227;o: III</bold>
    </p>
    <p>
      <bold>5. Grupo portadores de cardiomiopatias e miocardites</bold>
    </p>
    <p>
      <bold>5.1. Cardiomiopatia hipertr&#243;fica (CH) </bold>
    </p>
    <p>A cardiomiopatia hipertr&#243;fica &#233; uma doen&#231;a autoss&#244;mica dominante que se caracteriza por um desarranjo miofibrilar dos mi&#243;citos, acompanhado de hipercontratilidade, hipodiastolia, hipertrofia septal assim&#233;trica com ou sem obstru&#231;&#227;o da via de sa&#237;da de VE. Essa doen&#231;a &#233; a principal causa de morte s&#250;bita relacionada com o exerc&#237;cio e o esporte em indiv&#237;duos abaixo de 30-35 anos na Am&#233;rica do Norte, enquanto que na Europa prevalece a displasia arritmog&#234;nica de VD como principal causa de morte s&#250;bita naquela faixa et&#225;ria<sup>3,82</sup>.</p>
    <p>At&#233; o momento s&#227;o conhecidos 12 genes implicados na g&#234;nese dessa doen&#231;a com mais de 400 muta&#231;&#245;es gen&#233;ticas relacionadas com as prote&#237;nas contr&#225;teis do mioc&#225;rdio<sup>83</sup>. Os portadores de CH podem ser totalmente assintom&#225;ticos ou apresentar tonteiras, s&#237;ncope, especialmente relacionadas com o exerc&#237;cio, dispneia, palpita&#231;&#245;es e angina. A morte s&#250;bita nesses pacientes pode ocorrer devido a arritmias ventriculares, supraventriculares (com ou sem pr&#233;-excita&#231;&#227;o), bloqueio AV total, assistolia e infarto do mioc&#225;rdio<sup>3</sup>.</p>
    <p>
      <bold>5.2. Exames complementares na CH</bold>
    </p>
    <p>
      <bold>5.2.1. Eletrocardiograma</bold>
    </p>
    <p>Em torno de 95% dos pacientes com CH apresentam altera&#231;&#245;es eletrocardiogr&#225;ficas, sendo o segmento ST e a onda T comumente afetados. Cerca de 50% dos eletrocardiogramas apresentam sinais de sobrecarga ventricular esquerda<sup>84</sup> e as ondas Q patol&#243;gicas est&#227;o presentes em 30% dos casos. &#201; digno de nota que tal achado pode preceder a hipertrofia patol&#243;gica que se ir&#225; encontrar mais tardiamente no ecocardiograma<sup>85</sup>. As ondas Q da CH surgem por aumento das for&#231;as el&#233;tricas que s&#227;o geradas nas &#225;reas de hipertrofia. A sua dire&#231;&#227;o e magnitude est&#227;o relacionadas com o vetor resultante das zonas de maior hipertrofia ventricular<sup>84</sup>. McKenna e cols.<sup>86</sup> propuseram uma s&#233;rie de cinco crit&#233;rios ecocardiogr&#225;ficos, eletrocardiogr&#225;ficos e cl&#237;nicos para o diagn&#243;stico dessa doen&#231;a, especialmente quando ela tem origem familiar. A <xref ref-type="table" rid="tab8">tabela 8</xref> resume as principais altera&#231;&#245;es eletrocardiogr&#225;ficas nos pacientes com CH. </p>
    <table-wrap id="tab8">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt08.jpg"/></table-wrap>
    <p>
      <bold>5.2.2. Ecocardiografia</bold>
    </p>
    <p>A diferencia&#231;&#227;o entre a hipertrofia decorrente da MCH daquela secund&#225;ria ao treinamento f&#237;sico (hipertrofia ventricular do cora&#231;&#227;o do atleta) requer a integra&#231;&#227;o de informa&#231;&#245;es variadas como o padr&#227;o e a distribui&#231;&#227;o da hipertrofia, o espessamento parietal, o tamanho das cavidades, a avalia&#231;&#227;o da fun&#231;&#227;o diast&#243;lica pelo <italic>doppler</italic> tissular e ainda a hist&#243;ria familiar. Al&#233;m disso, &#233; importante avaliar a resposta ecocardiogr&#225;fica dos atletas sob suspeita a um per&#237;odo de destreinamento desportivo<sup>87</sup>. Em rela&#231;&#227;o ao progn&#243;stico, a identifica&#231;&#227;o de um septo maior do que 30 mm &#233; um fator de risco maior para morte s&#250;bita, principalmente em adolescentes e adultos jovens<sup>88</sup>. O ecocardiograma permite caracterizar o tipo e a extens&#227;o do comprometimento do ventr&#237;culo hipertr&#243;fico em um n&#250;mero expressivo de casos, mas a resson&#226;ncia magn&#233;tica pode ser &#250;til naqueles nos quais a ecocardiografia n&#227;o foi capaz de fazer o diagn&#243;stico<sup>89,90</sup>.</p>
    <p>
      <bold>5.2.3. Ecocardiograma <italic>doppler</italic> transtor&#225;cico</bold>
    </p>
    <p>
      <bold>Classe: I </bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: B</bold>
    </p>
    <p>Confirmar a suspeita cl&#237;nica de MCH, determinando o espessamento parietal e a presen&#231;a de gradiente din&#226;mico.</p>
    <p>Investigar a presen&#231;a de MCH em familiares de primeiro grau.</p>
    <p>Reavalia&#231;&#227;o da evolu&#231;&#227;o cl&#237;nica, assim como de interven&#231;&#245;es terap&#234;uticas.</p>
    <p>Eco de contraste mioc&#225;rdico p&#243;s-abla&#231;&#227;o septal para avaliar tamanho da &#225;rea infartada.</p>
    <p>Classe II </p>
    <p>N&#237;vel de evid&#234;ncia C</p>
    <p>IIa: reavalia&#231;&#227;o anual de familiares de pacientes com MCH naqueles com idade entre 12 e 18 anos. Nos indiv&#237;duos maiores de 21 anos a re-avalia&#231;&#227;o dever&#225; ser feita a cada 5 anos;</p>
    <p>IIa: <italic>doppler</italic> tissular para diferenciar MCH da hipertrofia ventricular fisiol&#243;gica do atleta ou da hipertrofia patol&#243;gica da hipertens&#227;o;</p>
    <p>IIb: ecoestresse com exerc&#237;cio em pacientes sintom&#225;ticos aos esfor&#231;os na sua vida habitual que n&#227;o evidenciam gradientes significativos em repouso ou com manobra de Valsalva.</p>
    <p>5.2.4. Ecocardiograma <italic>doppler</italic> transesof&#225;gico</p>
    <p>
      <bold>Classe: I </bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: B</bold>
    </p>
    <p>Pacientes com janela transtor&#225;cica inadequada;</p>
    <p>Para fins de avalia&#231;&#227;o do comprometimento valvar, do mecanismo e da magnitude da regurgita&#231;&#227;o mitral quando isso n&#227;o estiver claro na ecocardiografia transtor&#225;cica;</p>
    <p>Avalia&#231;&#227;o intraoperat&#243;ria na miomectomia e na abla&#231;&#227;o septal por alcooliza&#231;&#227;o.</p>
    <p>Classe: IIa </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: B</bold>
    </p>
    <p>Esclarecer o mecanismo de uma insufici&#234;ncia mitral at&#237;pica.</p>
    <p>5.2.5. Testes de exerc&#237;cio e (CH)</p>
    <p>O teste ergom&#233;trico (TE) apresenta valor independente para a identifica&#231;&#227;o de pacientes sob risco aumentado para morte s&#250;bita. A presen&#231;a de altera&#231;&#245;es marcadas do segmento ST em pacientes com CH pode indicar isquemia sem necessariamente representar enfermidade coron&#225;ria. Dessa feita o TE apresenta escasso valor diagn&#243;stico, mas pode ser um marcador progn&#243;stico que deve ser levado em considera&#231;&#227;o<sup>84</sup>. </p>
    <p>
      <italic>5.2.5.1. Indica&#231;&#227;o do TE em pacientes com CH</italic>
    </p>
    <p>
      <bold>Classe: I </bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: B</bold>
    </p>
    <p>Pacientes assintom&#225;ticos que n&#227;o apresentam crit&#233;rios de alto risco como elemento associado na estratifica&#231;&#227;o progn&#243;stica;</p>
    <p>Pacientes assintom&#225;ticos, que n&#227;o apresentam crit&#233;rios de alto risco, que desejam realizar atividade f&#237;sica recreativa;</p>
    <p>TE como elemento associado no diagn&#243;stico diferencial entre s&#237;ndrome do cora&#231;&#227;o do atleta e CH.</p>
    <p>Classe: IIa </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: C</bold>
    </p>
    <p>Pacientes com sintomas duvidosos n&#227;o associados com outros crit&#233;rios de alto risco;</p>
    <p>TE subm&#225;ximo em pacientes com desfibrilador implantado que desejam realizar atividade f&#237;sica de baixa intensidade com a finalidade de avalia&#231;&#227;o da capacidade funcional;</p>
    <p>TE subm&#225;ximo em pacientes com desfibrilador implantado que desejam realizar atividade f&#237;sica de baixa intensidade com a finalidade de avalia&#231;&#227;o da resposta da frequ&#234;ncia card&#237;aca ao exerc&#237;cio.</p>
    <p>
      <bold>Classe: III </bold>
    </p>
    <p>Pacientes com crit&#233;rios de alto risco sem desfibrilador;</p>
    <p>TE convencional com objetivo de diagn&#243;stico diferencial entre CH e hipertrofia fisiol&#243;gica do desportista.</p>
    <p>
      <bold>
        <italic>5.2.5.2. Papel do teste cardiopulmonar de exerc&#237;cio na CH</italic>
      </bold>
    </p>
    <p>Em atletas que se encontram na chamada zona cinza entre a hipertrofia fisiol&#243;gica do cora&#231;&#227;o do atleta e a patol&#243;gica da MCH, a mensura&#231;&#227;o do consumo de oxig&#234;nio e do pulso de oxig&#234;nio de pico por meio do teste cardiopulmonar de exerc&#237;cio (TCPE) pode ser de grande aux&#237;lio. Desportistas altamente treinadas normalmente apresentam valores entre 55-70 mL.Kg<sup>-1</sup>min<sup>-1</sup>. Sharma e cols.<sup>89</sup> demonstraram que aqueles atletas sem doen&#231;a de fato tinham um consumo de oxig&#234;nio de pico significativamente mais elevado do que atletas com CH (66,2 mL.Kg<sup>-1</sup>min<sup>-1</sup><italic>versus</italic> 34,3 mL.Kg<sup>-1</sup>min<sup>-1</sup>). &#201; importante frisar que n&#227;o houve sobreposi&#231;&#227;o entre os grupos. Por conseguinte, os investigadores postularam como ponto de corte a cifra de 50 mL.Kg<sup>-1</sup>min<sup>-1</sup> para discriminar a hipertrofia patol&#243;gica da CH daquela secund&#225;ria ao cora&#231;&#227;o do atleta.</p>
    <p>
      <bold>5.3. Esporte e CH</bold>
    </p>
    <p>Por que existe uma baixa preval&#234;ncia de CH em atletas de alto n&#237;vel? A resposta parece estar relacionada a um processo de sele&#231;&#227;o natural que exclui indiv&#237;duos com altera&#231;&#245;es funcionais e estruturais secund&#225;rias &#224; CH do treinamento regular de alta intensidade requerido para algu&#233;m virar atleta<sup>89</sup>. Ser atleta competitivo e ter CH &#233; sin&#244;nimo de morte s&#250;bita? A resposta &#233; n&#227;o. Todos n&#243;s conhecemos casos de atletas que receberam o diagn&#243;stico dessa enfermidade quando j&#225; haviam encerrado sua atividade competitiva profissional ou durante ela. O problema &#233; que o exerc&#237;cio intenso pode ser um gatilho para o desencadeamento de arritmias graves, aumento da obstru&#231;&#227;o da vida de sa&#237;da do ventr&#237;culo esquerdo e/ou isquemia por compress&#227;o dos pequenos vasos (poss&#237;vel fibrose por isquemias repetitivas), tanto durante o per&#237;odo de treinamento quanto nas competi&#231;&#245;es. De fato, n&#227;o existem estudos cl&#237;nicos ou gen&#233;ticos que assegurem um bom progn&#243;stico.</p>
    <p>Quando o diagn&#243;stico desta enfermidade &#233; feito, a exclus&#227;o para a pr&#225;tica de esportes competitivos tem sido a regra a ser seguida<sup>91</sup>. No entanto, &#233; poss&#237;vel que algumas exce&#231;&#245;es possam ser feitas para atletas assintom&#225;ticos e sem crit&#233;rios de alto risco que competem em esportes como golfe, cr&#237;quete, boliche ou tiro ao alvo. </p>
    <p>Persiste a recomenda&#231;&#227;o de exclus&#227;o para a pr&#225;tica de esportes competitivos para atletas com gen&#243;tipo positivo, mas com fen&#243;tipo negativo para CH, embora na atualidade n&#227;o se disponha de evid&#234;ncias suficientes, uma vez que elas n&#227;o possuam diagn&#243;stico cl&#237;nico nem apresentem crit&#233;rios de risco de risco para CH. Por&#233;m, algumas muta&#231;&#245;es no gene da troponina (cromossoma 1) podem n&#227;o se expressar como hipertrofia ventricular macrosc&#243;pica, mas expressar sim altera&#231;&#245;es histopatol&#243;gicas nas fibras musculares mioc&#225;rdicas, sendo de maior risco para morte s&#250;bita<sup>88</sup>.</p>
    <p>Em atletas com gen&#243;tipo positivo e fen&#243;tipo negativo que praticam esportes ac&#237;clicos (mudan&#231;as bruscas de velocidade com acelera&#231;&#245;es e desacelera&#231;&#245;es inesperadas, p.ex. futebol, basquete, t&#234;nis), parece-se ter mais risco do que para aqueles que competem em esportes c&#237;clicos (<italic>jogging</italic>, nata&#231;&#227;o, ciclismo)<sup>88</sup>.</p>
    <p>
      <bold>5.4. Estratifica&#231;&#227;o de risco de MS na cardiomiopatia hipertr&#243;fica</bold>
    </p>
    <p>Existem crit&#233;rios sugeridos por Rickers e cols.<sup>90</sup> e Colin Lizalde<sup>92</sup> para estabelecer os fatores de risco para MS em portadores de CH. Esses crit&#233;rios encontram-se na <xref ref-type="table" rid="tab9">tabela 9</xref>.</p>
    <table-wrap id="tab9">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt09.jpg"/></table-wrap>
    <p>
      <bold>5.5. Recomenda&#231;&#245;es para atletas com diagn&#243;stico de CH</bold>
    </p>
    <p>Atletas com diagn&#243;stico prov&#225;vel ou inequ&#237;voco de CH devem ser exclu&#237;dos da maior parte dos esportes competitivos, com poss&#237;vel exce&#231;&#227;o aqueles esportes de baixo componente din&#226;mico e est&#225;tico (IA). Essa recomenda&#231;&#227;o independe da idade, sexo, da apar&#234;ncia fenot&#237;pica do atleta, da presen&#231;a ou n&#227;o de sintomas, de obstru&#231;&#227;o da via de sa&#237;da do ventr&#237;culo esquerdo, de tratamento com drogas, abla&#231;&#227;o septal, uso de marcapasso ou desfibrilador implantado<sup>86</sup>.</p>
    <p>
      <bold>Classe: I </bold>
    </p>
    <p>
      <bold>N&#237;vel de evid&#234;ncia: C</bold>
    </p>
    <p>Os pacientes com diagn&#243;stico de CH devem ser exclu&#237;dos de competi&#231;&#245;es esportivas de car&#225;ter competitivo. Aqueles classificados como de baixo risco podem participar de golfe, biliar, boliche e tiro;</p>
    <p>Os esportes recreativos que requeiram alta intensidade ou mudan&#231;as bruscas de intensidade n&#227;o s&#227;o recomendados;</p>
    <p>Os sujeitos com gen&#243;tipo positivo e fen&#243;tipo negativo (sem evid&#234;ncias cl&#237;nicas de doen&#231;a) podem participar de esportes desde que avaliados de forma peri&#243;dica;</p>
    <p>Pacientes sem crit&#233;rios de alto risco e com teste de exerc&#237;cio normal podem realizar atividade f&#237;sica recreativa c&#237;clica de baixa intensidade;</p>
    <p>Pacientes com desfibrilador implantado devem ser exclu&#237;dos de esportes de contato.</p>
    <p>
      <bold>Classe: IIa</bold>
    </p>
    <p>Pacientes sem crit&#233;rios de alto risco e com teste de exerc&#237;cio normal podem participar em esportes de contato recreativos de baixa intensidade e baixo volume.</p>
    <p>
      <bold>Classe III</bold>
    </p>
    <p>Pacientes assintom&#225;ticos com CH, ainda que de baixo risco cl&#237;nico e gen&#233;tico, capacidade funcional alta e sem antecedentes familiares de morte s&#250;bita podem participar de esportes competitivos de alta intensidade. </p>
    <p>
      <bold>6. Grupo portadores de displasia arritmog&#234;nica do ventr&#237;culo direito (DAVD) ou cardiomiopatia de VD</bold>
    </p>
    <p>&#201; altera&#231;&#227;o do m&#250;sculo card&#237;aco de causa gen&#233;tica por altera&#231;&#227;o na forma&#231;&#227;o dos desmossomos que se caracteriza por substitui&#231;&#227;o fibrogordurosa patol&#243;gica do mioc&#225;rdio ventricular direito, podendo acometer tamb&#233;m o ventr&#237;culo esquerdo<sup>92-94</sup>. Essa enfermidade &#233; uma importante causa de morte s&#250;bita em jovens, incluindo a&#237; atletas competitivos. Inclusive, essa doen&#231;a tem sido descrita como a principal causa de morte s&#250;bita em atletas na regi&#227;o do V&#234;neto, It&#225;lia<sup>93,94</sup>. Uma vez que atletas altamente treinados podem ter hipertrofia do VD al&#233;m de uma variedade de altera&#231;&#245;es na despolariza&#231;&#227;o, repolariza&#231;&#227;o e na condu&#231;&#227;o do est&#237;mulo nervoso, o diagn&#243;stico diferencial entre a s&#237;ndrome do cora&#231;&#227;o do atleta e a DAVD deve ser sempre realizado. O ecocardiograma pode apresentar limita&#231;&#245;es t&#233;cnicas para acessar as imagens do VD, podendo ter sua an&#225;lise estrutural e funcional prejudicada<sup>95,96</sup>. A resson&#226;ncia magn&#233;tica card&#237;aca &#233; uma t&#233;cnica de imagem n&#227;o invasiva que tem se mostrado promissora<sup>96</sup>. A demonstra&#231;&#227;o de disfun&#231;&#227;o segmentar ou global do VD ou um aumento substancial da cavidade dessa c&#226;mara card&#237;aca associada &#224; afilamento do mioc&#225;rdio e presen&#231;a de fibrose (realce tardio na RM) d&#225; suporte ao diagn&#243;stico da DAVD<sup>83,97-100</sup>.</p>
    <p>
      <bold>6.1. Estratifica&#231;&#227;o de risco de MS na displasia arritmog&#234;nica de VE</bold>
    </p>
    <p>Alguns aspectos devem ser considerados na estratifica&#231;&#227;o de risco de MS na displasia arritmog&#234;nica de VD. </p>
    <p>
      <bold>Idade Classe: IIb, n&#237;vel de evid&#234;ncia: C</bold>
    </p>
    <p>Idade - H&#225; opini&#245;es divergentes se o aparecimento dos sintomas em idade inferior a 20 anos teria maior risco. </p>
    <p>
      <bold>S&#237;ncope Classe: IIb, n&#237;vel de evid&#234;ncia: A</bold>
    </p>
    <p>S&#237;ncope - grandes estudos n&#227;o conseguiram demonstrar uma rela&#231;&#227;o com aumento da mortalidade. </p>
    <p>
      <bold>ECG AR Classe: IIA, nivel de evid&#234;ncia: C</bold>
    </p>
    <p>Eletrocardiografia de alta resolu&#231;&#227;o - a presen&#231;a de potenciais tardios parece correlacionar-se positivamente com a gravidade da doen&#231;a e a ocorr&#234;ncia de taquicardia ventricular sustentada e fibrila&#231;&#227;o ventricular, quando est&#225; presente disfun&#231;&#227;o do ventr&#237;culo direito. Entretanto, novos estudos ser&#227;o necess&#225;rios para predizer o desenvolvimento de arritmias ventriculares. </p>
    <p>
      <bold>Ecocardiografia Classe: I, n&#237;vel de evid&#234;ncia: C</bold>
    </p>
    <p>Ecocardiografia - a morte s&#250;bita &#233; mais frequente em pacientes com dilata&#231;&#227;o difusa do ventr&#237;culo direito e naqueles com envolvimento do ventr&#237;culo esquerdo, pois a disfun&#231;&#227;o deste parece ser um marcador de risco para fibrila&#231;&#227;o ventricular e morte s&#250;bita. </p>
    <p>
      <bold>Estimula&#231;&#227;o el&#233;trica programada Classe: III, n&#237;vel de evid&#234;ncia: C</bold>
    </p>
    <p>Estimula&#231;&#227;o el&#233;trica programada - a indu&#231;&#227;o de taquicardia ventricular sustentada varia de 57% a 94% em pacientes com taquicardia ventricular sustentada monom&#243;rfica, por&#233;m &#233; baixa em pacientes que apresentaram fibrila&#231;&#227;o ventricular ou envolvimento do ventr&#237;culo esquerdo. Quando a indu&#231;&#227;o ocorre na presen&#231;a de disfun&#231;&#227;o de ventr&#237;culo direito, o valor preditivo para morte s&#250;bita &#233; maior. </p>
    <p>
      <bold>Resson&#226;ncia Magn&#233;tica Classe: I, n&#237;vel de evid&#234;ncia C</bold>
    </p>
    <p>A RM identifica a disfun&#231;&#227;o do VD, afilamento de paredes e presen&#231;a de realce tardio (fibrose mioc&#225;rdica) e a presen&#231;a de microaneurismas.</p>
    <p>Biopsia: pouco utilizada em nosso meio </p>
    <p>
      <bold>Holter de 24h, teste ergom&#233;trico e dispers&#227;o de QT Classe: III, n&#237;vel de evid&#234;ncia: C</bold>
    </p>
    <p>Holter de 24 horas, teste ergom&#233;trico e dispers&#227;o do QT n&#227;o apresentam valor para identificar pacientes com risco de morte s&#250;bita bem como o tipo de arritmia ventricular. </p>
    <p>Exerc&#237;cio - existem evid&#234;ncias de que o exerc&#237;cio pode ser um fator desencadeante de sintomas e arritmias potencialmente graves, sugerindo que essas consequ&#234;ncias s&#227;o dependentes do t&#244;nus simp&#225;tico, especialmente, em atletas<sup>99,100</sup>.</p>
    <p>Finalmente, &#233; importante salientar que a forma mais eficaz de se tentar detectar patologias card&#237;acas silenciosas que, por vezes, podem ser causas de morte s&#250;bita relacionada com o exerc&#237;cio e o esporte &#233; uma avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o criteriosa e que muitas das altera&#231;&#245;es encontradas nos exames de rotina e que podem ser confundidas com cardiopatias s&#227;o adapta&#231;&#245;es fisiol&#243;gicas resultantes do treinamento intensivo e regular, compondo as caracter&#237;sticas conhecidas como s&#237;ndrome do cora&#231;&#227;o de atleta, cardiomegalia, dist&#250;rbios do ritmo e da condu&#231;&#227;o e altera&#231;&#245;es da repolariza&#231;&#227;o ventricular no eletrocardiograma<sup>97,98,100,101</sup>.</p>
    <p>
      <bold>Recomenda&#231;&#245;es para atletas com diagn&#243;stico de displasia arritmog&#234;nica de VD</bold>
    </p>
    <p>Pacientes/atletas com diagn&#243;stico inequ&#237;voco de DVD devem ser exclu&#237;dos da pr&#225;tica de atividades competitiva<sup>92,93</sup>.</p>
    <p>
      <bold>7. Grupo portadores de miocardite</bold>
    </p>
    <p>&#201; uma enfermidade associada a um perfil cl&#237;nico heterog&#234;neo, sendo a prov&#225;vel causa da morte s&#250;bita em alguns atletas<sup>73,102,103</sup>. Geralmente a miocardite &#233; resultado de uma infec&#231;&#227;o, mas pode ser associada ao abuso de &#225;lcool ou de drogas<sup>103</sup>. A morte s&#250;bita pode ocorrer em sua fase ativa ou at&#233; mesmo quando j&#225; existe uma cicatriz no mioc&#225;rdio, sendo consequ&#234;ncia de arritmias complexas deflagradas a partir de um substrato el&#233;trico de instabilidade. No atleta podemos ter aumento ventricular esquerdo pela doen&#231;a <italic>per se,</italic> pela hipertrofia secund&#225;ria ao treinamento f&#237;sico ou pela mescla de ambas. O diagn&#243;stico diferencial nesses casos &#233; feito pela cl&#237;nica do atleta (presen&#231;a de arritmias, palpita&#231;&#245;es, pr&#233;-s&#237;ncope ou s&#237;ncope ou ainda pela disfun&#231;&#227;o sist&#243;lica). A resson&#226;ncia magn&#233;tica card&#237;aca e a realiza&#231;&#227;o de bi&#243;psia endomioc&#225;rdica em certas circunst&#226;ncias podem auxiliar no diagn&#243;stico. &#201; importante salientar que in&#250;meros estudos t&#234;m apontado a gripe H1N1 como respons&#225;vel por um tipo de miocardite grave, quase sempre acompanhada de choque cardiog&#234;nico. Recentemente, os comit&#234;s organizadores dos Jogos Asi&#225;ticos de Cingapura e dos Jogos Ol&#237;mpicos de Inverno no Canad&#225; recomendaram que todos os atletas participantes desses eventos chegassem a esses pa&#237;ses vacinados contra a gripe su&#237;na. Lembramos, tamb&#233;m, a possibilidade de miocardite pelo v&#237;rus da dengue em nosso meio em raz&#227;o das constantes epidemias dessa doen&#231;a no Brasil.</p>
    <p>
      <bold>7.1. Recomenda&#231;&#245;es para os atletas portadores de miocardite</bold>
    </p>
    <p>Atletas com o diagn&#243;stico de miocardite dever&#227;o ser retirados de todos os esportes competitivos e submetidos a um per&#237;odo de convalescen&#231;a por, pelo menos, 6 meses ap&#243;s o in&#237;cio das manifesta&#231;&#245;es cl&#237;nicas. Esses atletas poder&#227;o ser liberados para treinamentos e competi&#231;&#245;es ap&#243;s 6 meses se:</p>
    <disp-quote>
      <p>&#149; A fun&#231;&#227;o ventricular esquerda, a motilidade da parede ventricular e as dimens&#245;es card&#237;acas voltarem aos valores normais (baseados nos estudos ecocardiogr&#225;ficos e com radionucl&#237;deos em repouso e com esfor&#231;o);</p>
      <p>&#149; Formas complexas ou frequentes de arritmias ventriculares e supraventriculares e arritmias clinicamente relevantes estiverem ausentes;</p>
      <p>&#149; Marcadores inflamat&#243;rios e para insufici&#234;ncia card&#237;aca estiverem normalizados;</p>
      <p>&#149; O ECG de repouso estiver normalizado, embora a persist&#234;ncia de altera&#231;&#245;es de ST isoladamente n&#227;o seja crit&#233;rio impeditivo para retorno aos treinos e competi&#231;&#245;es.</p>
    </disp-quote>
    <p>
      <bold>8. Grupo portadores de doen&#231;a arterial coronariana</bold>
    </p>
    <p>A doen&#231;a isqu&#234;mica do cora&#231;&#227;o tem deca&#237;do ao longo das d&#233;cadas, no Brasil. Em 1980, a taxa padronizada de &#243;bitos por doen&#231;a arterial coronariana (DAC) era de 65/100.000 habitantes e, em 2005, os dados mostravam 46/100.000 habitantes<sup>104</sup>. A doen&#231;a arterial coronariana responde pela maioria dos eventos de morte s&#250;bita relacionados ao exerc&#237;cio em indiv&#237;duos com idade superior a 35 anos<sup>105</sup>. Os mecanismos respons&#225;veis por deflagrar eventos coronarianos, durante a atividade f&#237;sica vigorosa decorrem do aumento da atividade simp&#225;tica e da maior libera&#231;&#227;o de catecolaminas, ades&#227;o e ativa&#231;&#227;o plaquet&#225;rias (levando a risco de eventos tromboemb&#243;licos), altera&#231;&#245;es eletrol&#237;ticas por eleva&#231;&#227;o do pot&#225;ssio (servindo de gatilho para taquiarritmias ventriculares) e complica&#231;&#245;es como isquemia subendoc&#225;rdica,levando a ruptura da placa<sup>106,107</sup> ou poss&#237;vel eros&#227;o da placa<sup>108,109</sup>, fatos implicados como causas imediatas de eventos relacionados ao exerc&#237;cio em adultos. No individuo jovem, a principal causa de morte s&#250;bita durante a pr&#225;tica esportiva &#233; a cardiomiopatia hipertr&#243;fica<sup>110</sup>.</p>
    <p>Na &#250;ltima d&#233;cada, a pr&#225;tica da atividade f&#237;sica passou a ser recomendada como parte interven&#231;&#227;o prim&#225;ria e secund&#225;ria na preven&#231;&#227;o da doen&#231;a arterial coronariana est&#225;vel por proporcionar uma melhora na capacidade funcional (classe I), atenuando a angina em repouso (classe I), com melhora na gravidade da isquemia induzida pelo esfor&#231;o (classe IIa), al&#233;m da redu&#231;&#227;o de alguns fatores de risco cardiovasculares(classe IIa). Os mecanismos propostos e descritos para os benef&#237;cios do exerc&#237;cio f&#237;sico na DAC s&#227;o: incremento da fun&#231;&#227;o endotelial, regress&#227;o da placa ateroscler&#243;tica, forma&#231;&#227;o e aumento de fluxo da circula&#231;&#227;o colateral, vasculog&#234;nese, remodelamento e diminui&#231;&#227;o da apoptose108. Por&#233;m, para que essa popula&#231;&#227;o inicie uma pr&#225;tica f&#237;sica &#233; necess&#225;ria uma estratifica&#231;&#227;o quanto &#224; chance de ter um evento cardiovascular<sup>109,111</sup>. O algoritmo para a estratifica&#231;&#227;o do paciente inicia-se com anamnese e exame f&#237;sico detalhados e a posterior aplica&#231;&#227;o de um teste ergom&#233;trico progressivo e m&#225;ximo para uma poss&#237;vel indu&#231;&#227;o de arritmias card&#237;acas, isquemia de esfor&#231;o induzida, disfun&#231;&#227;o ventricular e dist&#250;rbios na condu&#231;&#227;o atrioventricular. Os dados fornecidos pelo teste ergom&#233;trico ir&#227;o orientar na prescri&#231;&#227;o da pr&#225;tica f&#237;sica, que deve seguir alguns princ&#237;pios fundamentais, como frequ&#234;ncia, dura&#231;&#227;o, intensidade e tipo de exerc&#237;cio<sup>112,113</sup>.</p>
    <p>Tipo de exerc&#237;cio: programa de exerc&#237;cios aer&#243;bicos s&#227;o os que trazem melhores benef&#237;cios para o sistema cardiovascular e controle dos fatores de risco. Esse tipo de programa &#233; caracterizado por exerc&#237;cios c&#237;clicos de grandes grupamentos musculares, como caminhadas, corridas, nata&#231;&#227;o, ciclismo, dan&#231;a, hidrogin&#225;stica, entre outros. </p>
    <p>Frequ&#234;ncia do exerc&#237;cio: a frequ&#234;ncia de exerc&#237;cios f&#237;sicos recomendada &#233; de 3-5 vezes por semana, sendo que em alguns grupos (hipertensos e obesos) a frequ&#234;ncia pode ser at&#233; 7 vezes semanais</p>
    <p>Intensidade do exerc&#237;cio: a melhor maneira de se mensurar a intensidade f&#237;sica do exerc&#237;cio &#233; por meio da frequ&#234;ncia card&#237;aca, determinada por teste ergom&#233;trico (TE) m&#225;ximo. A frequ&#234;ncia card&#237;aca de treinamento deve se situar entre 70 e 85% da FC m&#225;xima obtida no TE, podendo ser utilizada a f&#243;rmula de Karvonen (FC treino= (FCm&#225;xima-FCrepouso) x % da FCreserva recomendada + FCrepouso) ou pela frequ&#234;ncia card&#237;aca correspondente entre o limiar anaer&#243;bico e o ponto de compensa&#231;&#227;o respirat&#243;ria, avaliados pela ergoespirometria. Nos pacientes iniciantes dever&#225; ser usada a faixa de 50-60% da FC de reserva e 60-80% da FC de reserva para os condicionados. Nos pacientes em uso de betabloqueador devemos associar a FC de treinamento determinada pela prova funcional &#224; sensa&#231;&#227;o subjetiva de esfor&#231;o pela escala de Borg.</p>
    <p>Nos exerc&#237;cios de resist&#234;ncia muscular localizada para os principais grupos musculares, deve-se usar de 40-60% da contra&#231;&#227;o volunt&#225;ria m&#225;xima (baixa a moderada intensidade) com 8-15 repeti&#231;&#245;es, de uma a tr&#234;s s&#233;ries, ou de maneira emp&#237;rica, iniciando com cargas baixas e evoluindo at&#233; que a sensa&#231;&#227;o de esfor&#231;o seja de baixa a moderada.</p>
    <p><bold>Dura&#231;&#227;o dos exerc&#237;cios aer&#243;bicos:</bold> 30-60 minutos cont&#237;nuos</p>
    <p>
      <bold>8.1. Anamnese e exame f&#237;sico </bold>
    </p>
    <p>Os dados fornecidos pela anamnese e exame f&#237;sico do paciente s&#227;o imprescind&#237;veis para a avalia&#231;&#227;o da doen&#231;a arterial coronariana, se esta se encontra em curso est&#225;vel ou n&#227;o, auxiliando na estratifica&#231;&#227;o do individuo e programa&#231;&#227;o do exerc&#237;cio (classe IIa, n&#237;vel de evid&#234;ncia B).</p>
    <p>
      <bold>8.1.1. Hist&#243;ria cl&#237;nica</bold>
    </p>
    <p>A hist&#243;ria cl&#237;nica &#233; de extrema import&#226;ncia na estratifica&#231;&#227;o do paciente candidato a pr&#225;tica f&#237;sica supervisionada ou n&#227;o, orientando o m&#233;dico em rela&#231;&#227;o &#224; evolu&#231;&#227;o e ao est&#225;gio atual da doen&#231;a. Pode-se identificar a presen&#231;a ou n&#227;o de sintomas (dor, cansa&#231;o, falta de ar) e com que grau de esfor&#231;o eles s&#227;o desencadeados. Deve-se fazer um invent&#225;rio em rela&#231;&#227;o &#224;s medica&#231;&#245;es utilizadas, pois podem influenciar na din&#226;mica da programa&#231;&#227;o e pr&#225;tica dos exerc&#237;cios, devendo ater-se a algumas caracter&#237;sticas dos sintomas que orientam a probabilidade da presen&#231;a de angina como: </p>
    <p><bold>Localiza&#231;&#227;o:</bold> precordial, retroesternal, ombro, epig&#225;strio, cervical, hemit&#243;rax, dorso;</p>
    <p><bold>Tipo:</bold> constritiva, aperto, peso, opress&#227;o, desconforto, queima&#231;&#227;o, pontada;</p>
    <p><bold>Irradia&#231;&#227;o:</bold> membros superiores (direito, esquerdo, ambos), ombro, mand&#237;bula, pesco&#231;o, dorso, regi&#227;o epig&#225;strica;</p>
    <p><bold>Fatores desencadeantes:</bold> esfor&#231;o f&#237;sico, atividade sexual, posi&#231;&#227;o, alimenta&#231;&#227;o, respira&#231;&#227;o, componente emocional, espont&#226;nea;</p>
    <p><bold>Fatores de al&#237;vio: </bold>repouso, nitrato sublingual, analg&#233;sico, alimenta&#231;&#227;o, anti&#225;cido, posi&#231;&#227;o e apneia; </p>
    <p><bold>Sintomas associados: </bold>sudorese, n&#225;usea, v&#244;mito, palidez, dispneia, hemoptise, tosse, pr&#233;-s&#237;ncope e s&#237;ncope.</p>
    <p>A classifica&#231;&#227;o da dor tor&#225;cica torna-se fundamental, sendo divida esta classifica&#231;&#227;o em tr&#234;s grupos: t&#237;pica, at&#237;pica e n&#227;o card&#237;aca<sup>114,115</sup>.</p>
    <p><bold>Angina t&#237;pica</bold> (definitiva)</p>
    <disp-quote>
      <p>&#149; Desencadeada pelo exerc&#237;cio ou estresse emocional;</p>
      <p>&#149; Desconforto ou dor retroesternal;</p>
      <p>&#149; Aliviada com o repouso ou uso de nitroglicerina</p>
    </disp-quote>
    <p><bold>Angina at&#237;pica </bold>(prov&#225;vel)</p>
    <disp-quote>
      <p>&#149; Presen&#231;a de somente dois fatores acima</p>
      <p>&#149; Dor tor&#225;cica n&#227;o card&#237;aca</p>
      <p>&#149; Presen&#231;a de somente um ou nenhum dos fatores acima </p>
    </disp-quote>
    <p>Al&#233;m da hist&#243;ria cl&#237;nica da dor tor&#225;cica os fatores de risco para DAC devem ser considerados na estratifica&#231;&#227;o dos indiv&#237;duos, tais como: presen&#231;a de diabetes, hipertens&#227;o arterial, dislipidemia, tabagismo, historia familiar de DAC precoce (&lt;55 anos para homens e &lt;65 anos para mulheres), sedentarismo e estresse. </p>
    <p>
      <bold>8.1.2. Exame f&#237;sico</bold>
    </p>
    <p>O exame f&#237;sico pode ser normal ou apresentar algumas altera&#231;&#245;es identificadas pela ectoscopia, palpa&#231;&#227;o e ausculta, como um <italic>ictus</italic> desviado para a esquerda, a presen&#231;a de uma bulha acess&#243;ria (B3 e ou B4), identifica&#231;&#227;o de um sopro que podem dar ind&#237;cios sobre o "status" do cora&#231;&#227;o. A medida da press&#227;o arterial deve ser realizada em ambos os bra&#231;os, e nas posi&#231;&#245;es ortost&#225;tica, sentado e deitado e em pelo menos um membro inferior, com o objetivo de identificar hipotens&#227;o postural ou determinados problemas que podem fazer com que haja diferen&#231;a significativa da press&#227;o arterial entre os membros. O exame f&#237;sico &#233; usualmente normal nos pacientes com angina est&#225;vel<sup>27</sup>. Presen&#231;a de aterosclerose em outros s&#237;tios pode fornecer dados para uma investiga&#231;&#227;o de DAC em alguns indiv&#237;duos que apresentam pulsos de membros inferiores diminu&#237;dos, endurecimento arterial e aneurisma de aorta abdominal. Apesar do exame f&#237;sico nos indiv&#237;duos com DAC ser pouco elucidativo, a proped&#234;utica completa, em particular a do sistema cardiovascular, deve ser realizada cuidadosamente, pois pode fornecer informa&#231;&#245;es importantes sobre outras condi&#231;&#245;es associadas, como doen&#231;as valvares, cardiomiopatia hipertr&#243;fica e outras.</p>
    <p>
      <bold>8.2. Ecocardiograma na DAC cr&#244;nica:</bold>
    </p>
    <p>O uso do ecocardiograma transtor&#225;cico tem sido usado como importante m&#233;todo diagn&#243;stico na doen&#231;a arterial coron&#225;ria assim como m&#233;todo para a avalia&#231;&#227;o do progn&#243;stico nesses pacientes<sup>30</sup>. Nos pacientes que a hist&#243;ria cl&#237;nica e o eletrocardiograma s&#227;o inconclusivos, o ecocardiograma pode demonstrar anormalidades revers&#237;veis ou n&#227;o da motilidade segmentar, identificando &#225;reas de hipocinesia, acnesia, discinesia e aneurismas (classe I) e a extens&#227;o dessas altera&#231;&#245;es, fornecendo tamb&#233;m uma vari&#225;vel importante na avalia&#231;&#227;o da fun&#231;&#227;o ventricular esquerda, a fra&#231;&#227;o de eje&#231;&#227;o (classe I)<sup>116</sup>.</p>
    <p>
      <bold>8.3. Benef&#237;cios do exerc&#237;cio na doen&#231;a coronariana</bold>
    </p>
    <p>Existem v&#225;rios benef&#237;cios fisiol&#243;gicos elicitados pelo exerc&#237;cio em pacientes com DAC est&#225;vel. A <xref ref-type="table" rid="tab10">tabela 10</xref> resume os benef&#237;cios por grau de evid&#234;ncia.</p>
    <table-wrap id="tab10">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt10.jpg"/></table-wrap>
    <p><bold>Obs.:</bold> de acordo com a Diretriz da SBC sobre reabilita&#231;&#227;o card&#237;aca, a melhora da isquemia mioc&#225;rdica decorre do aumento do volume sist&#243;lico (n&#237;vel A), atenua&#231;&#227;o da taquicardia durante o exerc&#237;cio para cargas subm&#225;ximas de esfor&#231;o (n&#237;vel B), melhora da resposta vasodilatadora dependente do endot&#233;lio (n&#237;vel B) e aumento da perfus&#227;o na microcircula&#231;&#227;o coronariana (n&#237;vel B)<sup>117</sup>.</p>
    <p>
      <bold>8.4. Estratifica&#231;&#227;o de risco para inclus&#227;o de pacientes em programas de exerc&#237;cios e reabilita&#231;&#227;o card&#237;aca</bold>
    </p>
    <p>O risco de pacientes em programas de exerc&#237;cios e reabilita&#231;&#227;o card&#237;aca pode ser categorizado de acordo com a <xref ref-type="table" rid="tab11">tabela 11</xref><sup>117</sup>.</p>
    <table-wrap id="tab11">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt11.jpg"/></table-wrap>
    <p>
      <bold>8.5. Tomografia computadorizada, resson&#226;ncia magn&#233;tica e cora&#231;&#227;o de atleta</bold>
    </p>
    <p>A despeito da grande utilidade e aplicabilidade pr&#225;tica da <italic>doppler</italic>-ecocardiografia na avalia&#231;&#227;o de diferentes cardiopatias, existem situa&#231;&#245;es nas quais faz-se necess&#225;rio utilizar outras modalidades de imagem para o esclarecimento diagn&#243;stico e tamb&#233;m para a estratifica&#231;&#227;o de risco. Em especial na avalia&#231;&#227;o de atletas com suspeita de cardiopatia o emprego dessas metodologias pode ser importante, tais como a distin&#231;&#227;o entre cardiomiopatia hipertr&#243;fica discreta e hipertrofia mioc&#225;rdica secund&#225;ria &#224; atividade esportiva<sup>118,119</sup>. </p>
    <p>A complexidade dos movimentos card&#237;acos requer que os equipamentos que se destinam a <italic>image&#225;-lo </italic>sejam sofisticados o suficiente para reproduzir a anatomia do cora&#231;&#227;o sem artefatos resultantes da pr&#243;pria mobilidade do cora&#231;&#227;o<sup>118</sup>. Os equipamentos de resson&#226;ncia magn&#233;tica de 1,5 Tesla ou superior podem ser utilizados para essa finalidade<sup>118</sup>.</p>
    <p>Na tomografia os dados dispon&#237;veis na literatura se baseiam em estudos feitos em equipamentos de 64 fileiras de detectores. Os sistemas com pelo menos 32 fileiras de detectores podem ser utilizados de modo eficaz, havendo apenas a necessidade de uma prepara&#231;&#227;o mais adequada do paciente, para se aprimorar a qualidade das imagens obtidas<sup>118</sup>. </p>
    <p>Os profissionais envolvidos devem ter recebido treinamento adequado em centros especializados, para assegurar maior seguran&#231;a e melhor qualidade dos exames realizados<sup>118</sup>.</p>
    <p>O uso da resson&#226;ncia magn&#233;tica e da tomografia computadorizada para a estratifica&#231;&#227;o de risco e a libera&#231;&#227;o de indiv&#237;duos assintom&#225;ticos para a pr&#225;tica esportiva ainda &#233; limitado. N&#227;o existem trabalhos dispon&#237;veis na literatura avaliando a contribui&#231;&#227;o potencial que a resson&#226;ncia poderia ter nesse sentido. Al&#233;m disso, a tomografia tem, pelo menos em parte, sua aplica&#231;&#227;o limitada pelo fato de utilizar radia&#231;&#227;o ionizante, o que restringe seu uso indiscriminado, em especial na popula&#231;&#227;o mais jovem. Contudo, essa tecnologia tem papel definido em algumas condi&#231;&#245;es que podem estar presentes na avalia&#231;&#227;o de assintom&#225;ticos que desejam fazer atividades esportivas<sup>118,120,121</sup>.</p>
    <p>A presen&#231;a de sinais sugestivos de isquemia mioc&#225;rdica em jovens pode estar relacionada &#224; exist&#234;ncia de origem an&#244;mala de uma art&#233;ria coron&#225;ria. Essa &#233; uma condi&#231;&#227;o na qual a utiliza&#231;&#227;o da tomografia ou a resson&#226;ncia t&#234;m papel fundamental e bem definido<sup>122</sup>. </p>
    <p>Em indiv&#237;duos de idade mais avan&#231;ada que desejam praticar atividades f&#237;sicas, a tomografia tamb&#233;m pode contribuir, em especial se h&#225; conflitos entre os resultados de outros exames n&#227;o invasivos no que se refere &#224; exist&#234;ncia de isquemia mioc&#225;rdica silenciosa. A situa&#231;&#227;o mais habitual &#233; quando h&#225; teste ergom&#233;trico compat&#237;vel com a presen&#231;a de isquemia e cintilografia do mioc&#225;rdio normal ou duvidosa. Nessa condi&#231;&#227;o, o elevado poder preditivo negativo do exame pode ter papel fundamental para excluir a presen&#231;a de doen&#231;a coron&#225;ria obstrutiva ou para indicar a necessidade de se prosseguir na investiga&#231;&#227;o diagn&#243;stica invasiva. </p>
    <p>A elevada resolu&#231;&#227;o espacial da tomografia tamb&#233;m possibilita que ela seja utilizada para a investiga&#231;&#227;o diagn&#243;stica de outras condi&#231;&#245;es, tais como cardiopatias cong&#234;nitas, cardiomiopatias e anomalias vasculares, mas tais fins tamb&#233;m s&#227;o alcan&#231;ados com a resson&#226;ncia, que tem a vantagem adicional de n&#227;o utilizar radia&#231;&#227;o ionizante<sup>118</sup>. </p>
    <p>Outras condi&#231;&#245;es cl&#237;nicas que podem envolver a utiliza&#231;&#227;o de resson&#226;ncia para a libera&#231;&#227;o para a pr&#225;tica esportiva envolvem a exist&#234;ncia de cardiopatias subjacentes que n&#227;o tenham apresentado manifesta&#231;&#227;o cl&#237;nica at&#233; ent&#227;o. Nesses casos, as recomenda&#231;&#245;es cl&#237;nicas para o uso da resson&#226;ncia seguem as normas estabelecidas na pr&#225;tica cardiol&#243;gica habitual<sup>118</sup>.</p>
    <p>Para avalia&#231;&#227;o de cardiopatias em atletas que competem em categorias destinadas a indiv&#237;duos com mais de 40 anos e com testes n&#227;o invasivos conflitantes entre si<sup>118</sup>, a tomografia pode ser um exame &#250;til, pois apresenta poder preditivo negativo maior do que 97% e pode ser &#250;til para excluir a possibilidade de doen&#231;a obstrutiva. Em outras condi&#231;&#245;es cl&#237;nicas pode haver necessidade de investiga&#231;&#245;es adicionais, tais como a presen&#231;a de arritmias ou ainda o desenvolvimento de altera&#231;&#245;es ao eletrocardiograma<sup>120</sup>.</p>
    <p>O cora&#231;&#227;o do atleta profissionais ou amador de elite &#224; resson&#226;ncia se caracteriza por ter dimens&#245;es maiores de massa, volume diast&#243;lico final e volume sist&#243;lico final. Tais altera&#231;&#245;es, por outro lado, ocorrem sem que exista altera&#231;&#227;o da fra&#231;&#227;o de eje&#231;&#227;o, da contratilidade regional ou do padr&#227;o de contra&#231;&#227;o dos ventr&#237;culos. Esse aspecto deve ser sempre considerado, pois casos de cardiomiopatia hipertr&#243;fica habitualmente mostram altera&#231;&#227;o do padr&#227;o de contratilidade card&#237;aca, mesmo que exista discreto aumento da espessura do mioc&#225;rdio ventricular. Assim, a forma de tor&#231;&#227;o ventricular, tanto no plano longitudinal como no plano transverso, encontra-se preservada em atletas, mesmo os de elite, o que n&#227;o ocorre nos casos de cardiomiopatia hipertr&#243;fica<sup>119</sup>.</p>
    <p>Nos casos de adapta&#231;&#227;o do cora&#231;&#227;o ao esfor&#231;o encontrado nos atletas de elite o grau de hipertrofia que compromete o ventr&#237;culo esquerdo difere daquele que interessa ao ventr&#237;culo direito, sendo mais pronunciado na cavidade sist&#234;mica. Al&#233;m disso, quando h&#225; hipertrofia fisiol&#243;gica a rela&#231;&#227;o entre os volumes, as dimens&#245;es e a fra&#231;&#227;o de eje&#231;&#227;o do ventr&#237;culo esquerdo em rela&#231;&#227;o ao ventr&#237;culo direito s&#227;o superpon&#237;veis nos atletas e nos indiv&#237;duos sedent&#225;rios sem cardiopatia estrutural<sup>119,120</sup>. </p>
    <p>Uma das principais causa de morte em atletas jovens &#233; a cardiomiopatia hipertr&#243;fica condi&#231;&#227;o que deve ser lembrada e pesquisada sempre que surgirem ind&#237;cios de anormalidades para esse subgrupo. A literatura reporta existirem casos de at&#233; 13 mm de espessura no mioc&#225;rdio ventricular esquerdo como resposta adaptativa, em especial no caso de atletas de elite do sexo masculino. &#201; importante lembrar que em diferentes esportes dentre os quais o levantamento de peso, o remo, o ciclismo, a nata&#231;&#227;o, maratonas e futebol profissional os atletas tamb&#233;m podem ter aumentos expressivos das dimens&#245;es card&#237;acas, sem apresentar cardiopatia<sup>121</sup>.</p>
    <p>A miocardiopatia hipetr&#243;fica &#224; resson&#226;ncia tamb&#233;m pode compreender a presen&#231;a de realce tardio, que pode indicar a exist&#234;ncia de fibrose e estar presente em graus distintos, independentemente da manifesta&#231;&#227;o cl&#237;nica da cardiopatia. Alguns estudos t&#234;m associado esse padr&#227;o de imagem &#224; maior presen&#231;a de arritmias e &#224; evolu&#231;&#227;o para a forma dilatada da doen&#231;a, sendo um achado que deve aumentar a cautela na condu&#231;&#227;o do caso<sup>118,119</sup>.</p>
    <p>A displasia arritmog&#234;nica mostra-se tamb&#233;m como um desafio em atletas, em especial devido &#224; ampla variedade de padr&#245;es de imagem que ela pode apresentar. Deve ser lembrado que a simples presen&#231;a de tecido gorduroso no mioc&#225;rdio n&#227;o &#233; patognom&#244;nica dessa entidade, uma vez que a presen&#231;a de gordura no m&#250;sculo card&#237;aco pode ser uma consequ&#234;ncia de outras condi&#231;&#245;es inflamat&#243;rias, degenerativas e isqu&#234;micas, al&#233;m de ser um achado habitual em pacientes acima dos 65 anos. O diagn&#243;stico de displasia &#233; feito a partir da exist&#234;ncia de anormalidades regionais nos ventr&#237;culos, al&#233;m da exist&#234;ncia de &#225;reas de realce tardio nas paredes ventriculares, o que traduz a presen&#231;a de processo inflamat&#243;rio e/ou fibrose mioc&#225;rdica. A combina&#231;&#227;o desses achados, com ou sem a presen&#231;a de gordura associada, &#233; que possibilita a identifica&#231;&#227;o da displasia. Um dado de import&#226;ncia nesses casos resulta do fato de que, devido &#224; natureza evolutiva dessa entidade, o diagn&#243;stico implica no afastamento de atividades esportivas<sup>121,122</sup>.</p>
    <p>Outra condi&#231;&#227;o que tem import&#226;ncia cl&#237;nica &#233; a miocardite. Essa entidade pode ter sua ocorr&#234;ncia facilitada pela exist&#234;ncia de condi&#231;&#245;es que levam &#224; diminui&#231;&#227;o da atividade imunol&#243;gica, tal como a que ocorre quando h&#225; treinamento excessivo por per&#237;odo prolongado, condi&#231;&#227;o habitual dos atletas de elite. A resson&#226;ncia tem-se mostrado como uma forma eficaz na avalia&#231;&#227;o desses pacientes, revelando a presen&#231;a de realce tardio, at&#233; mesmo nos casos em que n&#227;o h&#225; modifica&#231;&#227;o da contratilidade ventricular, que permitem definir a presen&#231;a destas altera&#231;&#245;es. Alguns autores mencionam que o padr&#227;o de imagem pode at&#233; mesmo permitir que se infira o agente causador da entidade<sup>121</sup>. As altera&#231;&#245;es na presen&#231;a, na extens&#227;o e na intensidade do realce tardio nessas condi&#231;&#245;es t&#234;m import&#226;ncia progn&#243;stica<sup>121,122</sup>.</p>
    <p>A resson&#226;ncia e a tomografia computadorizada podem ser importantes aliados na estratifica&#231;&#227;o de risco e na avalia&#231;&#227;o de cardiopatia estrutural em atletas. Embora seu uso rotineiro seja o de, essencialmente, complementar a avalia&#231;&#227;o realizada pelo exame cl&#237;nico, eletrocardiogr&#225;fico e eventualmente pela ecocardiografia, em algumas condi&#231;&#245;es tais como a origem an&#244;mala de art&#233;rias coron&#225;rias, na pesquisa de displasia arritmog&#234;nica e da miocardite, eles podem compor a linha de frente e s&#227;o, indiscutivelmente, etapas importantes da avalia&#231;&#227;o diagn&#243;stica <xref ref-type="table" rid="tab12">tabela 12</xref>.</p>
    <table-wrap id="tab12">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt12.jpg"/></table-wrap>
    <p>
      <bold>9. Estratifica&#231;&#227;o de risco de MS relacionada com exerc&#237;cio/esporte nas s&#237;ndromes gen&#233;ticas arritmog&#234;nicas.</bold>
    </p>
    <p>
      <bold>9.1. Canalopatias</bold>
    </p>
    <p>As canalopatias s&#227;o doen&#231;as card&#237;acas heredit&#225;rias arritmog&#234;nicas, sem comprometimento estrutural, causadas por altera&#231;&#245;es gen&#233;ticas que resultam em disfun&#231;&#227;o dos canais i&#244;nicos card&#237;acos, expondo os seus portadores a um risco de morte s&#250;bita<sup>123</sup>. As canalopatias mais conhecidas s&#227;o a s&#237;ndrome do QT longo (SQTL), a s&#237;ndrome do QT curto, a s&#237;ndrome de Brugada e a taquicardia ventricular polim&#243;rfica catecolamin&#233;rgica TVPC. A doen&#231;a do n&#243; sinusal e doen&#231;a de Lenegre ou doen&#231;a do sistema de condu&#231;&#227;o tamb&#233;m s&#227;o exemplos de canalopatias. </p>
    <p>Os canais i&#244;nicos, as correntes de &#237;ons que transitam atrav&#233;s desses canais, as prote&#237;nas que ligam a estrutura da membrana das c&#233;lulas mioc&#225;rdicas e as jun&#231;&#245;es entre essas estruturas fazem parte da forma&#231;&#227;o do impulso el&#233;trico e da transmiss&#227;o desses impulsos em todo o m&#250;sculo card&#237;aco de forma sincr&#244;nica, gerando o potencial de a&#231;&#227;o card&#237;aco<sup>124,125</sup>. O desempenho de cada uma dessas fun&#231;&#245;es &#233; determinado por diferentes genes. As muta&#231;&#245;es que ocorrem em tais genes causam disfun&#231;&#245;es espec&#237;ficas e ocasionam as doen&#231;as conhecidas como canalopatias<sup>126,127</sup>. Os canais i&#244;nicos presentes na membrana celular permitem a entrada e a sa&#237;da de &#237;ons, seguindo um gradiente de voltagem. A altera&#231;&#227;o causada pela muta&#231;&#227;o gen&#233;tica em cada um desses canais pode gerar um ganho ou uma perda da fun&#231;&#227;o. Existem canais i&#244;nicos respons&#225;veis pela despolariza&#231;&#227;o e repolariza&#231;&#227;o da membrana celular. O primeiro canal, da direita para a esquerda, chamado de canal eletrog&#234;nico, permite a entrada de 3 &#237;ons s&#243;dio (Na+) para cada sa&#237;da de &#237;on c&#225;lcio (Ca<sub>2</sub>+) atrav&#233;s da membrana. Os canais de despolariza&#231;&#227;o s&#227;o: 1) I<sub>Na</sub>, canal de s&#243;dio carreado pelo gene SCN5A, cujas muta&#231;&#245;es que geram ganho da fun&#231;&#227;o resultam na SQTL 3, enquanto a perda da fun&#231;&#227;o gera s&#237;ndrome de Brugada e doen&#231;a do n&#243; sinusal cong&#234;nita; 2) I<sub>CaL</sub> canal de c&#225;lcio tipo L; 3) I<sub>Na/Ca</sub> canal de s&#243;dio e c&#225;lcio, chamado de canal eletrog&#234;nico. Os canais envolvidos na repolariza&#231;&#227;o da c&#233;lula mioc&#225;rdica s&#227;o: 1) I<sub>K1</sub> canal de pot&#225;ssio gene KCNJ2. Este canal &#233; respons&#225;vel pela sa&#237;da de pot&#225;ssio no final da fase 3 do potencial de a&#231;&#227;o. O ganho de fun&#231;&#227;o desse canal resulta na <bold>s&#237;ndrome do QT curto tipo 3</bold>. enquanto a perda da fun&#231;&#227;o desse canal resulta na <bold>sindrome do QT longo tipo 7 e s&#237;ndrome de Andersen</bold>. 2) I<sub>To1</sub> e I<sub>To2</sub>, respons&#225;vel pelo in&#237;cio da repolariza&#231;&#227;o - fase 1 do potencial de a&#231;&#227;o; 3) I<sub>Kr</sub> - Canal de pot&#225;ssio - Gene KCNH2/KCNE2. Este canal &#233; respons&#225;vel pela sa&#237;da de pot&#225;ssio no in&#237;cio da fase 3 do potencial de a&#231;&#227;o. O <bold>ganho</bold> de fun&#231;&#227;o deste canal resulta na <bold>s&#237;ndrome do QT curto tipo 1.</bold> 4) I<sub>Ks</sub> canal de pot&#225;ssio gene KCNQ1/KCNE1. Esse canal &#233; respons&#225;vel pela sa&#237;da de pot&#225;ssio no meio da fase 3 do potencial de a&#231;&#227;o. O <bold>ganho</bold> de fun&#231;&#227;o desse canal resulta na <bold>s&#237;ndrome do QT curto tipo 2</bold>. A <bold>perda</bold> da fun&#231;&#227;o do gene KCNQ1 (que forma a subunidade alfa nos poros da membrana celular) e do gene KCNE1 (que codifica a prote&#237;na que forma o componente lento do canal I<sub>Ks</sub>) causa a <bold>s&#237;ndrome do QT longo tipo 1.</bold></p>
    <p>
      <bold>9.2. S&#237;ndrome do QT longo</bold>
    </p>
    <p>A s&#237;ndrome do QT longo &#233; o prot&#243;tipo das canalopatias. Relatada h&#225; mais de 50 anos, inicialmente como doen&#231;a autoss&#244;mica recessiva a s&#237;ndrome de Jervell e Lange-Nielsen<sup>128</sup> (surdez cong&#234;nita, aumento do intervalo QTc e s&#237;ncope ou morte s&#250;bita) e, posteriormente, autoss&#244;mica dominante s&#237;ndrome de Romano-Ward (QTc prolongado sem surdez), a SQTL demonstrou uma caracter&#237;stica heredit&#225;ria de morte s&#250;bita em pacientes sem cardiopatia estrutural. Atualmente, existem v&#225;rios tipos de SQTL conhecidas, determinadas por muta&#231;&#245;es em genes que causam altera&#231;&#245;es distintas na despolariza&#231;&#227;o e repolariza&#231;&#227;o ventricular (<xref ref-type="table" rid="tab13">tabela 13</xref>). </p>
    <table-wrap id="tab13">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt13.jpg"/></table-wrap>
    <p>As caracter&#237;sticas cl&#237;nicas t&#237;picas da SQTL incluem s&#237;ncope ou morte s&#250;bita associada a aumento do intervalo QTc e presen&#231;a de taquiarritmia ventricular e <italic>torsadesdepointes</italic>. Classicamente, existem fatores desencadeantes da s&#237;ncope na SQTL, atividade adren&#233;rgica na SQTL 1 e despertar s&#250;bito ou est&#237;mulo auditivo na SQTL 2. Entretanto, existe uma ampla variedade de apresenta&#231;&#245;es, podendo o portador da muta&#231;&#227;o ser desde assintom&#225;tico, sem aumento do intervalo QTc, at&#233; ter s&#237;ncope ou morte s&#250;bita j&#225; nos primeiros dias de vida. Por isso, foram desenvolvidos crit&#233;rios diagn&#243;sticos com pontua&#231;&#227;o para as altera&#231;&#245;es em 3 crit&#233;rios principais: hist&#243;ria cl&#237;nica, hist&#243;ria familiar e altera&#231;&#227;o eletrocardiogr&#225;fica<sup>129</sup> (<xref ref-type="table" rid="tab14">tabela 14</xref>).</p>
    <table-wrap id="tab14">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt14.jpg"/></table-wrap>
    <p>
      <bold>9.2.1. Altera&#231;&#245;es gen&#233;ticas da s&#237;ndrome do QT longo (SQTL)</bold>
    </p>
    <p>As altera&#231;&#245;es gen&#233;ticas s&#227;o conhecidas em aproximadamente 60% dos casos cl&#237;nicos de SQTL. S&#227;o conhecidos atualmente 7 genes respons&#225;veis por essas s&#237;ndromes. Entretanto, centenas de muta&#231;&#245;es j&#225; foram descritas, sendo essa a canalopatia card&#237;aca com maior n&#250;mero de muta&#231;&#245;es descritas<sup>130</sup>.</p>
    <p>A muta&#231;&#227;o mais comum ocorre no gene KCNQ1, respons&#225;vel pela SQTL 1 (40-50%) e pela s&#237;ndrome de Jervell-Lange-Nielsen tipo 1. Essa muta&#231;&#227;o causa uma perda da fun&#231;&#227;o da corrente de pot&#225;ssio I<sub>Ks</sub>, que tem papel importante na repolariza&#231;&#227;o celular e na adapta&#231;&#227;o do intervalo QT &#224; frequ&#234;ncia card&#237;aca. O gene KCNE1, cuja muta&#231;&#227;o causa a SQTL5, &#233; muito menos frequente (2-3%) e tamb&#233;m &#233; respons&#225;vel pela fun&#231;&#227;o de I<sub>Ks</sub><sup>123,131,132</sup>.</p>
    <p>Os genes KCNH2 (HERG), que codifica a subunidade alfa dos canais r&#225;pidos de pot&#225;ssio e KCNE2, que codifica a subunidade beta, s&#227;o respons&#225;veis pela entrada r&#225;pida de pot&#225;ssio durante a fase 3 do potencial de a&#231;&#227;o<sup>131,133</sup>. A perda da fun&#231;&#227;o da subunidade alfa representa 40% das SQTL genotipadas e &#233; respons&#225;vel pela SQTL 2<sup>134</sup>.</p>
    <p>A SQTL 3 representa aproximadamente 10% de todas as muta&#231;&#245;es diagnosticadas na SQTL, ocorre por altera&#231;&#245;es no gene SCN5A, cujo ganho de fun&#231;&#227;o produz uma entrada cont&#237;nua de s&#243;dio durante a fase de plat&#244;, facilitando despolariza&#231;&#245;es precoce da c&#233;lula card&#237;aca. Centenas de outras muta&#231;&#245;es tem sido descritas. Entretanto, as aplica&#231;&#245;es cl&#237;nicas de se identificar estas muta&#231;&#245;es para tratamento e acompanhamento dos pacientes e familiares de SQTL s&#227;o restritas &#224;s formas mais conhecidas<sup>125</sup>.</p>
    <p>
      <bold>9.2.2. Estratifica&#231;&#227;o de risco na SQTL</bold>
    </p>
    <p>A an&#225;lise gen&#233;tica tem sido muito utilizada na estratifica&#231;&#227;o do risco e em interven&#231;&#245;es terap&#234;uticas espec&#237;ficas em pacientes com intervalo QT prolongado, assim como em seus familiares, para a identifica&#231;&#227;o de portadores com intervalo QT normal.</p>
    <p>A recomenda&#231;&#227;o de estrat&#233;gias de estratifica&#231;&#227;o de risco e tratamento, por serem condi&#231;&#245;es cl&#237;nicas pouco frequentes, e, portanto, os dados sobre a doen&#231;a obtidos mediante estudos de coorte, alguns com grande n&#250;mero de participantes, com seguimento longo, outros com n&#250;mero mais limitado ou seguimento mais restrito, limita o n&#237;vel de evid&#234;ncia para as recomenda&#231;&#245;es para B.</p>
    <p>O marcador de risco mais robusto identificado &#233; um epis&#243;dio pr&#233;vio de morte card&#237;aca s&#250;bita abortada e sua causa mais comum, s&#227;o epis&#243;dios de taquicardia ventricular polim&#243;rfica, degenerando ou n&#227;o para fibrila&#231;&#227;o ventricular. Pacientes que experimentaram tal condi&#231;&#227;o t&#234;m risco 12,9 vezes maior de novos epis&#243;dios de morte s&#250;bita. S&#237;ncope pr&#233;via tamb&#233;m &#233; um marcador de risco extremamente desfavor&#225;vel<sup>135</sup>.</p>
    <p>Para pacientes assintom&#225;ticos, foram identificados como fatores de risco: intervalo QTc &gt; 500 ms para pacientes com SQTL 1 e 2 e pacientes do sexo masculino na SQTL 3, independentemente do intervalo QT. Muta&#231;&#245;es que envolvem um segmento do gene que codifica o poro do canal tamb&#233;m s&#227;o relacionadas com pior progn&#243;stico. Portanto, mais uma vez fica claro o valor da genotipagem em pacientes com essa s&#237;ndrome. A presen&#231;a de morte s&#250;bita na fam&#237;lia n&#227;o se mostrou marcador de maior risco de eventos<sup>136</sup>.</p>
    <p>
      <bold>9.2.3. Recomenda&#231;&#245;es</bold>
    </p>
    <p>Restri&#231;&#227;o de atividade f&#237;sica: embora nas SQTL 2 e 3 os epis&#243;dios de arritmia ventricular n&#227;o sejam relacionados aos esfor&#231;os, &#233; recomend&#225;vel que todos os pacientes acometidos evitem esfor&#231;os f&#237;sicos competitivos. Essa recomenda&#231;&#227;o &#233; particularmente importante no caso da nata&#231;&#227;o para SQTL1. Em pacientes com SQTL 2 devem-se evitar est&#237;mulos ac&#250;sticos, especialmente durante o sono, como despertador e telefone. Obviamente, drogas que sabidamente prolongam o intervalo QT n&#227;o devem ser utilizadas, assim como drogas que reduzem os n&#237;veis plasm&#225;ticos de pot&#225;ssio e magn&#233;sio (interven&#231;&#245;es classe I).</p>
    <p>Todos os pacientes com intervalo QT prolongado devem receber betabloqueadores, embora a prote&#231;&#227;o seja incompleta para portadores de SQTL 2 e 3 (interven&#231;&#227;o classe I). Para pacientes portadores de muta&#231;&#227;o, mas com intervalo QT normal, tamb&#233;m se recomenda o uso profil&#225;tico de betabloqueadores (recomenda&#231;&#227;o IIa)<sup>137,138</sup>.</p>
    <p>O marcapasso tem sido considerado uma terapia adjuvante, sempre em conjunto com o betabloqueador<sup>139,140</sup>. &#201; eficaz na preven&#231;&#227;o da recorr&#234;ncia de <italic>torsades de pointes</italic>, embora seu papel n&#227;o esteja bem definido. Os mecanismos envolvidos s&#227;o a supress&#227;o das pausas que antecedem e precipitam as <italic>torsades de pointes</italic>, e por meio do encurtamento do intervalo QT. Em linhas gerais, est&#225; indicado na preven&#231;&#227;o de bradicardia severa ou em pausas decorrentes do uso de betabloqueadores, em pacientes que n&#227;o toleram doses adequadas, que permanecem sintom&#225;ticos a despeito do seu uso correto ou quando h&#225; evid&#234;ncia de arritmias pausa-dependentes. Determinados gen&#243;tipos da SQTL podem se beneficiar mais do que outros com o implante de marcapasso. O efeito da bradicardia sobre a dispers&#227;o transmural da repolariza&#231;&#227;o seria mais marcante na SQTL3 e na SQTL2 e pouco expressivo na SQTL1. A correta programa&#231;&#227;o do marcapasso &#233; importante na preven&#231;&#227;o de arritmias na SQTL. A estimula&#231;&#227;o em frequ&#234;ncias mais elevadas encurta o intervalo QT e reduz a dispers&#227;o da repolariza&#231;&#227;o ventricular. O limite de frequ&#234;ncia m&#237;nimo deve ser programado para 70 a 80 bpm, podendo ser aumentado em situa&#231;&#245;es de risco mais elevado, como em procedimentos cir&#250;rgicos e per&#237;odo p&#243;s-parto. A ocorr&#234;ncia de bloqueio atrioventricular funcional em alguns pacientes (principalmente crian&#231;as com QT muito prolongado) imediatamente antes do in&#237;cio de <italic>torsades de pointes</italic> faz do DDD o modo de estimula&#231;&#227;o mais utilizado. N&#227;o h&#225; consenso sobre a melhor programa&#231;&#227;o quanto &#224; resposta de frequ&#234;ncia e tempo de atraso atrioventricular. Algumas caracter&#237;sticas da programa&#231;&#227;o que permitem quedas de freq&#252;&#234;ncia card&#237;aca baixas devem ser desligadas, como a histerese e a fun&#231;&#227;o sono.</p>
    <p>O implante de cardioversor-desfibrilador &#233; recomendado para todos os sobreviventes de morte s&#250;bita com bom estado funcional e com expectativa de vida maior que 1 ano (recomenda&#231;&#227;o classe I). Pacientes que venham apresentando s&#237;ncope apesar do uso de betabloqueadores tamb&#233;m podem se beneficiar do desfibrilador (recomenda&#231;&#227;o IIa). O desfibrilador pode ser considerado em pacientes com risco elevado para morte s&#250;bita, como SQTL 2 e 3, mesmo assintom&#225;ticos (recomenda&#231;&#227;o classe IIb)<sup>141,142</sup>. </p>
    <p>A denerva&#231;&#227;o simp&#225;tica pode ser considerada para pacientes com s&#237;ncope ou taquicardia ventricular polim&#243;rfica que j&#225; est&#227;o em uso de beta-bloqueadores (recomenda&#231;&#227;o IIb)<sup>143,144</sup>.</p>
    <p>
      <bold>9.3. S&#237;ndrome do QT curto</bold>
    </p>
    <p>Nesta doen&#231;a ocorre um encurtamento da repolariza&#231;&#227;o, favorecendo a g&#234;nese de arritmias ventriculares por reentrada. Caracteriza-se por um intervalo QT curto QTc&lt;320 ms com ondas T apiculadas, que podem ter amplitude aumentada, com sua fase ascendente normal e fase descendente r&#225;pida<sup>125,127,145,146</sup>. Como os par&#226;metros cl&#237;nicos para diagn&#243;stico ainda n&#227;o est&#227;o claros, a an&#225;lise gen&#233;tica &#233; &#250;til para confirmar o diagn&#243;stico em casos suspeitos. Muta&#231;&#245;es em 3 genes foram descritas KCNH2, KCNQ1 e KCNJ2 todas resultando em ganhos de fun&#231;&#227;o dos canais IKr, IKs e IK1, respectivamente, e determinando as s&#237;ndromes de QT curto tipo 1, 2 e 3. Como o n&#250;mero de pacientes com diagn&#243;stico confirmado &#233; baixo, ainda n&#227;o est&#225; determinado se algum tipo espec&#237;fico de muta&#231;&#227;o determina um pior progn&#243;stico. Fatores de risco para a ocorr&#234;ncia de arritmias tamb&#233;m n&#227;o s&#227;o conhecidos.</p>
    <p>O tratamento para essa afec&#231;&#227;o ainda &#233; motivo de controv&#233;rsia. Em pacientes com muta&#231;&#227;o no gene KCNH2, o uso de quinidina mostrou prolongar a refratariedade e suprimir a indu&#231;&#227;o de arritmias durante estudo eletrofisiol&#243;gico<sup>146</sup>, para as outras muta&#231;&#245;es, sua utilidade n&#227;o foi estabelecida. A doen&#231;a parece ter alta letalidade, por&#233;m, pode existir um vi&#233;s de diagn&#243;stico apenas nos casos graves. O uso do desfibrilador pode ser considerado, por&#233;m, deve-se ter em mente o inconveniente da possibilidade de ocorr&#234;ncia de choques inapropriados pelo fen&#244;meno de dupla contagem (complexos QRS e ondas T)<sup>147,148</sup>.</p>
    <p>
      <bold>9.4. S&#237;ndrome de Brugada</bold>
    </p>
    <p>Esta s&#237;ndrome &#233; caracterizada pela ocorr&#234;ncia de s&#237;ncope ou morte s&#250;bita causada por taquicardia ventricular polim&#243;rfica, em cora&#231;&#245;es estruturalmente normais. Seu aspecto mais peculiar &#233; a ocorr&#234;ncia de supradesnivelamento do ponto J nas deriva&#231;&#245;es precordiais direitas V1 a V3, embora esse fen&#244;meno j&#225; tenha sido descrito nas deriva&#231;&#245;es inferiores<sup>149</sup>. Talvez seja influenciada pelo sexo 90% dos casos ocorrem em homens. At&#233; o momento, foram identificadas apenas muta&#231;&#245;es no gene SCN5A, que est&#227;o presentes em cerca<sup>123</sup> de 1/3 dos afetados<sup>123,150</sup>. Clinicamente, a doen&#231;a manifesta-se com s&#237;ncope ou morte s&#250;bita, preponderantemente na terceira ou quarta d&#233;cadas de vida. A febre &#233; um fator desencadeante para as arritmias.</p>
    <p>Na estratifica&#231;&#227;o do risco, indiv&#237;duos com supradesnivelamento do ponto J que ocorre espontaneamente t&#234;m pior progn&#243;stico, quando comparados &#224;queles em que o padr&#227;o t&#237;pico foi observado apenas ap&#243;s infus&#227;o de flecainida, procainamida ou ajmalina. A ocorr&#234;ncia de s&#237;ncope, associada &#224; ocorr&#234;ncia espont&#226;nea do supradesnivelamento, aumenta o risco de morte s&#250;bita em 6 vezes. A presen&#231;a de morte s&#250;bita na fam&#237;lia n&#227;o mostrou ser &#250;til para estratifica&#231;&#227;o do risco, assim como a detec&#231;&#227;o da muta&#231;&#227;o no gene SCN5A<sup>151,152</sup>. </p>
    <p>O uso da estimula&#231;&#227;o ventricular programada na estratifica&#231;&#227;o do risco &#233; controverso. Na s&#233;rie de Brugada e cols.<sup>152</sup>, a aus&#234;ncia de arritmias indut&#237;veis durante estudo eletrofisiol&#243;gico teve valor preditivo negativo de 93% em 3 anos, para eventos cl&#237;nicos. Entretanto, na s&#233;rie de pacientes de Priori e cols.<sup>136</sup>, o estudo eletrofisiol&#243;gico teve baixa acur&#225;cia como preditor de eventos. Atualmente, o uso da estimula&#231;&#227;o ventricular programada &#233; indica&#231;&#227;o classe IIb para estratifica&#231;&#227;o do risco em pacientes assintom&#225;ticos<sup>153,154</sup>. </p>
    <p>Como recomenda&#231;&#245;es terap&#234;uticas, o uso de desfibrilador &#233; indica&#231;&#227;o classe I para pacientes recuperados de morte s&#250;bita. &#201; indica&#231;&#227;o classe IIa para pacientes com supradesnivelamento espont&#226;neo do ponto J que manifestaram s&#237;ncope ou que tiveram taquicardia ventricular documentada previamente.</p>
    <p>A infus&#227;o de isoproterenol pode ser &#250;til no tratamento da tempestade el&#233;trica (classe IIa), assim como o uso de quinidina para essa mesma situa&#231;&#227;o (classe IIb)</p>
    <p>
      <bold>9.5. Taquicardia ventricular polim&#243;rfica catecolamin&#233;rgica</bold>
    </p>
    <p>A doen&#231;a &#233; caracterizada por epis&#243;dios de taquicardia ventricular polim&#243;rfica, desencadeada durante esfor&#231;os ou emo&#231;&#245;es, em crian&#231;as e adultos jovens que apresentam cora&#231;&#245;es estruturalmente normais<sup>155,156</sup>. O eletrocardiograma em repouso &#233; normal, exceto, por uma bradicardia relativa para a idade e presen&#231;a frequente de onda U. Manifesta-se clinicamente como s&#237;ncope desencadeada por situa&#231;&#245;es de estresse f&#237;sico ou emocional<sup>155,156</sup>. Foram descritas duas muta&#231;&#245;es, nos genes RyR2 e CASQ2, que codificam o receptor rianodina, prote&#237;na respons&#225;vel pela libera&#231;&#227;o do c&#225;lcio do ret&#237;culo sarcoplasm&#225;tico, e a calsequestrina, prote&#237;na que se liga ao c&#225;lcio no ret&#237;culo sarcoplasm&#225;tico. A an&#225;lise gen&#233;tica n&#227;o contribui para a estratifica&#231;&#227;o do risco, mas &#233; importante na identifica&#231;&#227;o de portadores da muta&#231;&#227;o que ainda n&#227;o manifestaram sintomas.</p>
    <p>A manifesta&#231;&#227;o t&#237;pica &#233; a ocorr&#234;ncia de arritmias durante exerc&#237;cio, mais frequentemente quando se atingem 120 a 130 batimentos por minuto, iniciando-se com extrass&#237;stoles ventriculares isoladas, progredindo para epis&#243;dios de taquicardia ventricular n&#227;o sustentada e sustentada, se o esfor&#231;o for mantido (figura 3). </p>
    <p>O uso de beta-bloqueadores &#233; bastante efetivo para redu&#231;&#227;o dos sintomas, sendo indica&#231;&#227;o classe I para pacientes com manifesta&#231;&#245;es cl&#237;nicas, IIa para crian&#231;as portadoras da muta&#231;&#227;o, mas que n&#227;o manifestaram sintomas, e classe IIb para adultos nessa mesma situa&#231;&#227;o<sup>157,158</sup>.</p>
    <p>O uso do desfibrilador &#233; indica&#231;&#227;o classe I nos recuperados de morte s&#250;bita e classe IIa nos pacientes que permanecem com s&#237;ncope ou taquicardia ventricular sustentada apesar do uso de betabloqueadores.</p>
    <p>Tem sido sugerido recentemente o tratamento com denerva&#231;&#227;o card&#237;aca simp&#225;tica esquerda como uma alternativa terap&#234;utica para pacientes que n&#227;o podem fazer uso de betabloqueadores. O mecanismo de a&#231;&#227;o dessa terap&#234;utica parece muito atrativo para tais pacientes, visto que reduz a estimula&#231;&#227;o catecolamin&#233;rgica card&#237;aca, o que em tese reduziria o est&#237;mulo deflagrador da arritmia. Alguns autores relataram experi&#234;ncias iniciais promissoras, mas ainda h&#225; poucos dados para que essa alternativa seja incorporada de rotina, sendo atualmente recomendada apenas nos casos de falha ou contra-indica&#231;&#227;o dos betabloqueadores.</p>
    <p>As recomenda&#231;&#245;es com rela&#231;&#227;o &#224; libera&#231;&#227;o para atividade esportiva levam em considera&#231;&#227;o o tipo de atividade e o diagn&#243;stico estabelecido a partir da avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o e eventuais exames complementares que se fizerem necess&#225;rios. Os esportes s&#227;o classificados em est&#225;ticos e din&#226;micos conforme a <xref ref-type="table" rid="a01tab15">tabela 15</xref>. As recomenda&#231;&#245;es est&#227;o resumidas nas <xref ref-type="table" rid="a01tab16">tabelas 16</xref>, <xref ref-type="table" rid="a01tab17">17</xref> e <xref ref-type="table" rid="a01tab18">18</xref>. </p>
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    <p content-type="asset">
      <table-wrap id="a01tab16">
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      <table-wrap id="a01tab17">
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    <p content-type="asset">
      <table-wrap id="a01tab18">
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    <p>
      <bold>10. Suporte b&#225;sico de vida no atleta</bold>
    </p>
    <p>
      <bold>10. 1. Morte s&#250;bita no atleta</bold>
    </p>
    <p>Apesar de rara, a morte s&#250;bita (MS) no esporte &#233; um evento que causa como&#231;&#227;o p&#250;blica, principalmente quando envolve atletas de alta performance. Estat&#237;sticas de diferentes pa&#237;ses mostram que sua preval&#234;ncia varia de 0,28 a 1 por 100.000 atletas<sup>159,160</sup>. Diferentes altera&#231;&#245;es estruturais e arritmog&#234;nicas s&#227;o respons&#225;veis pelos casos de parada card&#237;aca s&#250;bita no atleta, no entanto, a mais frequente &#233; a miocardiopatia hipertr&#243;fica, representando de 25 a 36% dos casos<sup>159,160</sup>. O exerc&#237;cio vigoroso associado &#224; cardiopatias ocultas parece ser o gatilho que desencadeia a arritmia respons&#225;vel pela parada cardiorrespirat&#243;ria (PCR).</p>
    <p>Diretrizes nacionais<sup>3</sup> e internacionais<sup>161</sup> aconselham o rastreio cardiovascular pr&#233;-participa&#231;&#227;o, que se constitui, de uma forma geral, em uma anamnese detalhada, exame f&#237;sico e eletrocardiograma de 12 deriva&#231;&#245;es. Tal rastreio seria capaz de detectar cerca de 90% dos atletas que sofreram um evento fatal, havendo, entretanto, relatos de esportistas v&#237;timas de MS que n&#227;o possu&#237;am qualquer altera&#231;&#227;o estrutural ou de condu&#231;&#227;o<sup>162</sup> Isoladamente, o rastreio n&#227;o &#233; capaz de diminuir consideravelmente o n&#250;mero de mortes por parada cardiorrespirat&#243;ria s&#250;bita nesse grupo de risco, principalmente pela n&#227;o realiza&#231;&#227;o dessa avalia&#231;&#227;o por parte dos atletas e pelos poss&#237;veis resultados falso-negativos, sendo necess&#225;ria a implanta&#231;&#227;o e fortalecimento de um segundo pilar, o suporte b&#225;sico de vida.</p>
    <p>
      <bold>10.2. Atendimento inicial ao atleta</bold>
    </p>
    <p>Os cuidados para um melhor atendimento de emerg&#234;ncia s&#227;o resumidos a um conjunto de a&#231;&#245;es efetuadas nos primeiros minutos que se seguem ap&#243;s um evento s&#250;bito. Tais a&#231;&#245;es podem ser resumidas em dois pilares: a organiza&#231;&#227;o e o planejamento da equipe de atendimento de emerg&#234;ncia, estabelecida no local onde &#233; realizada a atividade f&#237;sica, e o treinamento dos socorristas em RCP e manuseio do desfibrilador externo autom&#225;tico (DEA). Locais em que ocorrem atividades f&#237;sicas, tais como centros de treinamento, escolas, faculdades, gin&#225;sios, etc. precisam ter um plano de atendimento emergencial bem organizado, com profissionais treinados em suporte b&#225;sico de vida (SBV) e comunica&#231;&#227;o r&#225;pida e efetiva com servi&#231;os preparados para realizar o suporte avan&#231;ado de vida em cardiologia (SAVC).</p>
    <p>O tratamento efetivo de um atleta que sofre uma PCR s&#250;bita depende de uma sequ&#234;ncia de a&#231;&#245;es interdependentes, para que assim, quando ligadas entre si, formem um efeito em cadeia, aumentando a sobrevida das v&#237;timas, batizado pela <italic>American Heart Association</italic>, de "corrente da sobreviv&#234;ncia", formada pelos seguintes elos: acesso r&#225;pido, RCP precoce, desfibrila&#231;&#227;o precoce e SAVC precoce.</p>
    <p>A maior parte das PCR s&#250;bitas em atletas ocorre devido a uma taquiarritmia<sup>163</sup> (fibrila&#231;&#227;o ventricular), logo, pode ser tratada com a desfibrila&#231;&#227;o. A redu&#231;&#227;o na mortalidade nos atletas surpreendidos por tal evento requer programas de treinamento em RCP e manuseio do DEA, al&#233;m de socorristas equipados e treinados para reconhecer emerg&#234;ncias, ativar o sistema de emerg&#234;ncia, prover RCP de qualidade e usar o DEA. Existem orienta&#231;&#245;es atuais para que instala&#231;&#245;es esportivas que tenham mais de 2.500 frequentadores ou desenvolvam programas de atividade f&#237;sica a indiv&#237;duos pertencentes a certos grupos de risco, como cardiopatas e idosos, possuam desfibriladores estrategicamente alocados<sup>131</sup>.</p>
    <p>J&#225; se encontra bem estabelecido que para cada minuto sem ressuscita&#231;&#227;o cardiopulmonar (RCP) a sobrevida de uma v&#237;tima de PCR testemunhada diminui de 7 a 10%. No entanto, arritmias ventriculares no contexto de doen&#231;as estruturais parecem ser mais suscept&#237;veis a pequenos atrasos na desfibrila&#231;&#227;o<sup>129</sup> se comparados a um contexto de um cora&#231;&#227;o estruturalmente sadio, o que, possivelmente, traz aos atletas v&#237;timas de uma PCR s&#250;bita um decl&#237;nio mais significativo na sobrevida ao esperar por um DEA, salientando a extrema import&#226;ncia do terceiro elo da corrente, a desfibrila&#231;&#227;o precoce.</p>
    <p>O aumento da sobrevida consequente a programas de acesso p&#250;blico &#224; desfibrila&#231;&#227;o tem sido bem documentado em in&#250;meros estudos, incluindo loca&#231;&#245;es como cassinos<sup>164</sup>, avi&#245;es<sup>165</sup> e aeroportos<sup>132</sup> no entanto, pouco se sabe sobre o impacto dessa iniciativa sobre o grupo de risco espec&#237;fico dos atletas, principalmente por tratar-se de um evento raro.</p>
    <p>Importante marcador de risco, a avalia&#231;&#227;o m&#233;dica pr&#233;-participa&#231;&#227;o deve ser obrigat&#243;ria para praticantes de atividades f&#237;sico-esportivas, j&#225; que &#233; capaz de detectar altera&#231;&#245;es cardiovasculares que predisp&#245;em &#224; morte s&#250;bita. Apesar das diferentes recomenda&#231;&#245;es internacionais, existe um consenso de que todo atleta deva realizar, necessariamente, uma hist&#243;ria cl&#237;nica, exame f&#237;sico e ECG de 12 deriva&#231;&#245;es, complementando a investiga&#231;&#227;o com outros exames de acordo com o grau de suspei&#231;&#227;o.</p>
    <p>Esportistas v&#237;timas de MS devem ser prontamente atendidos e necessitam de RCP de qualidade imediata, provendo uma quantidade vital de fluxo sangu&#237;neo para o c&#233;rebro e o cora&#231;&#227;o. A equipe de emerg&#234;ncia local deve ser capaz de realizar um tempo ideal entre o colapso e a desfibrila&#231;&#227;o de 3 a 5 minutos, aumentando assim, as chances de sucesso do choque. Como, na maioria dos casos, o ritmo p&#243;s-desfibrila&#231;&#227;o n&#227;o &#233; capaz de atingir uma perfus&#227;o efetiva, a RCP dever&#225; ser reiniciada imediatamente ap&#243;s o choque.</p>
    <p>Finalmente, a avalia&#231;&#227;o m&#233;dica peri&#243;dica, um efetivo protocolo local para emerg&#234;ncias e socorristas treinados em SBV e capazes de prover RCP de qualidade, desfibrila&#231;&#227;o precoce e contato r&#225;pido com centros habilitados em SAVC constituem os pilares de sustenta&#231;&#227;o para um objetivo comum: a diminui&#231;&#227;o do n&#250;mero de casos de morte s&#250;bita em atletas e o aumento da sobrevida das v&#237;timas.</p>
    <p>
      <bold>10.3. Aspectos especiais da preven&#231;&#227;o de MS relacionada com o exerc&#237;cio e o esporte</bold>
    </p>
    <p>10.3.1. <italic><bold>Doping</bold></italic>: subst&#226;ncias il&#237;citas no esporte (<ext-link ext-link-type="uri" xlink:href="http://www.wada-ama.org"><bold>www.wada-ama.org</bold></ext-link>)</p>
    <p>Algumas subst&#226;ncias utilizadas como <italic>doping</italic> s&#227;o capazes de provocar repercuss&#245;es delet&#233;rias, especialmente no aparelho cardiovascular, inclusive morte s&#250;bita. Dentre as subst&#226;ncias mais usadas destacam-se os esteroides anabolizantes, a efedrina e a anfetamina. Dentre as drogas sociais as mais utilizadas s&#227;o a coca&#237;na, a maconha e a 3,4-metilenodioximetanfetamina MDMA, conhecida como ecstasy.</p>
    <p>
      <italic>10.3.1.1. Esteroides anabolizantes (EA)</italic>
    </p>
    <p>Essas subst&#226;ncia provocam diversos efeitos colaterais, incluindo, efeitos cardiovasculares indesej&#225;veis. Os EA podem induzir &#224; hipertens&#227;o arterial (HA) secund&#225;ria e nefroesclerose. A testosterona pode provocar um aumento da resposta vascular &#224; norepinefrina e, como conseq&#252;&#234;ncia, promover reten&#231;&#227;o h&#237;drica e aumento da resist&#234;ncia vascular perif&#233;rica levando &#224; HA3.</p>
    <p>Outro efeito importante foi descrito por Tagarakis e cols.<sup>166</sup>, que demonstraram, pela primeira vez em n&#237;vel microsc&#243;pico, uma adapta&#231;&#227;o de capilares card&#237;acos e mi&#243;citos com a utiliza&#231;&#227;o concomitante de esteroides anabolizantes e treinamento f&#237;sico. Isso provocaria um aumento desproporcional da massa mioc&#225;rdica em rela&#231;&#227;o aos capilares card&#237;acos. Os resultados desse trabalho sugeriram que o uso de EA poderia desenvolver um desequil&#237;brio entre a oferta e o consumo de O<sub>2</sub>, especialmente durante o exerc&#237;cio.</p>
    <p>
      <italic>10.3.1.2. Efedrina </italic>
    </p>
    <p>Estimulantes em geral acarretam taquicardia e aumento do consumo mioc&#225;rdico de oxig&#234;nio, podendo gerar arritmias e infarto agudo do mioc&#225;rdio em indiv&#237;duos suscept&#237;veis. A efedrina pode provocar taquicardias ventriculares sintom&#225;ticas, extrass&#237;sstoles ventriculares frequentes, fibrila&#231;&#227;o atrial e morte s&#250;bita. &#201; importante salientar que muitos produtos ditos naturais e "derivados da flora" possuem subst&#226;ncias como efedrina em sua f&#243;rmula sem fazerem parte da bula.</p>
    <p>
      <italic>10.3.1.3. Coca&#237;na</italic>
    </p>
    <p>O uso de coca&#237;na acarreta vasoconstric&#231;&#227;o generalizada, tendo como principal consequ&#234;ncia, a hipertens&#227;o arterial. Apesar de uso de coca&#237;na causar vasoconstric&#231;&#227;o mais intensa no sistema nervoso central, esta pode repercutir tamb&#233;m em outros &#243;rg&#227;os, como os rins provocando insufici&#234;ncia renal<sup>1</sup>. O uso de coca&#237;na pode provocar, ainda, IAM, arritmias card&#237;acas, cardiomiopatia congestiva, miocardite, hemorragia subaracnoidea, ruptura de aorta, hipertens&#227;o arterial, isquemia mioc&#225;rdica espont&#226;nea ou induzida pelo exerc&#237;cio e morte s&#250;bita card&#237;aca.</p>
    <p>
      <italic>10.3.1.4. Anfetaminas</italic>
    </p>
    <p>&#201; o prot&#243;tipo dos estimulantes do SNC. Possui grande variedade de sais e misturas sob diversas formas de apresenta&#231;&#227;o, sendo a mais usada o sulfato de dextroanfetamina. Essa subst&#226;ncia possui uma a&#231;&#227;o direta por estimula&#231;&#227;o dos receptores adren&#233;rgicos em n&#237;vel cortical e sistema reticular ativador ascendente e uma a&#231;&#227;o indireta, deslocando as catecolaminas end&#243;genas de seus s&#237;tios nas termina&#231;&#245;es nervosas. Seus efeitos colaterais mais pronunciados s&#227;o: gerais ins&#244;nia, tonteiras, sudorese profusa, tremores e euforia; Cardiovasculares palpita&#231;&#245;es, taquicardia, desconforto precordial: neurol&#243;gicos hemorragia cerebral.</p>
    <p>
      <italic>10.3.1.5. MDMA (3,4- metilenodioximetanfetamina) (ecstasy) </italic>
    </p>
    <p>&#201; um alucin&#243;geno similar &#224; anfetamina. Em fun&#231;&#227;o de seu baixo custo e disponibilidade em comprimidos, sua popularidade e consumo t&#234;m aumentado de forma importante. A ingest&#227;o de MDMA aumenta a libera&#231;&#227;o de serotonina, dopamina e noradrenalina pelos neur&#244;nios pr&#233;-sin&#225;pticos. Al&#233;m disso, previne o metabolismo desses neurotransmissores por meio da inibi&#231;&#227;o da monoaminooxidase. Seus principais efeitos cardiovasculares s&#227;o a HA, taquicardia e arritmias, podendo levar &#224; MS<sup>167,168</sup>. </p>
    <p>
      <bold>10.4. Avalia&#231;&#227;o do atleta, organiza&#231;&#227;o e planejamento do atendimento</bold>
    </p>
    <p>A morte s&#250;bita relacionada com o exerc&#237;cio e o esporte &#233; um evento dram&#225;tico e os m&#233;dicos e algumas medidas podem e devem ser tomadas para tentar prevenir essa rara, mas tem&#237;vel, complica&#231;&#227;o da pr&#225;tica de esportes/exerc&#237;cio.</p>
    <p>Descrevemos, a seguir, algumas medidas preventivas relacionadas a MS relacionada com o exerc&#237;cio e o esporte.</p>
    <p>
      <bold>10.4.1 Aspectos relacionados ao atleta</bold>
    </p>
    <p>
      <italic>10.4.1.1 - Avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o</italic>
    </p>
    <p>Considerando-se que na grande maioria dos casos a MS relacionada com o esporte &#233; provocada por cardiopatias conhecidas ou n&#227;o diagnosticadas, todo candidato &#224; pr&#225;tica da atividade f&#237;sica dever&#225; se submeter a exame cl&#237;nico pr&#233;vio, independente da faixa et&#225;ria. Esse exame cl&#237;nico dever&#225; ser precedido de uma boa anamnese com particular aten&#231;&#227;o para a hist&#243;ria familiar de doen&#231;a cardiovascular e morte s&#250;bita. A avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o na tentativa de se detectar essas patologias &#233; a forma mais eficiente para se prevenir um evento cardiovascular fatal<sup>3</sup>. Em recente documento, o Comit&#234; Ol&#237;mpico Internacional ratifica a import&#226;ncia da avalia&#231;&#245;es m&#233;dicas peri&#243;dica em atletas de elite<sup>2</sup>.</p>
    <p>Embora reconhecendo que o exame cl&#237;nico isolado pode falhar ao n&#227;o detectar todas as cardiopatias com potencial de provocar MS, esse procedimento com &#234;nfase para o exame do aparelho cardiovascular, antecedido de uma anamnese minuciosa e hist&#243;ria patol&#243;gica pregressa e hist&#243;ria familiar, &#233; o primeiro passo para uma avalia&#231;&#227;o adequada do atleta.</p>
    <p>O exame cl&#237;nico dever&#225; ser acompanhado, idealmente, por um eletrocardiograma de 12 deriva&#231;&#245;es. Embora haja uma discord&#226;ncia entre a escola americana (esta s&#243; recomenda a anamnese e exame f&#237;sico) e a escola europeia (esta recomenda acrescentar o eletrocardiograma de 12 deriva&#231;&#245;es &#224; anamese e exame cl&#237;nico)<sup>52</sup>, lembramos que na diretriz da SBC <italic>Crit&#233;rios para solicita&#231;&#227;o de exames complementares do aparelho cardiovascular</italic> essa entidade considera o eletrocardiograma de 12 deriva&#231;&#245;es como exame <bold>obrigat&#243;rio</bold> numa primeira consulta cardiol&#243;gica (ECG-1-1096)<sup>169</sup>. Por outro lado, sabe-se que in&#250;meras doen&#231;as card&#237;acas el&#233;tricas que podem levar &#224; MS s&#227;o pass&#237;veis de serem diagnosticadas pelo ECG de repouso, entre elas a s&#237;ndrome do QT longo, a s&#237;ndrome de Brugada, a s&#237;ndrome de Lenegre-Lev e a s&#237;ndrome de Wolf-Parkinson-White<sup>170</sup>. O protocolo europeu que inclui anamnese, exame f&#237;sico e eletrocardiograma &#233; adotado, atualmente, pelo Comit&#234; Ol&#237;mpico Internacional, Comit&#234; Ol&#237;mpico Italiano, FIFA e Uni&#227;o Europeia de futebol (UEFA)<sup>171</sup>. O exame cl&#237;nico deve incluir uma hist&#243;ria familiar e pessoal e um <italic>screening</italic> espec&#237;fico para a s&#237;ndrome de Marfan<sup>172</sup>.</p>
    <p>Uma abordagem mais detalhada sobre avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o em atividades f&#237;sico-desportivas est&#225; dispon&#237;vel em outra sess&#227;o dessa diretriz.</p>
    <p>
      <italic>10.4.1.2 Quanto &#224; prepara&#231;&#227;o do atleta </italic>
    </p>
    <p>O acompanhamento do atleta tem que ser feito de forma hol&#237;stica. Assim sendo, para evitar eventos cl&#237;nico-cardiovasculares, tamb&#233;m s&#227;o importantes medidas preventivas b&#225;sicas, nutri&#231;&#227;o e hidrata&#231;&#227;o adequadas, respeitar os per&#237;odos de repouso e evitar treinamentos e competi&#231;&#245;es nos hor&#225;rios mais quentes do dia. Al&#233;m disso, &#233; importante o acompanhamento e a observa&#231;&#227;o dos atletas nos treinos e competi&#231;&#245;es por profissionais qualificados da equipe m&#233;dica, preferencialmente, com experi&#234;ncia em medicina do esporte e no&#231;&#245;es de primeiros socorros em casos de situa&#231;&#245;es cl&#237;nico-emergenciais.</p>
    <p>10.4.2 Aspectos relacionados aos locais de treinos e competi&#231;&#245;es</p>
    <p>
      <italic>10.4.2.1 Atendimento emergencial e plano de conting&#234;ncia m&#233;dica</italic>
    </p>
    <p>Al&#233;m de todo o material necess&#225;rio ao atendimento de uma parada cardiorrespirat&#243;ria, dever&#225; ser elaborado um plano de conting&#234;ncia m&#233;dica nos locais de treinos e competi&#231;&#245;es, com pessoal treinado em ressuscita&#231;&#227;o cardiorrespirat&#243;ria, para a eventualidade de uma emerg&#234;ncia cl&#237;nica ou cardiovascular, otimizando o transporte de atletas para unidade hospitalar de maior complexidade, quando for o caso<sup>173,174</sup>.</p>
    <p>
      <italic>10.4.2.2 Desfibrilador externo autom&#225;tico </italic>
    </p>
    <p>O desfibrilador externo autom&#225;tico (DEA) dever&#225; estar dispon&#237;vel para sua utiliza&#231;&#227;o em menos de 5 minutos nos locais de treinos e competi&#231;&#245;es, clubes, arenas, est&#225;dios, academias e cl&#237;nicas de reabilita&#231;&#227;o cardiovascular com equipe treinada em ressuscita&#231;&#227;o cardiopulmonar<sup>174,175</sup>. </p>
    <p>Entre atletas jovens as paradas cardiorrespirat&#243;rias ocorrem, geralmente, ap&#243;s sess&#245;es de treinamento intenso ou durante uma competi&#231;&#227;o. Embora a ocorr&#234;ncia desses eventos seja rara (correspondendo a 1% daquelas que ocorrem em indiv&#237;duos de meia idade ou idosos), o valor de um pronto atendimento e ressuscita&#231;&#227;o com sucesso aumenta a sobrevida em longo prazo<sup>176</sup>. </p>
    <p>
      <bold>11. Paratletas ou atletas portadores de necessidades especiais.</bold>
    </p>
    <p>
      <bold>11.1. Avalia&#231;&#227;o cardiol&#243;gica: pr&#233;-participa&#231;&#227;o e reavalia&#231;&#245;es </bold>
    </p>
    <p>Todos os atletas paraol&#237;mpicos devem ser submetidos a avalia&#231;&#227;o independente de idade, sexo e defici&#234;ncia associada; a avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o deve incluir crian&#231;as, adolescentes, adultos, <italic>master</italic> / idosos; homens e mulheres, sob responsabilidade exclusiva do m&#233;dico assistente (grau de recomenda&#231;&#227;o: I, n&#237;vel de evid&#234;ncia: C). </p>
    <p>A avalia&#231;&#227;o deve ser global, levando em considera&#231;&#227;o o organismo como um todo, salientando-se os aspectos f&#237;sicos e som&#225;ticos; deve-se ter em mente as intera&#231;&#245;es entre defici&#234;ncias f&#237;sicas, co-morbidades, e respectivas sequelas no treinamento f&#237;sico e desempenho esportivo (grau de recomenda&#231;&#227;o: I, n&#237;vel de evid&#234;ncia: C) (<xref ref-type="fig" rid="fig4">Figura 4</xref>).</p>
    <fig id="fig4">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gf02.jpg"/></fig>
    <p>A periodicidade das reavalia&#231;&#245;es deve ficar a crit&#233;rio do m&#233;dico assistente, segundo as caracter&#237;sticas de cada caso; entretanto, a periodicidade deve ter por finalidade prec&#237;pua a pr&#225;tica do esporte seguro (grau de recomenda&#231;&#227;o: I, n&#237;vel de evid&#234;ncia: C). </p>
    <p>A avalia&#231;&#227;o dos atletas paraol&#237;mpicos obedece a protocolo definido, resumido na <xref ref-type="table" rid="tab21">Tabela 21</xref></p>
    <table-wrap id="tab21">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt19.jpg"/></table-wrap>
    <p>Ap&#243;s a avalia&#231;&#227;o inicial, segundo os achados devem ser indicados exames especializados, a crit&#233;rio do m&#233;dico assistente, tais como teste cardiopulmonar (TCP), ecocardiograma (ECO), vetorcardiograma (VCG), tomografia computadorizada, resson&#226;ncia magn&#233;tica, ultrassom, eletroforese de hemoglobina (pesquisa de anemia falciforme) e avalia&#231;&#245;es cardiol&#243;gica, oft&#225;lmica (pesquisa de Marfan, glaucoma, descolamento de retina) e ortop&#233;dica<sup>177,178</sup> (grau de recomenda&#231;&#227;o: I, n&#237;vel de evid&#234;ncia: C).</p>
    <p>Em atletas com paralisia cerebral pode-se utilizar o escore de avalia&#231;&#227;o de espasticidade (QSFC <italic>quantitative sports and functional classification</italic>), baseado nas condi&#231;&#245;es musculares de membros superiores, inferiores e tronco, para uso em investiga&#231;&#245;es cl&#237;nicas, tratamento cl&#237;nico e treinamento f&#237;sico<sup>179</sup>.</p>
    <p>Atletas cadeirantes e portadores de pr&#243;teses devem ser seguidamente e minuciosamente examinados para detec&#231;&#227;o de escaras de dec&#250;bito ou escaras no coto de implanta&#231;&#227;o da pr&#243;tese. A presen&#231;a de ulcera&#231;&#245;es nesses locais torna o atleta temporariamente ineleg&#237;vel, at&#233; que sejam restauradas as condi&#231;&#245;es locais do tegumento (grau de Recomenda&#231;&#227;o: I, n&#237;vel de evid&#234;ncia: C). A pr&#225;tica de reten&#231;&#227;o urin&#225;ria em cadeirantes deve ser proscrita, dado o risco de grandes eleva&#231;&#245;es de press&#227;o arterial e acidente vascular cerebral. Nos casos de bexiga neurog&#234;nica deve-se atentar &#224; presen&#231;a de infec&#231;&#245;es urin&#225;rias subcl&#237;nicas. </p>
    <p>
      <bold>11.2. Teste cardiopulmonar</bold>
    </p>
    <p>Os fundamentos dos protocolos do teste cardiopulmonar incluem: 1) reprodutibilidade do ato esportivo, segundo o princ&#237;pio da especificidade; 2) adequa&#231;&#227;o &#224; modalidade desportiva e aos meios de locomo&#231;&#227;o do atleta; 3) realiza&#231;&#227;o dos testes com estabilidade e seguran&#231;a, assegurando a precis&#227;o e a reprodutibilidade das aferi&#231;&#245;es11 (grau de recomenda&#231;&#227;o: I, n&#237;vel de evid&#234;ncia: B). </p>
    <p>Cuidados especiais devem ser tomados em rela&#231;&#227;o ao tipo e grau de defici&#234;ncia, &#224; postura do atleta, &#224; temperatura ambiente, ao esvaziamento vesical pr&#233;vio, &#224; preven&#231;&#227;o de hipotens&#227;o, ao risco de crises convulsivas e acidentes, &#224;s aferi&#231;&#245;es da press&#227;o arterial e ao velamento adequado das m&#225;scaras. In&#250;meros fatores podem limitar o desempenho nas avalia&#231;&#245;es: 1) cl&#237;nicos: defici&#234;ncias intelectual e sensorial (visual, t&#225;ctil, auditiva, epilepsia, disreflexia auton&#244;mica, bexiga neurog&#234;nica, depriva&#231;&#227;o simp&#225;tica, s&#237;ndrome p&#243;s-p&#243;lio, taquipneia de esfor&#231;o, desnutri&#231;&#227;o; 2) locomotores: redu&#231;&#227;o da massa, for&#231;a e flexibilidade musculares, aumento do t&#244;nus muscular, redu&#231;&#227;o da mobilidade articular, incoordena&#231;&#227;o motora, les&#245;es osteoarticulares secund&#225;rias &#224;s pr&#225;ticas desportivas, les&#245;es de cotos de amputa&#231;&#227;o; 3) cardiovasculares: eventuais afec&#231;&#245;es associadas; 4) fisiol&#243;gicos: redu&#231;&#227;o do VO2 PICO, limiar anaer&#243;bio, ponto de compensa&#231;&#227;o respirat&#243;rio, fadiga precoce, inatividade f&#237;sica; 4) socioecon&#244;micas e culturais: exclus&#227;o social, falta de patroc&#237;nio<sup>177</sup>.</p>
    <p>Segundo o princ&#237;pio da especificidade, tem-se utilizado erg&#244;metros de bra&#231;os para tenistas, arremessadores, halterofilistas, esgrimistas e nadadores, bicicleta para ciclistas e esteira para as demais modalidades<sup>177</sup>; ciclistas podem utilizar o equipamento pr&#243;prio acoplado ao sistema Mag 850 Minoura<sup>180</sup> (grau de recomenda&#231;&#227;o: I, n&#237;vel de evid&#234;ncia: C). </p>
    <p>Os testes cardiopulmonares podem ser executados por in&#250;meros protocolos espec&#237;ficos, citando-se como exemplo o resumido na <xref ref-type="table" rid="tab22">tabela 22</xref>.</p>
    <table-wrap id="tab22">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt20.jpg"/></table-wrap>
    <p>O protocolo de Knechtle e K&#246;plif (Institute of Sports Medicine Swiss Paraplegic Centre) para teste em esteira em cadeirantes, se inicia em velocidade de 8 km/h e inclina&#231;&#227;o de 1%, com incrementos de 0,5%, a cada 2 minutos e velocidade constante at&#233; exaust&#227;o<sup>181,182</sup>. </p>
    <p>Testes de campo tamb&#233;m podem ser realizados com vantagens<sup>183,184</sup>. Varia&#231;&#245;es entre 48-80% foram descritas nas equa&#231;&#245;es de regress&#227;o para determina&#231;&#227;o da capacidade f&#237;sica em parapl&#233;gicos e tetrapl&#233;gicos. Essas varia&#231;&#245;es podem ser explicadas pelo n&#237;vel e grau de les&#227;o medular, idade, g&#234;nero, atividade f&#237;sica e peso corporal<sup>183</sup>. Em nosso meio, os valores referentes &#224; pot&#234;ncia aer&#243;bia de atletas paraol&#237;mpicos t&#234;m sido semelhantes (<xref ref-type="table" rid="tab23">tabela 23</xref>)<sup>180,185</sup>.</p>
    <table-wrap id="tab23">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt21.jpg"/></table-wrap>
    <p>A avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o para atividades de lazer &#233; semelhante, em fun&#231;&#227;o do estresse f&#237;sico e mental. Em muitas ocasi&#245;es, dada a carga emocional envolvida e o menor n&#237;vel de treinamento, o estresse f&#237;sico e psicol&#243;gico pode ser de grande intensidade, de grau semelhante ao relativo &#224;s competi&#231;&#245;es.</p>
    <p>
      <bold>12. Preven&#231;&#227;o de eventos/morte s&#250;bita em esportes </bold>
    </p>
    <p>A preven&#231;&#227;o de eventos deve incluir a preven&#231;&#227;o de acidentes, de agravamento das les&#245;es e comorbidades preexistentes e da morte s&#250;bita. </p>
    <p>Os objetivos de um protocolo de preven&#231;&#227;o de eventos em esportes baseiam-se no rastreamento pr&#233;-participa&#231;&#227;o:</p>
    <disp-quote>
      <p>1. Identificar condi&#231;&#245;es predisponentes, ou seja, doen&#231;as cardiovasculares que potencialmente podem causar morte s&#250;bita;</p>
      <p>2. Definir se h&#225; medidas que podem ser tomadas para reduzir o risco de morte s&#250;bita: Quais s&#227;o? Como devem ser desenvolvidas?</p>
      <p>3. Padronizar a conduta a ser adotada em cada cardiopatia e discutir a eventual desqualifica&#231;&#227;o do atleta do exerc&#237;cio de sua profiss&#227;o. </p>
    </disp-quote>
    <p>A preven&#231;&#227;o de eventos e morte s&#250;bita em esportes e lazer &#233; realizada levando-se em conta o diagn&#243;stico precoce e tratamento das afec&#231;&#245;es cardiovasculares, bem como a aplica&#231;&#227;o dos crit&#233;rios de inexigibilidade vigentes e espec&#237;ficos para as v&#225;rias afec&#231;&#245;es descritos nas partes I e II deste documento e devidamente aplicados aos atletas paraol&#237;mpicos<sup>187</sup>. Torna-se imperioso que nos locais de competi&#231;&#227;o existam recursos m&#233;dicos e param&#233;dicos, devidamente equipados, para atendimento de emerg&#234;ncias.</p>
    <p>Nas v&#225;rias institui&#231;&#245;es, o diretor cl&#237;nico e/ou o m&#233;dico respons&#225;vel pelo atendimento respondem perante o respectivo Conselho Regional de Medicina pelo cumprimento dessas normas.</p>
    <p>Indiv&#237;duos rec&#233;m-hospitalizados ou sedent&#225;rios h&#225; longa data necessitam de treinamento progressivo com incrementos graduais na frequ&#234;ncia e dura&#231;&#227;o das sess&#245;es e na intensidade dos exerc&#237;cios; al&#233;m do risco de les&#245;es e seq&#252;elas f&#237;sicas, o aparecimento dessas pode ser fator de desencorajamento ao treinamento, prejudicando a auto-imagem, e predispondo ao abandono do programa (grau de recomenda&#231;&#227;o I, n&#237;vel de evid&#234;ncia C).</p>
    <p>
      <bold>12.1. Aspectos &#233;ticos</bold>
    </p>
    <p>A avalia&#231;&#227;o m&#233;dica deve incluir especialistas de v&#225;rias &#225;reas, destacando-se a medicina do exerc&#237;cio e esporte, a cardiologia, a ortopedia e a fisiatria. </p>
    <p>Em se tratando de atletas portadores de defici&#234;ncias, torna-se importante ressaltar que &#233; de compet&#234;ncia exclusiva do m&#233;dico dirigir o treinamento, diagnosticar as eventuais patologias e sequelas, solicitar exames, prescrever terap&#234;utica e afastar os atletas das atividades esportivas, sendo vedado ao m&#233;dico atribuir ou delegar fun&#231;&#245;es de sua exclusiva compet&#234;ncia para profissionais n&#227;o habilitados ao exerc&#237;cio da medicina. (<bold>Conselho Federal de Medicina, Resolu&#231;&#227;o n&#186; 1236/87</bold>). Por outro lado, a execu&#231;&#227;o do treinamento deve ser realizada por professores de educa&#231;&#227;o f&#237;sica e fisioterapeutas. A intera&#231;&#227;o entre m&#233;dicos, professores de educa&#231;&#227;o f&#237;sica, fisioterapeutas, fisiologistas, nutricionistas e psic&#243;logos &#233; fundamental para o sucesso do programa. A prescri&#231;&#227;o do treinamento deve ser feita em receitu&#225;rio m&#233;dico, constando modalidade, freq&#252;&#234;ncia e dura&#231;&#227;o das sess&#245;es, intensidade do treinamento e outras observa&#231;&#245;es, a crit&#233;rio do m&#233;dico assistente. Essa conduta est&#225; ratificada pelo <bold>Conselho Federal de Medicina Parecer 4141/2003:</bold> "Por todo o exposto, compete exclusivamente ao m&#233;dico, ap&#243;s o diagn&#243;stico da patologia, prescrever a terap&#234;utica adequada ao paciente e, inclusive, a prescri&#231;&#227;o de atividade f&#237;sica em face da patologia diagnosticada ou para a preven&#231;&#227;o de diversas patologias." </p>
    <p>Nas v&#225;rias institui&#231;&#245;es, o diretor cl&#237;nico e/ou o m&#233;dico respons&#225;vel pelo atendimento respondem pelo cumprimento dessas normas perante o respectivo Conselho Regional de Medicina. </p>
    <p>As rela&#231;&#245;es do m&#233;dico com os demais profissionais em exerc&#237;cio na &#225;rea de sa&#250;de devem basear-se no respeito m&#250;tuo, na liberdade e independ&#234;ncia profissional de cada um, buscando sempre o interesse e o bem-estar do paciente (<bold>C&#243;digo de &#201;tica M&#233;dica de 08/01/1988 artigo 18</bold>). A intera&#231;&#227;o entre m&#233;dicos e para-m&#233;dicos professores de educa&#231;&#227;o f&#237;sica, fisioterapeutas, nutricionistas, psic&#243;logos e treinadores &#233; fundamental para o sucesso do programa de treinamento e deve ser estimulada a cada momento.</p>
    <p>
      <bold>12.2. Recomenda&#231;&#245;es</bold>
    </p>
    <p>Na atualidade, dada a escassez de relatos na literatura especializada, os crit&#233;rios de atendimento de atletas paraol&#237;mpicos se baseiam, em geral, em consenso de especialistas (n&#237;vel de evid&#234;ncia: C).</p>
    <p>A determina&#231;&#227;o da elegibilidade esportiva deve seguir o protocolo da International Paralympic Committee Classification Code and International Standards<sup>188</sup> e do Comit&#234; Ol&#237;mpico Brasileiro<sup>189</sup>. Dessa forma, o para-atleta pode ser eleg&#237;vel a uma modalidade e ineleg&#237;vel a outra. Os crit&#233;rios de elegibilidade esportiva s&#227;o definidos para cada modalidade paraol&#237;mpica pela respectiva federa&#231;&#227;o internacional<sup>190</sup>. </p>
    <p>As recomenda&#231;&#245;es para o atendimento de atletas paraol&#237;mpicos v&#234;m citadas na <xref ref-type="table" rid="tab24">Tabela 24</xref>.</p>
    <table-wrap id="tab24">
      <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt22.jpg"/></table-wrap>
    <p>
      <bold>13. Ap&#234;ndice</bold>
    </p>
    <p>
      <bold>13.1. Elabora&#231;&#227;o de atestado de aptid&#227;o ou liberat&#243;rio para o exerc&#237;cio e esporte<sup>173</sup></bold>
    </p>
    <p>O atestado m&#233;dico para libera&#231;&#227;o de atividades f&#237;sicas competitivas e amadoras &#233; parte integrante do ato m&#233;dico e um direito do paciente. Deve ser objetivo, esclarecedor quanto ao tipo de atividade f&#237;sica permitida e de prefer&#234;ncia com a intensidade de treinamento f&#237;sico sendo sugerida. Nos casos em que existem limita&#231;&#245;es &#224; pr&#225;tica de alguma modalidade, estas dever&#227;o estar claramente mencionadas no documento. Toda e qualquer informa&#231;&#227;o a respeito do quadro cl&#237;nico, exame f&#237;sico e exames complementares dever&#227;o estar contidos no atestado m&#233;dico quando solicitados e autorizados pelo paciente.</p>
    <p>Com base na medicina baseada em evid&#234;ncias &#233; mais apropriada a estratifica&#231;&#227;o do risco individual, considerando a condi&#231;&#227;o cl&#237;nica e a aptid&#227;o f&#237;sica, sexo, idade e condi&#231;&#245;es nas quais essa pr&#225;tica ser&#225; realizada. Para a grande maioria das situa&#231;&#245;es &#233; poss&#237;vel contrastar o risco de um dado indiv&#237;duo com aquele esperado para seus pares de mesma idade e assim caracterizar o risco como muito menor, menor, similar,maior ou muito maior. Especificamente, pode ser ainda conveniente caracterizar a pr&#225;tica como terap&#234;utica, recreativa ou competitiva. Em adendo, fatores ambientais, notadamente clim&#225;ticos podem ser relevantes. </p>
    <p>Quando da emiss&#227;o de um atestado, este dever&#225; caracterizar ou especificar qualquer restri&#231;&#227;o cl&#237;nica, seja de natureza cardiorrespirat&#243;ria ou locomotora. Idealmente, a frase conclusiva dever&#225; se ater aos limites do que foi efetivamente examinado ou avaliado, evitando senten&#231;as gen&#233;ricas e pouco fundamentadas tais como "apto para a pr&#225;tica de esportes", sendo provavelmente mais adequado algo como "n&#227;o foram encontradas contraindica&#231;&#245;es cl&#237;nicas formais para a pr&#225;tica de exerc&#237;cio f&#237;sico recreativo ou competitivo".</p>
    <p>Quando a decis&#227;o for pela desqualifica&#231;&#227;o profissional, o principal interessado na informa&#231;&#227;o deve ser o atleta ou seu representante legal (quando menor), mesmo que o primeiro fa&#231;a parte de uma equipe e sua avalia&#231;&#227;o tenha sido oferecida pelo clube ou associa&#231;&#227;o a qual est&#225; vinculado. Nesses casos &#233; prudente que o laudo seja assinado pelo m&#233;dico respons&#225;vel e por pelo menos mais dois outros que acompanham a decis&#227;o, al&#233;m do pr&#243;prio atleta, sendo realizado em pelo menos duas vias, uma delas arquivada no prontu&#225;rio m&#233;dico do atleta. Cuidado especial deve ser tomado para manter a integridade do atleta, sendo guardado o sigilo necess&#225;rio a cada caso.</p>
    <p>
      <bold>14. Refer&#234;ncias</bold>
    </p>
    <p>
      <fn id="end" fn-type="corresp">
        <label>
          <bold>Correspond&#234;ncia:</bold>
        </label>
        <p> Sociedade Brasileira de Cardiologia </p>
        <p> Av. Marechal C&#226;mara, 160/330 - Centro </p>
        <p> Rio de Janeiro - CEP: 20020-907 </p>
        <p> e-mail: </p>
        <p>
          <email xlink:href="sbc@cardiol.br">sbc@cardiol.br</email>
        </p>
      </fn>
    </p>
    <p>
      <bold>15. Rela&#231;&#227;o das Tabelas</bold>
    </p>
    <p><xref ref-type="table" rid="tab1"><bold>Tabela 1</bold></xref> - Particularidades que devem fazer parte da hist&#243;ria pessoal e familiar de atletas</p>
    <p><xref ref-type="table" rid="tab2"><bold>Tabela 2</bold></xref> - Diferentes tipos de anormalidades eletrocardiogr&#225;ficas em rela&#231;&#227;o &#224; idade, em uma popula&#231;&#227;o n&#227;o selecionada de 32.652 individuos21 submetidas a avalia&#231;&#227;o pr&#233;-participa&#231;&#227;o esportiva na Europa. </p>
    <p><xref ref-type="table" rid="tab3"><bold>Tabela 3</bold></xref> - Crit&#233;rios para considerar um eletrocardiograma de 12 deriva&#231;&#245;es como positivo para cardiomiopatia - Sociedade Europ&#233;ia de Cardiologia</p>
    <p><xref ref-type="table" rid="tab4"><bold>Tabela 4</bold></xref> - Altera&#231;&#245;es Consideradas Fisiol&#243;gicas X Sugestivas de Cardiopatias</p>
    <p><xref ref-type="table" rid="tab5"><bold>Tabela 5</bold></xref> - Principais diferen&#231;as entre o TE convencional e o TCPE</p>
    <p><xref ref-type="table" rid="tab6"><bold>Tabela 6</bold></xref> - Principais causas de morte s&#250;bita em atletas </p>
    <p><xref ref-type="table" rid="tab7"><bold>Tabela 7</bold></xref> - Recomenda&#231;&#245;es segundo faixa et&#225;ria e n&#237;vel competitivo</p>
    <p><xref ref-type="table" rid="tab8"><bold>Tabela 8</bold></xref> - Altera&#231;&#245;es eletrocardiogr&#225;ficas na CH</p>
    <p><xref ref-type="table" rid="tab9"><bold>Tabela 9</bold></xref> - Fatores de risco para M.S. em portadores de C.H.</p>
    <p><xref ref-type="table" rid="tab10"><bold>Tabela 10</bold></xref> - Benef&#237;cios do Exerc&#237;cio na Doen&#231;a Coronariana.</p>
    <p><xref ref-type="table" rid="tab11"><bold>Tabela 11</bold></xref> - Estratifica&#231;&#227;o de risco para inclus&#227;o de pacientes em programas de reabilita&#231;&#227;o card&#237;aca</p>
    <p><xref ref-type="table" rid="tab12"><bold>Tabela 12</bold></xref> - Op&#231;&#245;es de avalia&#231;&#227;o diagn&#243;stica pela Tomografia e pela Resson&#226;ncia</p>
    <p><xref ref-type="table" rid="tab13"><bold>Tabela 13</bold></xref> - Tipos de SQTL conhecidas</p>
    <p><xref ref-type="table" rid="tab14"><bold>Tabela 14</bold></xref> - Crit&#233;rios diagn&#243;sticos da s&#237;ndrome do QT longo</p>
    <p><xref ref-type="table" rid="a01tab15"><bold>Tabela 15</bold></xref> - Classifica&#231;&#227;o dos esportes</p>
    <p><xref ref-type="table" rid="a01tab16"><bold>Tabela 16</bold></xref> - Atletas com cardiopatias cong&#234;nitas</p>
    <p><xref ref-type="table" rid="a01tab17"><bold>Tabela 17</bold></xref> - Atletas com doen&#231;a valvular</p>
    <p><xref ref-type="table" rid="a01tab18"><bold>Tabela 18</bold></xref> - Atletas com miocardiopatias, miocardites e pericardites</p>
    <p><ext-link ext-link-type="uri" xlink:href="http://www.cob.org.br"><bold>Tabela 19</bold></ext-link> - Atletas com doen&#231;a card&#237;aca isqu&#234;mica</p>
    <p><xref ref-type="table" rid="a01tab20"><bold>Tabela 20</bold></xref> - Atletas com arritmias e condi&#231;&#245;es arritmog&#234;nicas</p>
    <p content-type="asset">
      <table-wrap id="a01tab20">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt23.jpg"/></table-wrap>
    </p>
    <p><xref ref-type="table" rid="tab21"><bold>Tabela 21</bold></xref> - Protocolo de avalia&#231;&#227;o dos atletas paraol&#237;mpicos segundo o Departamento M&#233;dico do Comit&#234; Paraol&#237;mpico Brasileiro</p>
    <p><xref ref-type="table" rid="tab22"><bold>Tabela 22</bold></xref> - Protocolos para testes cardiopulmonares em atletas paraol&#237;mpicos (Centro de Estudos em Fisiologia do Exerc&#237;cio - UNIFESP / Escola Paulista de Medicina)</p>
    <p><xref ref-type="table" rid="tab23"><bold>Tabela 23</bold></xref> - Pot&#234;ncia aer&#243;bia de atletas paraol&#237;mpicos brasileiros participantes dos Jogos de Atlanta</p>
    <p><xref ref-type="table" rid="tab24"><bold>Tabela 24</bold></xref> - Recomenda&#231;&#245;es para o atendimento de paratletas</p>
    <p>
      <bold>ERRATA</bold>
    </p>
    <p>
      <bold>Edi&#231;&#227;o de Janeiro de 2013, vol. 100 (1), Supl. 2, p&#225;g. 6</bold>
    </p>
    <p>A "Diretriz em Cardiologia do Esporte e do Exerc&#237;cio da Sociedade Brasileira de Cardiologia e da Sociedade Brasileira de Medicina do Esporte", publicada como suplemento n&#250;mero dois da edi&#231;&#227;o de janeiro de 2013 dos Arquivos Brasileiros de Cardiologia [Arq Bras Cardiol. 2013;100(1Supl.2):1-41], sofreu a seguinte corre&#231;&#227;o:</p>
    <p>Corrigir o texto:</p>
    <p>Atividade f&#237;sica como lazer, de intensidade leve ou moderada, em indiv&#237;duo assintom&#225;tico e sem fator de risco cardiovascular: realizar teste ergom&#233;trico ao iniciar programa de atividade f&#237;sica.</p>
    <p>Grau de recomenda&#231;&#227;o: IIa</p>
    <p>N&#237;vel de evid&#234;ncia: A</p>
    <p>E considerar o texto seguinte:</p>
    <p>Atividade f&#237;sica como lazer, de intensidade leve ou moderada, em indiv&#237;duo assintom&#225;tico e sem fator de risco cardiovascular: realizar teste ergom&#233;trico ao iniciar programa de atividade f&#237;sica.</p>
    <p>Grau de recomenda&#231;&#227;o: III</p>
    <p>N&#237;vel de evid&#234;ncia: C</p>
  </body>
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  <sub-article article-type="translation" id="TRen" xml:lang="en">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Guidelines</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="en">Guideline in Cardiology of Sport and Exercise of the Brazilian Society of Cardiology and the Brazilian Society of Sports Medicine</article-title>
      </title-group>
    </front-stub>
    <body>
      <p>
        <bold>GUIDELINES</bold>
      </p>
      <p>
        <fn id="enda-body2">
          <label>
            <bold>Guideline in Cardiology of Sport and Exercise of the Brazilian Society of Cardiology and the Brazilian Society of Sports Medicine</bold>
          </label>
          <p>
            <bold>Ghorayeb N., Costa R.V.C., Daher D.J., Oliveira Filho J.A., Oliveira M.A.B. et al.</bold>
          </p>
        </fn>
      </p>
      <p>
        <bold>Mail</bold>
      </p>
      <p>
        <xref ref-type="undefined" rid="en_a01img01-body2">Clique para ampliar</xref>
      </p>
      <p content-type="asset">
        <undefined id="en_a01img01-body2">
          <inline-graphic xlink:href="https://minio.scielo.br/documentstore/1678-4170/ZyzdWXbWwLmYTWhJ7fGzGMF/d09fc77b287be8467ab713d219e5e603829ec341.jpg"/>
        </undefined>
      </p>
      <p>
        <xref ref-type="undefined" rid="en_a01img02-body2">Clique para ampliar</xref>
      </p>
      <p content-type="asset">
        <undefined id="en_a01img02-body2">
          <inline-graphic xlink:href="https://minio.scielo.br/documentstore/1678-4170/ZyzdWXbWwLmYTWhJ7fGzGMF/7f4ffb707d4ca6cdcc91bd4cbe91e9e9e178d69c.jpg"/>
        </undefined>
      </p>
      <p>
        <bold>Presentation</bold>
      </p>
      <p>In the year of 1986 in Belo Horizonte during the XLII Brazilian Cardiology Congress it was formalized, by gathering the signatures of all members, the creation of the Study Group in Sports Cardiology, which was in the beginning directly linked to SBC board, and afterwards a component of DERC.</p>
      <p>The scientific fulfillment of this true practice of Brazilian cardiology was concluded with the first Guideline in Sports Cardiology. In the same rhythm of Societies of Sports Medicine and Cardiology all over the world, no doubt, the number of researchers and interested professionals that have their practice in sports and in the physical exercises of sports professionals and population in general will grow. The interest, even governmental, in heart disease prevention starts by the dissemination of physical activities for all. The current reality is the growth of people of all ages practicing physical activities in various modalities of sports.</p>
      <p>The need of having a queries base compatible with our habits and usages was fulfilled with this text. The members are cardiologists and sports physicians, which facilitated the necessary integration and a legacy, the guideline, elaborated and within the difficulties of being the first one, to be optimized and periodically changed. The Sports Cardiology, being a new area of cardiology, is based in experience, but seeks to create its evidences in a global level.</p>
      <p>Each day new modalities with increasing sports difficulties and intensities are "invented" and immediately incorporated to fitness centers, thousands of new long street races participants turn to us for technical evaluations and questioning, it all demands that the doctor keeps its practice updated, on behalf of more safety to sportsmen. It must be clear that there is no zero risk, despite the specialized emergency apparatus and acquired knowledge.</p>
      <p>The fundamental is described in this Guideline, which was further studied in many heart disease aspects to facilitate reader's comprehension. Difficulties and lack of more consistent evidences in certain clinical situations will remain, but throughout the text you can find more pertinent solutions. Consistency with other BSC Guidelines was also sought.</p>
      <p>This Guideline sought to approach the pre-participation evaluation and recommendations to prevent fatal and non-fatal events for the athletes, for people in general who practice sports and for para-athletes.</p>
      <p>To conclude we would like to remember that, for the first time in a Guideline from Brazilian Society of Cardiology a chapter was added for disabled individuals, the cheered PARA-ATHLETES.</p>
      <p>To the collaborators our best regards and congratulations. To the colleagues to use it we hope it can be useful for the good practice of Medicine.</p>
      <p>
        <bold>Nabil Ghorayeb</bold>
      </p>
      <p>
        <bold>1. Introduction</bold>
      </p>
      <p>The pre-participation clinical evaluation (APP, PPE) for physical/sports activities should be understood as a systematic medical examination, uniform, able to comprehend the ample population of sports practitioners and athletes before their release to physical training. Its goal is to identify, or at least improve, the suspicion over cardiovascular diseases that are incompatible with the practice of physical activities seeking efficiency.</p>
      <p>This evaluation, performed previous to the physical activity and periodically in its maintenance, has as its mean goal to prevent the development of cardiovascular system diseases (CSD) and sudden death by means of temporary or definite prohibition to practice physical activities or of treatment of the conditions that may be potentially fatal and triggered by physical exercise. The American Heart Association, as well as European Cardiology Society and Brazilian Society of Sports Medicine<sup>1-3</sup> agree on recommending the PPE for all professional athletes. There is also an indication to prescribe correctly exercises for non-professional sports practitioners that perform high intensity activities.</p>
      <p>Currently, the main argument against PPE implementation is over the costs involved in this evaluation. Due to the low prevalence of conditions capable of triggering sudden death during sports activities and to the big population of sports practitioners in the country, , a lot has been discussed on which would be the evaluation model with best cost-effectiveness. While some societies as a American Heart Association defend the simple implementation of a questions form and physical examination, believing that the financial and psychological cost bounded to false positive results in the performance of complementary exams do not justify the benefits that might be found, others, like European Cardiology Society, reinforce the use of complementary diagnosis methods, as its use is capable of modifying the occurrence of sudden death in the athletes population<sup>3-7</sup>. Although we do not have randomized works comparing the two evaluation methods, we suggest, like Brazilian Society of Sports Medicine, that PPE should be associated to complementary methods for professional athletes, considering its indication is completely justifiable in the pursue of guaranteeing the athlete's physical integrity and all the costs involved in their training. Another controversial aspect concerns the PPE in children, over which until now there is no consensus about protocols to be followed<sup>6,8,9</sup>.</p>
      <p>These aspects will be approached in this document, which intends to establish the regulations for PPE in Brazil. For didactic purposes, and also because of the differences concerning physiology, epidemiology and clinical aspects, we have chosen to divide the individuals to be evaluated in three groups: one formed by sports practitioners, other by professional athletes and a third contemplating children and adolescents and also para-athletes or disabled athletes. There will always be an intersection zone among them, when several aspects of the exercise, like intensity, frequency, training volume, etc. are considered. The common sense of medicine practice and the individual experience of the evaluation doctor will be essential in the choice of a path for PPE performance in these cases.</p>
      <p>
        <bold>2. Sports group</bold>
      </p>
      <p>It is characterized by adult individuals who practice regular physical and sport activities, which intensity may vary from moderate to high, eventually competing, but without professional approach to the sport.</p>
      <p>
        <bold>2.1. Anamnesis and clinical examination</bold>
      </p>
      <p>The ideal would be that every individual who is candidate to practice sports in moderate/high intensity level be submitted, necessarily, to a medical examination that will allow the detection of risk factors, signs and symptoms of cardiovascular, pulmonary, metabolic or locomotor system diseases<sup>1,10,11</sup>. The classical techniques of clinical anamnesis must be employed with some differences, especially those that favor aspects related to exercise and to the history of family diseases or cardiovascular events related to the practice of sports.</p>
      <p>During the anamnesis the Physical Activity Readiness Questionnaire (PAR-Q) developed in Canada, coupled with basic questionings applied by a doctor (<xref ref-type="table" rid="tab1-body2">Table 1</xref>), can be systematically applied. We must pay attention to sudden death or congenital heart disease cases in the family; family history for sickle cell anemia or other hemonoglobinopathies; provenience from endemic areas for Chagas disease or regions in which there is a prevalence of congenital diseases, like descendants from immigrants from the region of Veneto, in Italy, where there is a prevalence arrhythmogenic right ventricular dysplasia<sup>3-12,13</sup>. Special care must be taken when obtaining information related to the use of licit or illicit drugs that may be considered as doping, even involuntary, or that are hazardous to health or can cause sudden death<sup>13,14</sup>.</p>
      <table-wrap id="tab1-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt01-en.jpg"/></table-wrap>
      <p>Among the symptoms, we must pay attention to palpitations, syncope, precordial pain or thoracic discomfort; dyspnea on exertion; dizziness/lipothymy; asthenia; or any other symptom triggered by physical exercise. Accurate sensibility is required to evaluate whether the abovementioned symptoms are indicative of a pathological condition or are merely the consequence of a competition or of a more intense training. As for the syncope in athletes, a detail investigation is required, for until evidence to the contrary it should be treated as an episode of sudden death spontaneously aborted<sup>14</sup>.</p>
      <p>In the physical examination some clinical conditions should be highlighted, as: anemia; postural changes; infectious focuses (e.g., dental); systemic or severe infectious diseases; bronchial asthma, obesity, diabetes mellitus; systemic arterial hypertension; changes in cardiac and pulmonary auscultation; and special situations as pregnancy.</p>
      <p>One must prioritize the search for characteristic signs related to the possibility of a heart disease, as: the presence of heart murmur, splitting in the third or fourth heart sounds, valve disease, changes in the palpation of superior and inferior limbs, Marfan syndrome physical features, besides the adequate measuring of blood pressure (on both arms in the first evaluation)<sup>15,16</sup>.</p>
      <p>Also, in the physical examination one must characterize the eventual muscle-tendon shortening, especially from some muscle groups: hamstrings, quadriceps, iliopsoas, calf, thigh adductors, iliotibial tract, back and shoulder muscles, as the adequate therapeutic guidance can help preventing and treating muscle injuries, improving the sport performance.</p>
      <p>
        <bold>Recommendation Grade: I</bold>
      </p>
      <p>
        <bold>Evidence level: C</bold>
      </p>
      <p>
        <bold>2.2. Complementary exams (non-cardiovascular)</bold>
      </p>
      <p>We highlight, among routine laboratory exams aiming health: complete hemogram, fasting glycaemia, urea and creatinine, complete lipidgram, uric acid, hepatogram (AST, ALT, gamma-GT, bilirrubines, PAT/INR), urine exam, feces parasitological exam.</p>
      <p>
        <bold>Recommendation Grade: I</bold>
      </p>
      <p>
        <bold>Evidence level: B</bold>
      </p>
      <p>In individuals subject to practice exercises or compete in heights superior to 2.000 m, it is important the performance of hemoglobin electrophoresis to discharge the possibility of hemoglobinopathies (e.g., sickle cell anemia). In our environment, especially on those with compatible epidemiology, the serology for Chagas disease is recommended<sup>6,7</sup> (IA). Thoracic teleradiography in PA (posteroanterior) and left profile must be routinely required, because of its low cost and by providing relevant information about cardiovascular diseases, pulmonary diseases and thoracic structure diseases.</p>
      <p>
        <bold>2.2.1. Electrocardiogram</bold>
      </p>
      <p>
        <italic>2.2.1.1. Introduction </italic>
      </p>
      <p>It is known that there are controversies in the approach of younger athletes; the American guideline (AHA/ACC/ACSM) does not contemplate the ECG inclusion, but the Italian protocol, already followed by the European Society of Cardiology (ESC), justifies and recommends its performance.</p>
      <p>As regards individuals classified as master or aged, the rest ECG is mandatory; add to that the method's wide availability and low cost. At this age there is a bigger prevalence of cardiovascular diseases, being coronary artery disease the main one. This indication applies even to asymptomatic individuals and/or individuals without knowledge of previous cardiovascular pathology.</p>
      <p>
        <italic>2.2.1.2. Method</italic>
      </p>
      <p>The conventional 12 lead ECG should be performed de 12 with the individual in supine position, registered in speed of 25 mm/s and obtained at least 24 hours after the last sport activity. Previous rest of at least 5 minutes is mandatory<sup>17,18</sup>.</p>
      <p>
        <italic>2.2.1.3 Analysis</italic>
      </p>
      <p>The exam must be evaluated by a professional physician, cardiologist and with experience in the sport area, so that physiologic changes in the athlete's heart are not mistaken by eventual heart diseases.</p>
      <p>
        <italic>2.2.1.4. Changes</italic>
      </p>
      <p>The 12 lead ECG has limited diagnosis value for detection of coronary artery disease in population of asymptomatic individuals, mainly because of electrocardiographic patterns variations associated to physical training<sup>17</sup>. It is more useful when performed as part of a pre-participation evaluation, when it can identify non-expected changes, as previous myocardial infarction (in high age brackets), arrhythmias, and conduction disorders, among others.</p>
      <p>It can also help in the diagnosis of less prevalent diseases, as MHCM, long QT syndrome, short QT syndrome, Brugada syndrome, WPW syndrome and pre-excitement, besides arrhythmogenic right ventricular dysplasia.</p>
      <p>The 12 lead ECG may help in the diagnosis evaluation of aortic and mitral valvopathies, ectopic beatings (ventricular and supraventricular extrasystoles), bradyarrhythmia and tachyarrhythmia, other ventricular and supraventricular arrhythmias, disorders in the conduction system (LBB, RBB, AVB of varying grades). It can also detect changes in the ST segment, as early repolarization, St segment depression or elevation ST, T wave inversion in precordial and/or peripheral leads, raise in the R/S waves voltage suggesting LVE<sup>2,19</sup>.</p>
      <p>There may be variations in the prevalence of electrocardiography changes, those being greater in the female gender than in the male gender; regarding the age, in the population of masters or aged, we find a greater frequency of inverted T waves in precordial and/or peripheral leads, increased R/S waves suggesting LVE and stimulus conduction disorders.</p>
      <p>The variations found in conventional 12 lead electrocardiograms are also statistically significant regarding the type of sport practiced and depending on the age bracket evaluated in <xref ref-type="table" rid="tab2-body2">table 2</xref>.</p>
      <table-wrap id="tab2-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt02-en.jpg"/></table-wrap>
      <p>
        <bold>Recommendation grade: I</bold>
      </p>
      <p>
        <bold>Evidence level: A</bold>
      </p>
      <p>
        <bold>2.2.2. Exercise testing</bold>
      </p>
      <p>The exercise testing (ET) may be indicated in the initial evaluation of a sport practitioner in the early identifying of cardiovascular disease, as well as contribute to prognosis analysis in asymptomatic individuals or when there is reference to some symptom potentially indicative of this condition. Its indication also stands with goal to cardiorespiratory aptness evaluation in training evolution in some sport modalities, notoriously the ones with predominance of aerobic component<sup>21-23</sup>.</p>
      <p>The cardiovascular overload imposed by physical activity stress, performed as leisure, during the practice of some sport or in competition, requires a great metabolic demand and peripheral hemodynamic. To cover this demand, there is a progressive increase in oxygen consumption by the heart with the objective of making possible the elevation of cardiac debt. The identification of eventual limitations to cover this crescent demand of oxygen by the cardiac muscle can be evaluated by ET.</p>
      <p>Although the ET should always be indicated in the PPE, in the specific condition of leisure activities of light and moderate intensities asymptomatic individuals can be released without the need of examination. In further conditions, the ET will always be recommended<sup>24</sup>.</p>
      <p>In adults up to 65 years old the coronary artery disease is the main responsible by mortality and the ET indication to those individuals aims predominantly the identification of myocardial ischemia, reflecting probable coronary disease (CAD). Also in asymptomatic people and even in those who have a known CAD the indication of ET is sustained by the need of an adequate prescription of physical activity.</p>
      <p>The presence of changes in the rest electrocardiogram, often recurring from the athlete's left ventricular hypertrophy, reduces the diagnosis capacity, in the electrocardiographic aspect, of myocardial ischemia in ET. The simultaneous analysis of other ET variables contributes to the evaluation<sup>25,26</sup>.</p>
      <p>The response evaluation of arterial blood pressure in the ET enables the adoption of early preventive and therapeutic measures, besides contributing to the correct exercise prescription.</p>
      <p>The occurrence of palpitation during physical activity shall be investigated by means of ET with the objective of reproducing under monitoring the patient's complaint. The cardiac arrhythmia diagnosis may then be performed, the adequate treatment being oriented.</p>
      <p>
        <italic>2.2.2.1. Variables to be evaluated in the exercise testing</italic>
      </p>
      <p>
        <italic>2.2.2.1.1. <underline>Exercise capacity</underline></italic>
      </p>
      <p>The low exercise capacity expresses a bad prognosis. Its identification will deserve investigation as to the reason of its existence<sup>27,28</sup>.</p>
      <p>
        <italic>2.2.2.1.2. <underline>Thoracic pain</underline></italic>
      </p>
      <p>Reproduce by ET the complaint of pain or thoracic discomfort during the exercise will allow the probable myocardial ischemia diagnosis by coronary disease, with consequent investigation proceeding e withdrawal from physical activities. If during the ET completely non-ischemic characteristics of pain are identified and the pain is indicated by the athlete as similar to the one that motivated the ET and there isn't change in any testing variable, the coronary disease probability becomes insignificant, therefore the athlete can be released for competition<sup>29</sup>.</p>
      <p>
        <italic>2.2.2.1.3. <underline>ST-T Segment</underline></italic>
      </p>
      <p>
        <bold>ST unlevelling</bold>
      </p>
      <p>ST segment sub-unlevelling or supra-unlevelling in slow, horizontal or descendant ascension may characterize CVD, in special CAD, especially when there is concomitantly the reference to thoracic pain or other manifestation that contributes to myocardial ischemia diagnosis<sup>30</sup>.</p>
      <p>In asymptomatic athletes, when there are ST changes during ET, even if they are not accompanied by thoracic pain and occur in high double product and in high exercise capacity, associated to frequent cardiac arrhythmias, the temporary withdrawal or the postponement of the physical activity start and the proceeding in the cardiovascular disease investigation are justifiable.</p>
      <p>This approach may be based on the bigger cardiovascular demand and the bigger risk of cardiovascular events, including sudden death, during exercise or during the practice of sports, noticeably for those over 35 years old and when one or more risk factors for CAD are present.</p>
      <p>The ST segment analysis should consider:</p>
      <p>The morphologic characteristics, being descendent more serious than horizontal and this more serious than slow lenta<sup>31,32</sup>.</p>
      <p>The earliness of its appearance during exertion and these changes persistence lately in the recovering phase are conditions that indicate bigger risk and more severe<sup>33,34</sup>.</p>
      <p>The reason between the depression variation in the ST segment concerning the heart rate variation [(delta ST in mm x 100) / delta HR]. It is considered potentially ischemic when equal or bigger than 1,6<sup>35,36</sup>.</p>
      <p>The ST depression when it is bigger than 10% in relation to the previous R wave amplitude. This adjustment in the ST segment evaluation deserves to be considered mainly because of the habitual presence of high R waves, expressing left ventricular hypertrophy physiologically present in the athletes<sup>37</sup>.</p>
      <p>Still related to the ventricular repolarization we must pay attention to the fact that, when starting from a variation in rest ECG, these variations normalization during exercise is an important sign of benignity and good prognosis. Inversely, variations that do not normalize or even get worse with the raise in HR and of double product are often a sign of the presence of subjacent coronariopathy or myocardiopathy<sup>38-40</sup>.</p>
      <p>
        <bold>Ventricular depolarization </bold>
      </p>
      <p>In the presence of a ST segment depression during exertion, an increase in R wave amplitude and simultaneously reduction or maintenance of Q wave amplitude in lateral leads (V4, V5, CM5, V6), increase the diagnosis efficacy for myocardial ischemia<sup>41,42</sup>.</p>
      <p>
        <italic>2.2.2.2. Systemic arterial blood pressure</italic>
      </p>
      <p>Excessive high arterial blood pressure values during the exercise test enable to infer that during the exercise or sport practice the arterial blood pressure shall be very high as well. Sports that require a bigger static component will possibly be accompanied by even higher systolic, diastolic, arterial blood pressure.</p>
      <p>The arterial hypertension laboratorial investigation and treatment should begin in sequence, and the sport activities should be interrupted temporarily until better control is reached<sup>43</sup>. On the other hand, progressive fall or systolic arterial blood pressure during ET, especially when systolic arterial blood pressure values inferior to pre-exertion are reached should deserve proceeding in the investigation of presence of cardiac disease.</p>
      <p>
        <italic>2.2.2.3. Heart rate</italic>
      </p>
      <p>Chronotropic incompetence indicates a bad prognosis and has been associated to endothelial malfunction, change in the autonomic modulation, elevated values in the inflammatory markers and coronary disease.</p>
      <p>The heart rate inadequate response may be considered by the inability of reaching 85% of the maximum estimated heart rate. The function 208 (age x 0.70) may be used to predict the maximum heart rate. Topic index under 80% is another method to identify chronotropic incompetency, and it has prognosis value. It is obtained by the reason [(Obtained HR Reserve /Estimated HR Reserve) x 100]<sup>44</sup>.</p>
      <p>The heart rate reduction in the recovery first minute related to the heart rate in the peak of exertion enables to infer the cardiac vagal modulation. This observation was first identified in athletes comparatively to cardiac insufficiency patients<sup>45,46</sup>. Reductions equal or inferior to 12 beatings per minute have been associated to bigger mortality incidence<sup>47</sup>.</p>
      <p>
        <italic>2.2.2.4. Cardiac Arrhythmias</italic>
      </p>
      <p>Cardiac arrhythmias of a lesser level of complexity, as eventual ventricular extrasystoles on ET, often express increase in the sympathetic autonomic modulation imposed by graduated exercise. Such conditions taken isolated, without the presence of other variations do not justify greater restriction to physical activities in asymptomatic individuals.</p>
      <p>Symptomatic or asymptomatic individuals, who develop complex ventricular arrhythmias, as ventricular tachycardia, sustained or not, will deserve investigation previous to release to physical activities.</p>
      <p>The presence of seven or more ventricular extrasystoles exclusively in recovery phase, or in recovery and exertion, express a potentially bigger risk of future cardiac events<sup>48</sup>.</p>
      <p>Recommendation Grade and Evidence Level</p>
      <p>Physical activity as leisure, of light or moderate intensity, in asymptomatic individual without cardiovascular risk factor: perform exercise test when initiating physical activity program.</p>
      <p>
        <bold>Recommendation Grade: IIa</bold>
      </p>
      <p>
        <bold>Evidence level: A</bold>
      </p>
      <p>Physical activity as leisure, of light or moderate intensity, in asymptomatic individual with cardiovascular risk factor: perform exercise test when initiating physical activity program.</p>
      <p>Recommendation Grade: IIa</p>
      <p>Evidence level: A</p>
      <p>High intensity leisure activity, sport and competition: perform exercise test when initiating physical activity program.</p>
      <p>
        <bold>Recommendation Grade: IIa</bold>
      </p>
      <p>
        <bold>Evidence level: A</bold>
      </p>
      <p>
        <bold>At any moment:</bold>
      </p>
      <p>Reference to thoracic pain or discomfort, tiredness or dyspnea of non-defined cause, palpitation, identification of previously inexistent arrhythmias, pre-syncope or syncope related to exercise or arterial blood pressure elevation in rest, compromising or not target organ: perform exercise test.</p>
      <p>
        <bold>Recommendation Grade: I</bold>
      </p>
      <p>
        <bold>Evidence Level: A</bold>
      </p>
      <p>Note: the exercise test requirement will depend on initial clinical evaluation and may be contraindicated or eventually anteceded or succeeded by other complementary exams, if necessary.</p>
      <p>
        <bold>2.2.3. Echocardiogram with Doppler</bold>
      </p>
      <p>It should be used in the cases of heart disease familiar/clinical history or suspect physical exam, as well as for cases of rest electrocardiogram with positive criteria for cardiomyopathy (<xref ref-type="table" rid="tab3-body2">Table 3</xref>)<sup>49</sup>. Also in known cases of congenital heart diseases, especially those of low complexity, in which the physical activity and even sports practice seeking efficacy are not contraindicated, the periodical echocardiogram performance helps in the evolutive evaluation and in the correct management of the condition in question. We should reinforce the importance of echocardiogram with Doppler associated to physical exertion in situations in which the cardiac function verification during exercise can help in diagnosis and conduct<sup>50</sup>.</p>
      <table-wrap id="tab3-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt03-en.jpg"/></table-wrap>
      <p>
        <bold>Recommendation Grade: IIa</bold>
      </p>
      <p>
        <bold>Evidence level: B</bold>
      </p>
      <p><xref ref-type="table" rid="tab3-body2">Table 3</xref> - Criteria to consider a 12 lead electrocardiogram as suggestive of heart disease and of indication of echocardiogram European Cardiology Society (adapted from Pelliccia A)<sup>18</sup>.</p>
      <p>Regarding athletes with age superior to 35 years old, the standard protocol associated with question form for coronary artery disease specific evaluation should be applied. In men &gt;40 years old and women &gt;55 years old and in individuals with more than 2 risk factors for coronary artery disease (besides gender and age) <sup>51,52</sup> the performance of functional test with exercise should be considered.</p>
      <p>In case of positive in the initial evaluation for coronary artery disease the investigation must go deeper with more accurate exams, like echocardiogram at rest, stress echocardiography or myocardial tomographic scintigraphy, evaluating each case individually.</p>
      <p>
        <bold>Recommendation Grade: IIa</bold>
      </p>
      <p>
        <bold>Evidence level: B</bold>
      </p>
      <p>
        <bold>2.2.4. Other complementary exams</bold>
      </p>
      <p>The use of other diagnosis tools, be it laboratory, charts, graphics methods, invasive or not, should comprise to clinical criteria and scientific evidences established in literature, as function of those found along the PPE.</p>
      <p>Specific details on the indication and interpretation of those complementary exams will be found on the topic about sudden death and cardiovascular events prevention in physical and sports activity in this guideline.</p>
      <p>
        <bold>3. Athletes group</bold>
      </p>
      <p>This group is characterized by individuals who practice physical and sports activities in a regular and professional basis, systematically competing, with professional attachment to sports through clubs and/or sponsors of any kind. This group works always in pursue of records and limits overcoming, often submitting themselves to high intensity training load which places them invariably under intense physical and psychological stress, with frequently hazardous consequences.</p>
      <p>
        <bold>3.1. Anamnesis and physical examination</bold>
      </p>
      <p>The athletes' pre-participation evaluation (PPE) demands a manageable strategy regarding economics, especially in a country in development such as Brazil, with continental dimensions, well-populated and with great social and economic diversity. The cardiologic approach deserves special attention, as the event of sudden death depends mainly on cardiovascular causes. In this context, it is fundamental a correct anamnesis and physical examination<sup>53,54</sup>.</p>
      <p>It should be considered in the anamnesis, contributing to a correct interpretation of the physical examination, that the cardiac adaptations to physical exercise depend on its frequency, quantity and intensity, varying according to different demands observed in several sports modalities, different training systems and also individual responses<sup>55</sup>. This last aspect is what makes it possible that individuals submitted to similar physical activities have different cardiac characteristics. Therefore, there are HR and SAP variations that depend on the habitual physical activity and also on characteristics proper of each individual. It should be noted that the variations that produce the athlete's heart syndrome should, for starters, be considered as normal physiologic adaptations to physical exercise, transitory and with no negative results on health<sup>56,57</sup>.</p>
      <p>Laboratory exams are not required at first; its requirement should come from the clinical data obtained, with emphasis on cardiovasculatory aspects. The laboratory exams listed in the first part of this document (sports group) should also be considered in the athletes' group.</p>
      <p>
        <bold>Recommendation Grade: I</bold>
      </p>
      <p>
        <bold>Evidence level: A</bold>
      </p>
      <p>
        <bold>3.1.1. Considerations on overtraining syndrome (OTS)</bold>
      </p>
      <p>Many times the magnitude and the clinical repercussions of cardiovascular variations configure a health problem as the overtraining syndrome should be considered. Because it is a profile that is difficult to ascertain and depends essentially on the clinical analysis for its presence to be suspected, we have chosen to include here its description and the recommendations to manage it. In the confirmation of diagnosis, the laboratory sometimes has a fundamental role.</p>
      <p>There are two types of overtraining: the sympathetic, or Basedow type, and the parasympathetic, or Addison type.</p>
      <p>The OTS of parasympathetic type is more common in veteran athletes. It is not always followed by decline in sports efficiency. Many times it manifests only by some lethargic state, consequence of great vagal predominance. The sympathetic reflex responses are inhibited, which can lead to orthostatic hypotension, dizziness, faintness and Stokes-Adams episodes in daily life situations.</p>
      <p>The OTS of sympathetic type, which is more common, usually causes decline in sports efficiency, irritability, insomnia, loss of appetite, profuse sweating, persistent tachycardia and other tachyarrhythmias, slow return to basal heart rate after physical exertion and arterial hypertension. It may indicate an accentuated catabolic process, with loss of weight by loss of muscle mass, and even osteoporosis and stress fractures. Laboratory variations may occur, with increase in urinary nitrogen excretion, reduction of anabolic hormones, like testosterone and growth hormone, and defense factors depletion with less immune resistance. By configuring the catabolic process, the anabolic hormones reduction is accompanied by increase of catabolic hormones, like cortisol. Thus, the reason serum cortisol / serum testosterone usually presents values above normal. The decrease in efficiency and the related symptoms demand immediate reduction or even interruption of physical exercises, in long resting period. The recovery time is variegated, requiring monitoring to indicate the best time to return to activities.</p>
      <p>
        <bold>3.2. Electrocardiogram</bold>
      </p>
      <p>Sports practice promotes morphofunctional variations in the heart related to training time and intensity, which are demonstrated in ECG at rest, like ventricular overload, atrioventricular conduction and rhythm disturbances, imposed by the exercise's vagal exacerbation. Abnormalities that can put the athlete in risk during sports practice can be detected, representing the expression of a subjacent heart disease. When an athlete's ECG is analyzed, the main goal is to discern between physiological patterns and those that require action and/or additional tests to exclude (or confirm) the suspicion of subjacent cardiovascular disease leading to increased risk of sudden death in sport<sup>58</sup>.</p>
      <p>Mistakes in the differentiation between physiologic and pathologic may have serious consequences. Athletes can be unnecessarily disqualified for competitions because of ECG variations which are inserted in the normal interval for athletes. On the other hand, they can be submitted to unnecessary exams, raising in much the evaluation costs. This is particular relevant for the professional, as the competitor disqualification generates psychological and eventually financial troubles. Alternatively, potentially fatal cardiovascular disease signs can be wrongly interpreted as variant from normal in an athlete's ECG.</p>
      <p>The peculiarities of athletes' electrocardiogram in rest imply that the exam interpretation should be performed by cardiologist doctors with experience in the exercise physiology area or sports doctor with training in the cardiology area.</p>
      <p>Currently available data enable to define the ECG usefulness and cost-effectiveness of use in pre-participation evaluation<sup>59,60</sup>. The Sociedade Brasileira de Cardiologia (Brazilian Cardiology Society) recommends it in every initial cardiologist appointment. The European Cardiology Society and the International Olympics Committee, the FIFA, indicate its performance in everyone who wishes to ingress in a leisure or competitive physical exercise program<sup>61</sup>. The American Heart Association does not indicate it as mandatory in pre-participation evaluation for the practice of exercise or sports<sup>62</sup>. In Brazil, in many institutions where athletes are evaluated its performance is mandatory.</p>
      <p>
        <bold>3.2.1. Variations considered physiologic X suggesting heart diseases</bold>
      </p>
      <p>The efforts concentrate on better understanding interpretation basis, defining ECG criteria to discern between athlete's heart and actual heart diseases. More studies are necessary to test if the accuracy, usefulness and cost-effectiveness of ECG presents criteria variations regarding gender, age, ethnics and different levels of training and/or type of sport<sup>63,64</sup>. The variations in athletes' ECG may be divided in two groups: commons and/or related to sports training (group1) or sporadic and/or suggestive of heart diseases (group2), as listed in <xref ref-type="table" rid="tab4-body2">table 4</xref>.</p>
      <table-wrap id="tab4-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt04-en.jpg"/></table-wrap>
      <p>Athletes often (up to 80%) show electrocardiographic variations as sinus bradycardia/arrhythmia (13-69%), first-degree atrioventricular block (35%), early repolarization (50-80%), resulting from physiological adaptations recurring from the increase in vagal tone. They can also present voltage criteria (i. e., based only in QRS amplitude measurings) for physiological left ventricular hypertrophy that reflects the remodeling of this cavity, without the concomitant presence of pathologic Q waves, electrical axle deviation, atrial overload and repolarization variations<sup>65,66</sup>.</p>
      <p>Those physiological variations in the ECG must be clearly separated from patterns suggestive of heart disease recognized by repolarization variations, pathological Q waves, electrical axle deviation, intraventricular conduction defect, pre-excitement, short/long QT interval and Brugada. Those findings are rare (5%), but may be the expression of heart diseases, genetic inheritance and canalopathies, which predispose to sudden death<sup>67</sup>.</p>
      <p>Variations caused by cardiac adaptation to physical exertion (group 1) should not cause alarm and the athlete may be released to practice competitive sports without further evaluation, as should continue under investigation athletes with signs suggestive of heart diseases even though asymptomatic, in the absence of positive family history or abnormal findings in the physical exam<sup>68-70</sup>.</p>
      <p>
        <bold>Recommendation Grade: I</bold>
      </p>
      <p>
        <bold>Evidence level: A</bold>
      </p>
      <p>
        <bold>3.3. Exercise test</bold>
      </p>
      <p>The exercise test (ET) may be indicated in the initial evaluation of athletes in any age bracket as part of the strategy for early identification of cardiovascular disease, as well as to contribute in the prognosis analysis, in asymptomatic or when there is reference to any symptom potentially indicating this condition<sup>71,72</sup>.</p>
      <p>Your requirement will depend on the initial clinical evaluation and may be contra-indicated or eventually anteceded or succeeded by other complementary exams, if necessary.</p>
      <p>The considerations on method made in the chapter dedicated to sports practitioners are totally applicable for professional athletes. We suggest, therefore, that the text quoted in this document be read.</p>
      <p>
        <bold>Recommendation Grade: I</bold>
      </p>
      <p>
        <bold>Evidence level: A</bold>
      </p>
      <p>
        <bold>3.4. Cardiopulmonary test</bold>
      </p>
      <p>For a long time, including in Brazil, athletes and individuals who participate in high efficiency physical activities have been submitted to the maximum cardiopulmonary exercise test (MCET), aiming performance evaluation and aerobic training prescription<sup>73</sup>. As described in <xref ref-type="table" rid="tab5-body2">table 5</xref>, MCET differs from conventional exercise test primarily by the addition of measuring and analysis of exhaled gases<sup>74,75</sup>. According to its primary objectives, when performed in athletes apparently healthy, contrary to exercise tests aiming clinical diagnosis, many times the arterial blood pressure measurings and even electrocardiogram are not performed, and the heart rate measuring is in this case obtained by the use of frequency meters.</p>
      <table-wrap id="tab5-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt05-en.jpg"/></table-wrap>
      <p>With hundreds of equipments available today (in laboratories, clinics, hospitals, sports clubs and centers) capable of performing these measurings, it actually makes little sense to perform athletes' aerobic condition evaluation by a conventional exertion test, in which there is approximately 20% error when estimates based on formulae developed for clinical protocols for treadmill or cycloergometers. It is apparently consensual among physicians and physical education professionals that work with athletes that when performing a MCET is impossible, the tendency is to choose field tests like the 2,400 m or even the traditional Cooper test instead of the conventional exercise test.</p>
      <p>In the clinical context of pre-participation evaluation of athletes and individuals who wish to start practicing intense aerobic exercises, the MCET has many advantages over the conventional exercise test, as illustrated in <xref ref-type="table" rid="tab5-body2">table 5</xref>, besides the objective and validated measurement of aerobic condition or maximum VO2. In certain clinical circumstances and for determined differentiated groups of athletes, for example master athletes or those individuals with cardiovascular and/or pulmonary infirmities who are involved with recreational sports competition (e.g., half marathon races, marathon races, high mountain climbing, road cycling competitions, water circuits, etc.) or professionally, the inclusion of MCET in their pre-participation evaluation may be recommended or even fundamental for the individual risk stratification, because of aggregated information by measure and analysis of exhaled gases. In these circumstances and whenever possible, the use of closest ergometer for the sports activity practiced should be preferred.</p>
      <p>With the crescent involvement of middle-aged individuals in mass sports events<sup>76</sup>, it is probable that MCET will be used to obtain objective and valid subsidies that orient the training more scientifically or to have more safety in the characterization of a low clinical risk for unfavorable cardiovascular events, especially those that have coronary risk factor.</p>
      <p>Among the several possibilities of additional clinical information derived exclusively from a MCET in the physically active healthy athlete or individual, two stand out: a) more accurate and objective identification of limiting factor(s) for maximum exertion (cardiovascular, respiratory and muscular or metabolic) and b) evaluation of systolic volume behavior, obtained by the analysis of curves and of oxygen pulse maximum values (VO2/FC) and of ventilatory equivalents (VE/VO2 and VE/VCO2) when an incremental and maximum protocol is performed during at least 8 to 10 minutes (more commonly ramp protocol)<sup>77</sup>.</p>
      <p>In many cases, especially when considering the high relative prevalence of electrocardiography abnormalities of male athletes with long years of predominantly aerobic training, compromising at least in part the diagnosis specificity and sensibility of tracings obtained in exertion, the behavior of cardiopulmonary variables obtained during the MCET may contribute to solve doubts and adequately stratify the individual risk of a given athlete. In other situations, a systolic arterial blood pressure reduction in the MCET last minutes in an apparently healthy athlete, when accompanied by normal ventilatory responses, probably reflects an accentuated reduction of peripheral vascular resistance resulting from metabolic acidosis with a preserved or even crescent cardiac debt and not an acute dysfunction of cardiac inotropism/lusitropism recurring from myocardial ischemia.</p>
      <p>The MCET is already incorporated in the cardiologic practice to evaluate heart failure patients<sup>56</sup> and to identify the etiology of exertional dyspnea<sup>57</sup> and recently considered as capable of identifying myocardial ischemia<sup>58</sup> or abnormal responses after cardiac surgeries<sup>59</sup>.</p>
      <p>With athletes, it is the procedure of choice when one wishes to obtain a valid measure and needs the aerobic condition and the determination of threshold heart rate to prescribe the exercise.</p>
      <p>
        <bold>Recommendation Grade: I</bold>
      </p>
      <p>
        <bold>Evidence level: A</bold>
      </p>
      <p>It is for a more accurate stratification of the exercise limiting factor.</p>
      <p>
        <bold>Recommendation Grade: II.a</bold>
      </p>
      <p>
        <bold>Evidence level: A</bold>
      </p>
      <p>When there are changes in the rest electrocardiogram that may interfere in its interpretation to exercise or suspect hemodynamic responses.</p>
      <p>
        <bold>Recommendation Grade: II.a</bold>
      </p>
      <p>
        <bold>Evidence level: B</bold>
      </p>
      <p>Its routine use in apparently healthy children and adolescents, just for the purpose of stratify the risk of sudden death to exercise do not seem particularly useful.</p>
      <p>
        <bold>Recommendation Grade: II.b</bold>
      </p>
      <p>
        <bold>Evidence level: B</bold>
      </p>
      <p>
        <bold>3.5. Echocardiogram</bold>
      </p>
      <p>The pre-participation evaluation's goal is to prevent occurrences that could risk the integrity of individuals who practice recreational or competitive physical activities, prioritizing the identification of structural and/or functional cardiovascular variations that could increase the risk of morbidity and mortality during this practice<sup>40,60,61</sup>.</p>
      <p>The use of complementary methods in the routinely cardiovascular evaluation is controversial, and the most relevant aspect of this strategy is the cost-efectiveness<sup>39</sup>. In this scenery, echocardiography has an essential role, by the possibility of diagnosing the main diseases implied in athletes' sudden death (<xref ref-type="table" rid="tab6-body2">Table 6</xref>) and differentiating athlete's heart physiological variations from hypertrophic cardiomyopathy pathologic hypertrophy in an innocuous, fast and relatively low cost way.</p>
      <table-wrap id="tab6-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt06-en.jpg"/></table-wrap>
      <p>The sudden death in young athletes (12-35 years old) affects, mostly, afro-descendants individuals (&gt;50%) and of the masculine gender (1:9). However, the risk of sudden death do not depend on the competition level (school, amateur, professional)<sup>63-65</sup>.</p>
      <p>
        <bold>3.6. Recommendations</bold>
      </p>
      <p>Institutions internationally known as the European Cardiology Society (ECS), the International Olympic Committee (IOC) and the American Heart Association (AHA) differ as to the definition of screening diagnosis exams to establish the public health investigation protocols<sup>66-68</sup>. This question's complexity lies in the relative infrequency of sudden death in young athletes (between 1:100.000 and 1:300.000 per year), besides the questionable efficiency in preventing its occurrence, being a fact that this event invariably causes repercussion and commotion in the society<sup>3,5</sup>.</p>
      <p>Considering this scenery, the European Cardiology Society (ECS) supported by the consistent Italian experience, which monitored athletes for 25 years, determines in its screening program for individuals between 12-35 years old an initial exam composed by family history, physical examination, 12-lead ECG, and additional exams will only be performed with positive findings during the initial evaluation. (<xref ref-type="fig" rid="fig1-body2">figure 1</xref>)<sup>17,69</sup>.</p>
      <fig id="fig1-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gf01-en.jpg"/></fig>
      <p>This strategy was effective in reducing in almost 90% the annual incidence of sudden death in athletes in the Italian northeast<sup>40</sup>.</p>
      <p>The use of echocardiography in population programs in young asymptomatic athletes (12-35 years old) proved to be a high cost strategy and to the moment there is no population study with adequate follow-up to prove its efficacy<sup>63-65</sup>.</p>
      <p>Regarding athletes with age superior to 35 years old, the standard protocol associated to questionnaire for specific evaluation of coronary artery disease should be applied. In men &gt;40 years old and women &gt; 55 years old should be considered the performance of functional test with exercise and in individuals with more than two risk factors for coronary artery disease (besides gender and age)<sup>1,70.</sup></p>
      <p>In case of positivity in the initial evaluation for coronary artery disease the investigation should proceed with more accurate exams, and echocardiogram at rest or stress echocardiography may be used, evaluating each individual case<sup>40,41</sup>.</p>
      <p>Several studies have suggested the introduction of limited echocardiographic modalities with restricted two dimensional examination being performed in 5 minutes. The results show a good sensibility and specificity for the diagnosis of several illnesses related to sudden death in athletes, especially the hypertrophic cardiomyopathy implied in more than 30% of the cases of sudden death in young athletes<sup>71</sup>.</p>
      <p>The recommendations in <xref ref-type="table" rid="tab7-body2">table 7</xref> take into consideration the formulation of a population screening investigative strategy for public health policies and cannot be fitted to take decisions in singular cases, based in studies result and population records founded in cost planning programs.</p>
      <table-wrap id="tab7-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt07-en.jpg"/></table-wrap>
      <p>Currently, professional athletes' associations and executive boards have their own protocols, due to legal and economic issues involved in the professional aspect<sup>40</sup>.</p>
      <p>The pre-participation evaluation based in initial medical appointment and 12-lead ECG enables the identification of athletes under greater risk of sudden death, however it is not a definite screening strategy in this segment. Other more accurate diagnosis methods will have more space as initial screening exam in the future<sup>72-74,78</sup>.</p>
      <p>Currently, echocardiography represents the confirmatory diagnosis modality to be performed after suspicion during initial pre-participation evaluation.</p>
      <p>
        <bold>Recommendation Grade: I</bold>
      </p>
      <p>Evidence level: A</p>
      <p>There is no evidence for its routinely use in population screening programs in asymptomatic individuals.</p>
      <p>
        <bold>Recommendation Grade: III</bold>
      </p>
      <p>
        <bold>4. Children and adolescents group</bold>
      </p>
      <p>Characterized by individuals who practice sports and physical activities in a very variable way, engaging mostly in recreational sports that reach moderate and high intensity levels, being as competitive as the athletic levels, even without systematic training, in certain situations they even surpass athletic levels. It is, therefore, impossible to discern between athletes and non-athletes in terms of intensity and energetic expenditure. They are children and adolescents that may compete systematically, sometimes already professionally linked with sports through clubs and sponsors of any nature. Sometimes they are submitted to intense physical and psychological stress, including, in some situations, by the parents or carers questionable positioning, when they should always be oriented as to inherent risks of such practice in this age bracket<sup>12,75</sup>.</p>
      <p>The main causes of sudden death more often related to physical activities in this age bracket<sup>3</sup> are: hypertrophic cardiomyopathy, congenital coronary artery anomaly, arrhythmogenic right ventricular dysplasia, Marfan syndrome cardiologic variations Marfan (aortic rupture), pre-excitement syndrome (WPW), Brugada syndrome, long QT syndrome, hemodynamic and arrhythmic repercussions of congenital heart diseases, myocarditis, comottio cordis, Chagas disease, infections and others like conduction dysfunction, hydroelectrolytic variations, sickle cell anemia, besides undetermined causes. In Brazil we don't have statistics epidemiologic records of sudden deaths related to sports practice in this age bracket, being restricted only to report of cases in publications. The above-mentioned order is therefore selective, and its prevalence in the population studied is not characterized.</p>
      <p>A competitive athlete is one which takes part on an organized team or individual sport that requires systematic training and regular competitions aiming a goal, be it a prize or excellence in the modality. In general they are federates and/or members of sports clubs. Especially at this age bracket, the differentiation between "competitive" athletes and non-athletes, as mentioned before, is almost impossible.</p>
      <p>The sports pre-participation evaluation has been developed and has become more formal, being a legal attitude in some countries, like Italy. An already established global consensus is that of the performance of a well-conducted clinical history, focusing mainly on symptoms and personal background as well as heart disease family history, mainly the occurrence of sudden death. The best strategy to perform the PPE on this age bracket is still a matter under discussion in several countries<sup>3,75</sup>. Such data may be obtained through validated questionnaires like the one of the American Heart Association (AHA) and of the Recommendations on Sudden Death of the International Olympics Committee (Lausanne), adapted on <xref ref-type="table" rid="tab1-body2">table 1</xref>.</p>
      <p>
        <bold>4.1. Specific evaluation: Tanner stages l <sup>79,80</sup></bold>
      </p>
      <p>In the growth and development process, we have a sequence of pubertal events that culminate with the emergence of secondary sexual characters resulting from hormonal maturation, systematized by Tanner and classified in five stages, taking into account, in the feminine gender, the mammary development and the quantity and distribution of pubic hair, and, in the masculine gender, the genital organs aspects and also the quantity and distribution of pubic hair. The evaluation of these parameters is essential, as the increase in muscle mass, height, weight, besides motor specialization are related to them. Although there is constancy in the Tanner stages sequence, the time to pass from one stage to another is much variable, and thus the sexual maturation may last from 2 to 5 years.</p>
      <p>The great increment in physical growth that occurs in puberty, the known growth spurt, is the phase in which the individual grows most. Usually, the growth acceleration in the feminine gender occurs in the beginning of puberty, between stages 2 and 3, and always antecedes the menarche, which usually coincides with the phase of growth deceleration, and with stage 4. In the masculine gender, the acceleration usually happens in stage 3 and its peak is in stage 4.</p>
      <p>Electrocardiogram at rest in this group follows the same controversy already described as routine examination. Because of the extreme regional differences in the country<sup>79,81</sup> and taking into account the scientific evidences available, we recommend the ECG as follows:</p>
      <p>Children and adolescents who are healthy and asymptomatic and have no important clinical fact observed in the initial medical evaluation with detailed clinical history and detailed physical examination, who meet the above-mentioned questionings.</p>
      <p>
        <bold>Recommendation Grade: IIa</bold>
      </p>
      <p>
        <bold>Evidence level: C</bold>
      </p>
      <p>In the PPE of children and adolescents of 5 to 18 years old starting organized and competitive training in sports schools, fitness centers and clubs.</p>
      <p>
        <bold>Recommendation Grade: I</bold>
      </p>
      <p>
        <bold>Evidence level: A</bold>
      </p>
      <p>In all children and adolescents with some suspicion of heart disease, detected with the data obtained during medical evaluation.</p>
      <p>
        <bold>Recommendation Grade: I</bold>
      </p>
      <p>
        <bold>Evidence level: A</bold>
      </p>
      <p>
        <bold>4.2. Laboratory exams</bold>
      </p>
      <p>Regarding the performance of laboratory exams, in the age bracket in question they assume some importance for the control of situations that are frequent in this population like parasitosis, anemia, alimentary mistakes and even some cases of malnutrition. We consider the exams listed below as passible of indication, always depending on previous clinical evaluation<sup>76,77</sup>:</p>
      <p>Hemogram: hemoglobin analysis, associated to anemia and leukopenia, very common mainly in young people in training, and can cause an increase in the risk of superior aerial ways infection.</p>
      <p>Iron and ferritin: it helps in the diagnosis of iron deficiency anemia and is also useful to detect overtraining syndrome, in which we find low levels of ferritin.</p>
      <p>Sodium, potassium and chloride: detection of hydroelectrolytic disorders.</p>
      <p>Lipid profile and glycemia: nowadays, due to constant mistakes in the nutrition of children and adolescents, it is becoming important in the primary prevention of hypercholesterolemia in adult age.</p>
      <p>Chagas Disease Serology: it is still an endemic disease in Brazil and South America, cause of myocardiopathy, frequently sub-diagnosed, mainly individuals of a lower socioeconomic level.</p>
      <p>Coprologic: identification of parasitosis.</p>
      <p>Hemoglobin electrophoresis: evaluation of hemoglobinopathies like sickle cell anemia, important in the eligibility of competitive individuals.</p>
      <p>
        <bold>Recommendation Grade: II</bold>
      </p>
      <p>
        <bold>Evidence level: C</bold>
      </p>
      <p>In selected cases with personal or family heart disease background, if variations in physical exam or electrocardiogram arouse, a deeper cardiologic evaluation is required before release for sports activity. This evaluation may include the performance of transthoracic echocardiogram, maximum exercise test and 24 hour holter<sup>77</sup>.</p>
      <p>In official statement, the Sociedade Brasileira de Medicina do Esporte (Brazilian Society of Sports Medicine) recommends that, from the public health point of view, children and adolescents may take part in recreational physical activities of low or moderate intensity without the need of a formal pre-participation examination. When the goal is competitive sport or high intensity physical activity, the youngster needs a medical and functional evaluation, including body composition and aerobic and anaerobic capacity<sup>76</sup>.</p>
      <p>
        <bold>Recommendation Grade: IIa</bold>
      </p>
      <p>
        <bold>Evidence level: B</bold>
      </p>
      <p>The American Heart Association, in document published in 2006 about exercise test in children and adolescents, describes among the main indications in this age bracket: 1- the specific evaluation of symptoms or signs induced or aggravated by exercise; 2- evaluate or identify abnormal response to exercise in children with heart diseases, pulmonary diseases or diseases in other systems, including the presence of myocardial ischemia and arrhythmias; 3- evaluation of the functional capacity for recreational or athletic activities<sup>77</sup>.</p>
      <p>
        <bold>Recommendation Grade: IIa</bold>
      </p>
      <p>
        <bold>Evidence level: B</bold>
      </p>
      <p>The 36th Bethesda conference and the Recommendations for competitive sports participation in athletes with cardiovascular disease refers that the exercise test performance is indicated in the pre-participation evaluation of individuals with congenital heart diseases, valve diseases, myocardiopathies, arterial hypertension, arrhythmias and other conditions of suspected or diagnosed disease with the goal of evaluating functional capacity, symptoms, arrhythmias and orientate the allowed intensity for exercise<sup>81</sup>.</p>
      <p>
        <bold>Recommendation Grade: I</bold>
      </p>
      <p>
        <bold>Evidence level: A</bold>
      </p>
      <p>
        <bold>4.2.1. Echocardiogram </bold>
      </p>
      <p>Echocardiography represents a confirmatory diagnosis modality to be performed after suspicion during initial pre-participation evaluation. In children and adolescents it becomes a extremely useful exam in the presence of abnormalities in the physical exam that induce to suspicion of structural heart disease, especially when heart murmur is detected.</p>
      <p>In cases in which ECG variations are detected, its performance is part of the arsenal for differential diagnosis of severe heart diseases that could potentially trigger sudden death during physical activity, as hypertrophic cardiomyopathy and arrhythmogenic right ventricular dysplasia<sup>1,12,79,80</sup>.</p>
      <p>
        <bold>Recommendation Grade: I</bold>
      </p>
      <p>
        <bold>Evidence level: A</bold>
      </p>
      <p>To the moment there is no evidence to justify its routinely use in population screen programs in asymptomatic individuals.</p>
      <p>
        <bold>Recommendation Grade: III</bold>
      </p>
      <p>
        <bold>5. Group of carriers of cardiomyopathies and myocarditis</bold>
      </p>
      <p>
        <bold>5.1. Hypertrophic cardiomyopathy (HCM) </bold>
      </p>
      <p>Hypertrophic cardiomyopathy is an autosomal dominant disease characterized by myocytes myofibrillar disarray, followed by hypercontractility, hypodyastoly, asymmetric septal hypertrophy with or without obstruction of left ventricle outlet. This disease is the main cause of sudden death related to exercise and sports in individuals under 30-35 years old in North America, while in Europe arrhythmogenic right ventricular dysplasia prevails as main cause of sudden death in this age bracket<sup>3,82</sup>.</p>
      <p>To the moment 12 genes are known which are implied in the genesis of this disease with more than 400 genetic mutations related to myocardial contractile proteins<sup>83</sup>. HCM carriers can be completely asymptomatic or present dizziness, syncope, especially related to exercise, dyspnea, palpitations and angina. Sudden death may occur to this patients due to ventricular and supraventricular arrhythmias (with pre-excitement or not), complete AV block, asystole and myocardial infarction<sup>3</sup>.</p>
      <p>
        <bold>5.2. HCM complementary exams</bold>
      </p>
      <p>
        <bold>5.2.1. Electrocardiogram</bold>
      </p>
      <p>About 95% of the patients with HCM present electrocardiographic variations, the ST segment and the T wave being commonly affected. Around 50% of the electrocardiograms present signs of left ventricular overload<sup>84</sup> and the pathologic Q waves are present in 30% of the cases. It should be noted that such finding may precede the pathologic hypertrophy that will be found lately in the echocardiogram<sup>85</sup>. The HCM Q waves arise by increase of the electrical forces generated in the hypertrophy areas. Its direction and magnitude are related to the vector that results from the areas with greater ventricular hypertrophy<sup>84</sup>. McKenna et al<sup>86</sup> proposed a series of five echocardiographic, electrocardiographic and clinical criteria for the diagnosis of this disease, especially when its origin is in the family. <xref ref-type="table" rid="tab8-body2">Table 8</xref> synthetizes the main electrocardiographic variations in patients with HCM.</p>
      <table-wrap id="tab8-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt08-en.jpg"/></table-wrap>
      <p>
        <bold>5.2.2. Echocardiography</bold>
      </p>
      <p>The differentiation between hypertrophy recurring from MHCM and that secondary to physical training (ventricular hypertrophy of the athlete's heart) requires the integration of several information with the pattern and distribution of the hypertrophy, parietal thickness, the size of the cavities, the evaluation of diastolic function by tissular Doppler and yet the family history. Furthermore, it is important to evaluate the echocardiographic response of athletes under suspicion to a sports untraining<sup>87</sup>. Regarding the prognosis, the identification of a septum bigger than 30 mm is a bigger risk factor for sudden death, especially among adolescents and young adults<sup>88</sup>. The echocardiogram enables the characterization of the type and extension of the compromising of the hypertrophic ventricle in an expressive number of cases, but magnetic resonance may be useful in those in which the echocardiography was not enough to reach diagnosis<sup>89,90</sup>.</p>
      <p>
        <bold>5.2.3. Transthoracic Doppler echocardiogram</bold>
      </p>
      <p>
        <bold>Class: I </bold>
      </p>
      <p>
        <bold>Evidence level: B</bold>
      </p>
      <p>Confirm the clinical suspicion of MHCM, determining the parietal thickness and the presence of dynamic gradient.</p>
      <p>Investigate the presence of MHCM in first-degree family members.</p>
      <p>Re-evaluation of clinical evolution and therapeutic interventions.</p>
      <p>Myocardial contrast echo post-septal ablation to evaluate the size of the infarcted area.</p>
      <p>
        <bold>Class II </bold>
      </p>
      <p>
        <bold>Evidence level C</bold>
      </p>
      <p>IIa: annual re-evaluation of family members of patients with MHCM between 12 and 18 years old. In individuals who are more than 21 years old the re-evaluation should be performed every 5 years;</p>
      <p>IIa: tissular Doppler to differentiate MHCM from athlete's physiologic ventricular hypertrophy or hypertension pathologic hypertrophy;</p>
      <p>IIb: stress echo with exercise in patients symptomatic to habitual routine exertion that do not put in evidence significant gradients at rest or with Valsalva's maneuver.</p>
      <p>
        <bold>5.2.4. Transesophageal Doppler echocardiogram</bold>
      </p>
      <p>
        <bold>Class: I</bold>
      </p>
      <p>
        <bold>Evidence level: B</bold>
      </p>
      <p>Patients with inadequate transthoracic window;</p>
      <p>To evaluate valve compromising, mechanism and magnitude of mitral regurgitation when it is not clear in the transthoracic echocardiography;</p>
      <p>Intraoperative evaluation in myomectomy and in septal ablation by alcoholization.</p>
      <p>
        <bold>Class: IIa </bold>
      </p>
      <p>
        <bold>Evidence level: B</bold>
      </p>
      <p>Clarify the mechanism of an atypical mitral insufficiency.</p>
      <p>
        <bold>5.2.5. Exercise tests and (HCM)</bold>
      </p>
      <p>The exercise test (ET) presents independent value for the identification of patients under increased risk of sudden death. The presence of marked variations of the ST segment in patients with HCM may indicate ischemia without necessarily representing coronary infirmity. In this case the ET presents little diagnosis value, but could be a prognostic marker that should be taken into consideration<sup>84</sup>.</p>
      <p>
        <italic>5.2.5.1. Indication of ET in patients with HCM</italic>
      </p>
      <p>
        <bold>Class: I </bold>
      </p>
      <p>
        <bold>Evidence level: B</bold>
      </p>
      <p>Asymptomatic patients that do not present high risk criteria as associated element in prognostic stratification;</p>
      <p>Asymptomatic patients that do not present high risk criteria and that wish to perform recreational physical activity;</p>
      <p>ET as associated element in differential diagnosis between athlete's heart syndrome and HCM.</p>
      <p>
        <bold>Class: IIa </bold>
      </p>
      <p>
        <bold>Evidence level: C</bold>
      </p>
      <p>Patients with doubtful symptoms not associated with other high risk criteria;</p>
      <p>Sub-maximum ET in patients with implanted defibrillator that wish to perform low intensity physical activity aiming to evaluate functional capacity;</p>
      <p>Sub-maximum ET in patients with implanted defibrillator that wish to perform low intensity physical activity aiming to evaluate heart rate response to exercise.</p>
      <p>
        <bold>Class: III</bold>
      </p>
      <p>Patients with high risk criteria without defibrillator;</p>
      <p>Conventional ET aiming differential diagnosis between HCM and sports practitioner physiologic hypertrophy.</p>
      <p>
        <italic>5.2.5.2. Role of exercise cardiopulmonary test in HCM</italic>
      </p>
      <p>In athletes that are in the so-called gray zone the athlete's heart physiologic and the MHCM pathologic hypertrophy, the oxygen consumption and peak oxygen pulse measuring through the exercise cardiopulmonary test (MCET) may be of great help. Sports practitioners highly trained generally present values between 55-70 mL.Kg<sup>-1</sup>min<sup>-1</sup>. Sharma et al<sup>89</sup> demonstrate that those athletes with no factual disease had a peak oxygen consumption significantly more elevated than athletes with HCM (66.2 mL.Kg<sup>-1</sup>min<sup>-1</sup> versus 34.3 mL.Kg<sup>-1</sup>min<sup>-1</sup>). It is important to highlight that there wasn't superposition among the groups. Therefore, the investigators established as cut-off the cypher of 50 mL.Kg<sup>-1</sup>min<sup>-1</sup> to distinguish HCM pathologic hypertrophy from that secondary to the athlete's heart.</p>
      <p>
        <bold>5.3. Sport and HCM</bold>
      </p>
      <p>Why is there low prevalence of HCM in high level athletes? The answer seems to be related to a natural selection process that excludes individuals with functional and structural variations secondary to HCM from the high intensity regular training required for someone to be an athlete<sup>89</sup>. Being a competitive athlete who has HCM is synonymous of sudden death? The answer is no. We all know cases of athletes who received a diagnosis for this infirmity when they already had quit their professional competitive activity or even while they were still on it. The problem is that intense exercise may be a trigger to launch severe arrhythmias, increase in the obstruction of left ventricle outlet and/or ischemia by compression of small vessels (possible fibrosis by repetitive ischemias), during the training and competition periods. As a matter of fact, there are no clinical or genetic studies to ensure a good prognosis.</p>
      <p>When this infirmity is diagnosed, the rule to be followed has been the exclusion from competitive sports<sup>91</sup>. However, it is possible that some exceptions be made for asymptomatic athletes without high risk criteria that compete in sports like golf, cricket, bowling and shooting.</p>
      <p>The recommendation for exclusion from competitive sports remains for athletes with positive genotype, but with negative phenotype for HCM, although currently we do not have enough evidences available, as they do not have clinical diagnosis nor present risk criteria for HCM. However, some mutations in the troponin gene (chromosome 1) may not express themselves as macroscopic ventricular hypertrophy, but express histopathologic variations in the myocardial muscle fibers, being of bigger risk for sudden death<sup>88</sup>.</p>
      <p>In athletes with positive genotype and negative phenotype that practice acyclic sports (drastic variations in speed with unexpected accelerations and decelerations, e. g. soccer, basketball, tennis), there seems to be more risk than for those who compete in cyclic sports (jogging, swimming, cycling)<sup>88</sup>.</p>
      <p>
        <bold>5.4. SD risk stratification in hypertrophic cardiomyopathy</bold>
      </p>
      <p>There are criteria suggested by Rickers et al<sup>90</sup> and Colin Lizalde<sup>92</sup> to establish risk factors for SD in HCM carriers. Those criteria are found in <xref ref-type="table" rid="tab9-body2">table 9</xref>.</p>
      <table-wrap id="tab9-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt09-en.jpg"/></table-wrap>
      <p>
        <bold>5.5. Recommendations for athletes with HCM diagnosis</bold>
      </p>
      <p>Athletes with probable or unequivocal HCM diagnosis should be excluded from most competitive sports, with possible exception to those sports of low dynamic and static component (IA). This recommendation does not depend on age, gender, phenotypic appearance of the athlete, presence or not of symptoms, obstruction of left ventricle outlet, treatment with drugs, septal ablation, use of pacemaker or implanted defibrillator<sup>86</sup>.</p>
      <p>
        <bold>Class: I </bold>
      </p>
      <p>
        <bold>Evidence level: C</bold>
      </p>
      <p>Patients with HCM diagnosis should be excluded from sports competitions of competitive feature. Those classified as low risk may participate on golf, pool, bowling and shooting;</p>
      <p>Recreational sports that require high intensity or drastic variations in intensity are not recommended;</p>
      <p>Individuals with positive genotype and negative phenotype (without clinical evidence of disease) may participate in sports as long as they are periodically evaluated;</p>
      <p>Patients without high risk criteria and with normal exercise test may perform cyclic recreational physical activity of low intensity;</p>
      <p>Patients with implanted defibrillator should be excluded from contact sports.</p>
      <p>
        <bold>Class: IIa</bold>
      </p>
      <p>Patients without high risk criteria and with normal exercise test may participate on recreational contact sports of low intensity and low volume.</p>
      <p>
        <bold>Class III</bold>
      </p>
      <p>Asymptomatic patients with HCM, even if of low clinical and genetic risk, high functional capacity and without family history of sudden death may participate in high intensity competitive sports.</p>
      <p>
        <bold>6. Group of carriers of arrhythmogenic right ventricular dysplasia (ARVD) or left ventricular cardiomyopathy</bold>
      </p>
      <p>It is a variation in the heart muscle of genetic cause by variation in the desmosome formation that is characterized by pathologic fibro-fatty replacement of right ventricular myocardium, and it may manifest also in the left ventricle<sup>92-94</sup>. This infirmity is an important cause of sudden death in youngsters, including competitive athletes. This disease has been described as the main cause of sudden death in athletes in the region of Veneto, Italy<sup>93,94</sup>. As highly trained athletes may have right ventricular hypertrophy besides a variety of variations in depolarization, repolarization and conduction of nervous stimulus, the differential diagnosis between athlete's heart syndrome and ARVD must always be performed. The echocardiogram may present technical limitations to access right ventricle images, and its structural and functional analysis may be damaged<sup>95,96</sup>. The cardiac magnetic resonance is a non-invasive image technique that has shown itself to be promising<sup>96</sup>. The demonstration of global or segmental dysfunction of right ventricle or the substantial increase of this cardiac chamber cavity associated to myocardial tampering and presence of fibrosis (MR delayed equilibrium) gives support to the ARVD diagnosis<sup>83,97-100</sup>.</p>
      <p>
        <bold>6.1. SD risk stratification in arrhythmogenic left ventricular dysplasia</bold>
      </p>
      <p>Some aspects must be considered in the SD risk stratification in arrhythmogenic right ventricular dysplasia.</p>
      <p>
        <bold>Age Class: IIb, Evidence level: C</bold>
      </p>
      <p>Age - There are divergent opinions on whether the appearance of symptoms in age to 20 years old would be of more risk.</p>
      <p>
        <bold>Syncope Class: IIb, Evidence level: A</bold>
      </p>
      <p>Syncope - great studies could not demonstrate a relation with increase in mortality.</p>
      <p>
        <bold>ECG AR Class: IIA, Evidence level: C</bold>
      </p>
      <p>High resolution electrocardiography - the presence of late potentials seems to positively co-relate with the seriousness of the disease and the occurrence of sustained ventricular tachycardia and ventricular fibrillation, when right ventricular dysfunction is present. However, new studies will be required to predict the development of ventricular arrhythmias.</p>
      <p>
        <bold>Echocardiography Class: I, Evidence level: C</bold>
      </p>
      <p>Echocardiography - sudden death is more frequent in patients with right ventricular diffuse dilatation and in those in who the left ventricle is involved, because its dysfunction seems to be a marker of risk of ventricular fibrillation and sudden death.</p>
      <p>
        <bold>Programmed electrical stimulation Class: III, Evidence level: C</bold>
      </p>
      <p>Programmed electrical stimulation - the induction of sustained ventricular tachycardia varies from 57% to 94% in patients with monomorphic sustained ventricular tachycardia, but is low in patients who present ventricular fibrillation or left ventricle involved. When the induction occurs in the presence of right ventricular dysfunction, the predictive value for sudden death is bigger.</p>
      <p>
        <bold>Magnetic Resonance Class: I, Evidence level C</bold>
      </p>
      <p>The MR identifies the right ventricular dysfunction, walls tapering and presence of delayed equilibrium (myocardial fibrosis) and the presence of microaneurysms.</p>
      <p>Biopsy: little used in our milieu</p>
      <p>
        <bold>24 hour Holter, exercise test and QT dispersion Class: III, Evidence level: C</bold>
      </p>
      <p>24 hour Holter, exercise test and QT dispersion do not present value to identify patients in risk of sudden death as well as the type of ventricular arrhythmia.</p>
      <p>Exercise - there are evidences that the exercise can be a triggering factor of potentially serious symptoms and arrhythmias, suggesting that these consequences depend on the sympathetic tone, especially in athletes<sup>99,100</sup>.</p>
      <p>Finally, it is important to highlight that the most efficient way of detecting silent cardiac pathologies that sometimes may be the cause of sudden death related to exercise and sports is a careful pre-participation evaluation and that many variations found in routine exams and that may be confused with heart diseases are physiological adaptations resulting from intensive and regular training, composing the characteristics known as athlete's heart syndrome, cardiomegaly, conduction and rhythm disturbances and variations of ventricular repolarization in the electrocardiogram<sup>97,98,100,101</sup>.</p>
      <p>Recommendations for athletes with arrhythmogenic right ventricular dysplasia diagnosis</p>
      <p>Patients/athletes with unequivocal diagnosis of right ventricular dysplasia should be excluded from the practice of competitive activities<sup>92,93</sup>.</p>
      <p>
        <bold>7. Group of myocarditis carriers</bold>
      </p>
      <p>It is an infirmity associated to a heterogeneous clinical profile, being the probable cause of sudden death in some athletes<sup>73,102,103</sup>. Usually, myocarditis is result of an infection, but it can be associated to alcohol or drugs abuse<sup>103</sup>. Sudden death may occur in its active phase or even when there is already a scar in the myocardium, consequence of complex arrhythmias deflagrated from an instability electric substrate. In the athlete we can have left ventricular increase by the disease per se, by hypertrophy secondary to physical training or by a mix of both. The differential diagnosis in this cases is made by the athlete's clinic (presence of arrhythmias, palpitations, pre-syncope or syncope or yet by systolic dysfunction). The cardiac magnetic resonance and the performance of endomyocardial biopsy in certain circumstances can help in the diagnosis. It is important to highlight that several studies have shown H1N1 flu as responsible for a kind of serious myocarditis, almost always accompanied by cardiogenic shock. Recently, the organizing committees of the Singapore Asian Games and of the Winter Olympics in Canada recommended that all athletes participating in these events came to these countries vaccinated against swine flu. We also remind here of the possibility of myocarditis by dengue virus in our country because of the constant outbreaks of this disease in Brazil.</p>
      <p>
        <bold>7.1. Recommendations for athletes carriers of myocarditis</bold>
      </p>
      <p>Athletes diagnosed with myocarditis should be removed from all competitive sports and undergo a recovery period of at least 6 months after the onset of clinical manifestations. These athletes may be released for training and competition after 6 months if:</p>
      <p>Left ventricular function, ventricular wall motility and cardiac dimensions return to normal (based on echocardiographic and radionuclide studies at rest and with exertion);</p>
      <p>Frequent or complex forms of ventricular and supraventricular arrhythmias and clinically relevant arrhythmias are absent;</p>
      <p>Inflammatory markers and heart failure are standardized;</p>
      <p>The ECG at rest is standard, although the persistence of ST alterations criterion alone is not impediment to return to training and competitions.</p>
      <p>
        <bold>8. Group of carriers of coronary artery disease</bold>
      </p>
      <p>The ischemic heart disease has declined over the decades, in Brazil. In 1980, the standardized death rate from coronary artery disease (CAD) was 65/100,000 inhabitants, and in 2005 the data showed 46/100,000 inhabitants<sup>104</sup>. Coronary artery disease accounts for the majority of the events of sudden death associated with exercise in people aged over 35 years old<sup>105</sup>. The mechanisms responsible for triggering coronary events during vigorous physical activity result from increased sympathetic activity and increased release of catecholamines, platelet adhesion and activation (leading to risk of thromboembolic events), electrolyte abnormalities by elevated potassium (serving as a trigger for ventricular tachyarrhythmias) and complications as subendocardial ischemia, leading to plaque rupture<sup>106, 107</sup> or possible plaque erosion<sup>108, 109</sup>, facts implicated as immediate causes of exercise-related events in adults. In the young individual, the leading cause of sudden death during sports is hypertrophic cardiomyopathy<sup>110</sup>.</p>
      <p>In the last decade, the practice of physical activity has been recommended as part of intervention in primary and secondary prevention of coronary artery disease by providing a steady improvement in functional capacity (Class I) alleviating angina at rest (Class I), with improvement in the severity of exercise-induced ischemia (Class IIa) and the reduction of some cardiovascular risk factors (Class IIa). Proposed mechanisms and described the benefits of physical exercise in CAD &#8203;&#8203;are: increment of endothelial function, regression of atherosclerotic plaque formation and increased flow of collateral circulation, vasculogenesis, remodeling and decreased apoptose<sup>108</sup>. However, for this population start a physical practice is needed as to the stratification chance of having an event cardiovascular <sup>109, 111</sup>. The algorithm for the stratification of the patient begins with history taking and physical examination and the subsequent application of a progressive exercise test and maximum for the induction of cardiac arrhythmias, ischemic stress induced ventricular dysfunction and atrioventricular conduction disturbances. Data provided by exercise testing will guide the prescription of physical practice, you must follow some basic principles, such as frequency, duration, intensity and type of exercise<sup>112, 113</sup>.</p>
      <p>Type of exercise: aerobic exercise program are those that yield better benefits for the cardiovascular system and control of risk factors. This type of program is characterized by cyclical exercises of large muscle groups, such as walking, jogging, swimming, cycling, dancing, aerobics, among others.</p>
      <p>Frequency of exercise: the recommended exercise frequency is 3-5 times a week, and in some groups (hypertensive and obese) the frequency can be up to 7 times a week.</p>
      <p>Exercise intensity: the best way to measure the intensity of physical exercise is through heart rate, determined by maximum exercise testing (ET). The training heart rate should be between 70 and 85% of maximal HR obtained in ET and can be used to Karvonen formula (HR training = (HR maximum - HR at rest) x% of HR reserve recommended + HR at rest) or the corresponding heart rate between the anaerobic threshold and respiratory compensation point, assessed by spirometry. In beginners patients the range 50-60% HR reserve and 60-80% HR reserve for contingent should be used. Patients on beta-blockers should associate with HR training determined by functional testing to feel exertion by the Borg scale.</p>
      <p>In muscular endurance exercises for the major muscle groups, you should use 40-60% of maximum voluntary contraction (low to moderate intensity) with 8-15 repetitions, three sets to one, or empirically, starting with low loads and evolving until the sense of effort is low to moderate.</p>
      <p>Duration of aerobic exercise: 30-60 continuous minutes</p>
      <p>
        <bold>8.1. Anamnesis and physical examination</bold>
      </p>
      <p>Data supplied by anamnesis and physical examination are essential for the evaluation of coronary artery disease, whether it is stable course or not, helping to stratify the individual and exercise schedule (Class IIa, Evidence level B).</p>
      <p>
        <bold>8.1.1. Clinical history</bold>
      </p>
      <p>The clinical history is extremely important in the stratification of candidate patient with physical practice supervised or not, guiding the physician regarding the evolution and the current stage of the disease. You can identify the presence or absence of symptoms (pain, fatigue, shortness of breath) and with what degree of effort they are triggered. One should make an inventory regarding medications, as they may influence the dynamics of programming and practice exercises, must abide by certain characteristics of the symptoms that drive the probability of the presence of angina as:</p>
      <p>Location: chest, retrosternal shoulder, epigastrium, cervical, hemithorax, back;</p>
      <p>Type: constrictive, tightness, heaviness, tightness, discomfort, burning, stabbing;</p>
      <p>Irradiation: upper (right, left, both), shoulder, jaw, neck, back, epigastrium;</p>
      <p>Trigger factors: physical exertion, sexual activity, position, power, breathing, emotional component, spontaneous;</p>
      <p>Factors relief, rest, sublingual nitrate, analgesic, food, antacid, position and apnea;</p>
      <p>Associated symptoms: sweating, nausea, vomiting, pallor, dyspnea, hemoptysis, cough, pre-syncope and syncope.</p>
      <p>The classification of chest pain becomes fundamental, and divide this into three groups: typical, atypical and not cardiac<sup>114, 115</sup>.</p>
      <p>Typical angina (definite)</p>
      <p>Triggered by exercise or emotional stress;</p>
      <p>Retrosternal discomfort or pain;</p>
      <p>Relieved by rest or nitroglycerin</p>
      <p>Atypical angina (probable)</p>
      <p>Presence of only two factors above</p>
      <p>Non-cardiac chest pain</p>
      <p>Presence of only one or none of the above factors</p>
      <p>Besides clinical history of chest pain risk factors for CAD should be considered in the stratification of individuals, such as diabetes, hypertension, dyslipidemia, smoking, family history of premature CAD (&lt;55 years for men and &lt;65 years for women), inactivity and stress.</p>
      <p>
        <bold>8.1.2. Physical examination</bold>
      </p>
      <p>Physical examination may be normal or show some changes identified by ectoscopy, palpation and auscultation, such as a stroke deflected to the left, the presence of an accessory heart sound (and B3 or B4), identifying a blow that may give clues about " status "of the heart. A blood pressure measurement should be performed in both arms, and in orthostatic, sitting and lying and at least one lower limb, with the goal of postural hypotension or identify certain problems that can cause there is a significant difference in blood pressure among members. The physical examination is usually normal in patients with stable angina<sup>27</sup>. Presence of atherosclerosis at other sites can provide data for an investigation of CAD in some individuals with lower limb pulses decreased, arterial stiffening and abdominal aortic aneurysm. Despite the physical examination in subjects with CAD be little instructive, complete workup, particularly the cardiovascular system should be performed carefully, because it can provide important information on other associated conditions such as valvular disease, hypertrophic cardiomyopathy and other.</p>
      <p>
        <bold>8.2. Echocardiography in chronic CAD:</bold>
      </p>
      <p>The transthoracic echocardiography has been used as an important diagnostic tool in coronary artery disease as well as a method for the evaluation of prognosis in these pacientes<sup>30</sup>. In patients clinical history and electrocardiogram are inconclusive, echocardiography can demonstrate reversible abnormalities of wall motion or not, identifying areas of hypokinesia, acnesia, dyskinesia and aneurysms (Class I) and extent of these changes, providing also an important variable in assessing left ventricular function, ejection fraction (Class I) <sup>116</sup>.</p>
      <p>
        <bold>8.3. Benefits of exercise on coronary disease</bold>
      </p>
      <p>There are several physiological benefits elicited by exercise in patients with stable CAD. <xref ref-type="table" rid="tab10-body2">Table 10</xref> summarizes the benefits for level of evidence.</p>
      <table-wrap id="tab10-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt10-en.jpg"/></table-wrap>
      <p>
        <bold>8.4. Risk stratification for inclusion of patients in exercise and cardiac rehabilitation programs</bold>
      </p>
      <p>The risk of patients in exercises and cardiac rehabilitation programs can be categorized according to <xref ref-type="table" rid="tab11-body2">table 11</xref><sup>117</sup>.</p>
      <table-wrap id="tab11-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt11-en.jpg"/></table-wrap>
      <p>
        <bold>8.5. Computed tomography, magnetic resonance and athlete's heart</bold>
      </p>
      <p>Despite the great usefulness and practical applicability of Doppler echocardiography in the evaluation of different heart diseases, there are situations where it is necessary to use other imaging modalities for the diagnosis and also for risk stratification. In particular in the evaluation of athletes with suspected heart disease using these methodologies can be important, such as the distinction between mild hypertrophic cardiomyopathy and myocardial hypertrophy secondary to sport activity<sup>118, 119</sup>.</p>
      <p>The complexity of the cardiac movements requires that equipment intended to produce image be sophisticated enough to reproduce the anatomy of the heart without artifacts resulting from the mobility of the heart itself <sup>118</sup>. The magnetic resonance equipment equal or greater than 1.5 Tesla can be used for this end<sup>118</sup>.</p>
      <p>Tomography data available in the literature are based on studies of equipment of 64 rows of detectors. Systems with at least 32 rows of detectors can be used effectively, there is only a need for more adequate preparation of the patient, to improve the quality of images obtained<sup>118</sup>.</p>
      <p>The professionals involved should have received appropriate training in specialized centers, to ensure greater safety and better quality of examinations performed<sup>118</sup>.</p>
      <p>The use of magnetic resonance imaging and computed tomography for the risk stratification of asymptomatic individuals and release for sports is still limited. There are no jobs available in the literature assessing the potential contribution that the resonance could have that effect. In addition, CT is at least in part, its limited application because it uses ionizing radiation, which restricts its indiscriminate use, especially in the younger population. However, this technology has definite role in some conditions that may be present in the evaluation of asymptomatic wanting to do sports activities<sup>118, 120,121</sup>.</p>
      <p>The presence of signs suggestive of myocardial ischemia in young people may be related to the existence of anomalous origin of a coronary artery. This is a condition in which the use of CT or MRI is fundamental and well defined<sup>122</sup>.</p>
      <p>In older individuals who wish to practice physical activities, CT can also help, especially if there is conflict between the results of other noninvasive tests with regard to the existence of silent myocardial ischemia. The most common situation is when there is stress test compatible with the presence of ischemia and myocardial scintigraphy normal or doubtful. In this condition, the high negative predictive power of the test may have a fundamental role to exclude the presence of obstructive coronary disease or to indicate the need for if further invasive diagnostic investigation.</p>
      <p>The high spatial resolution of CT also enables it to be used for diagnosis of other conditions such as congenital heart disease, cardiomyopathies, and vascular anomalies, but also those ends are achieved with MRI, which has the added advantage of not using ionizing radiation<sup>118</sup> .</p>
      <p>Other medical conditions that may involve the use of MRI for release for sports involve the existence of underlying heart disease that has not presented clinical manifestation previously. In these cases, the clinical recommendations for the use of resonance are within the regulations established in habitual cardiology<sup>118</sup>.</p>
      <p>For evaluation of heart disease in athletes who compete in categories aimed for people over 40 years and with conflicting non-invasive tests<sup>118</sup>, tomography can be a useful test, because it has a negative predictive value greater than 97% and may be useful for rule out obstructive disease. Other clinical conditions may need further investigation, such as arrhythmias or the development of changes to electrocardiogram<sup>120</sup>.</p>
      <p>The heart of the professional athlete or amateur elite to resonance is characterized by having larger dimensions mass, end-diastolic volume and end-systolic volume. Such changes, however, occur without altering ejection fraction, regional contractility or contraction pattern of the ventricles. This aspect should always be considered as cases of hypertrophic cardiomyopathy usually show changes in the pattern of cardiac contractility, even if there is slight increase in thickness of the ventricular myocardium. Thus, the shape of ventricular twist in both the longitudinal and in the transverse plane, is preserved in athletes, even elite, which does not occur in cases of hypertrophic cardiomyopathy<sup>119</sup>.</p>
      <p>In cases of heart adaptation to stress found in elite athletes the degree of hypertrophy that affects the left ventricle differs from that which interests the right ventricle, being more pronounced in the cavity systemic. Furthermore, when there is a relationship between physiological hypertrophy volumes, dimensions and ejection fraction of the left ventricle compared to the right ventricle are comparable in athletes and sedentary individuals without structural heart disease<sup>119, 120</sup>.</p>
      <p>A major cause of death in young athletes is hypertrophic cardiomyopathy condition that should always be remembered and researched evidence of abnormalities that arise for this subgroup. The literature reports cases there are up to 13 mm thickness in the left ventricular myocardium as an adaptive response, especially in the case of elite athletes male. It is important to remember that in different sports among them weightlifting, rowing, cycling, swimming, marathons and professional football athletes may also have significant increases of cardiac dimensions, without presenting heart disease<sup>121</sup>.</p>
      <p>Hypertrophic cardiomyopathy resonance can also understand the presence of delayed enhancement, which may indicate the existence of fibrosis and be present in varying degrees, regardless of the clinical manifestation of heart disease. Some studies have associated this image pattern to the occurrence of arrhythmias and changes to the dilated form of the disease, a finding that should raise caution in case driving<sup>118, 119.</sup></p>
      <p>The arrhythmogenic also shows up as a challenge in athletes, especially due to the wide variety of image patterns that it can present. It must be remembered that the simple presence of fat tissue in the myocardium is not pathognomonic of that entity, since the presence of fat in heart muscle may be a consequence of other inflammatory conditions, degenerative and ischemic besides being a usual finding in patients over 65. The diagnosis of dysplasia is made from the existence of regional abnormalities in the ventricles, and the existence of areas of delayed enhancement in the ventricular walls, reflecting the presence of inflammation and / or myocardial fibrosis. The combination of these findings, with or without the presence of fat associated, allows for the identification of dysplasia. Important data such cases arises from the fact that due to the evolving nature of this entity, the diagnosis involves the removal of sports activities<sup>121, 122</sup>.</p>
      <p>Another condition that has clinical importance is myocarditis. This entity can have your event facilitated by the existence of conditions that lead to decreased immune activity, such as occurs when there is excessive training for a long period, habitual condition of elite athletes. The resonance has been shown to be an effective evaluation of these patients revealed the presence of late enhancement, even in cases where there is no change in ventricular contractility, which allow defining the presence of these changes. Some authors mention that the image pattern may even allow them to infer the causative agent of entidade121. Changes in the presence, extent and intensity of delayed enhancement in these conditions are important prognosis<sup>121, 122</sup>.</p>
      <p>Resonance and computed tomography can be important allies in risk stratification and evaluation of structural heart disease in athletes. Although its routine use is to essentially complement evaluation by clinical examination, ECG and echocardiography may, under some conditions such as anomalous origin of the coronary arteries, in search of arrhythmogenic dysplasia and myocarditis, they can compose the line front and are arguably important stages of the diagnostic evaluation <xref ref-type="table" rid="tab12-body2">table 12</xref>.</p>
      <table-wrap id="tab12-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt12-en.jpg"/></table-wrap>
      <p>
        <bold>9. Risk stratification of SD-related exercise / sport in arrhythmogenic genetic syndromes.</bold>
      </p>
      <p>
        <bold>9.1. Canalopathies</bold>
      </p>
      <p>The canalopathies are inherited arrhythmogenic heart disease, no structural, caused by genetic alterations that result in dysfunction of cardiac ion channels, exposing their patients to a risk of sudden death<sup>123</sup>. Canalopathies The best known are the long QT syndrome (LQTS), short QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia TVPC. The sinus node disease and disease Lenegre or conduction system disease are also examples of canalopathies.</p>
      <p>The ion channels, ion currents passing through these channels, proteins that bind to cell membrane structure myocardial and the junctions between these structures are part of electrical impulse formation and transmission of these impulses throughout the heart muscle so synchronous generating the potential cardiac action<sup>124, 125</sup>. The performance of each of these functions is determined by different genes. Mutations that occur in these genes cause specific dysfunctions and diseases known to cause canalopathies<sup>126, 127</sup>. The ion channels present on the cell membrane allow entry and exit of ions, following a voltage gradient. The change caused by genetic mutation in each of these channels may generate a gain or loss of function. There are ion channels responsible for depolarization and repolarization of the cell membrane. The first channel from right to left, called electrogenic channel, allows entry of three sodium ions (Na +) to each output of calcium ion (Ca2 +) across the membrane. The depolarization channels are: 1) INa, sodium channel carried by SCN5A gene whose mutations that cause gain of function resulting in LQTS 3, while the loss of function causes Brugada syndrome and congenital sinus node disease, 2) channel iCal L-type calcium; 3) INa / Ca channel sodium and calcium channel called electrogenic. The channels involved in myocardial repolarization of the cell are: 1) IK1 potassium channel KCNJ2. This channel is responsible for the output of potassium at the end of phase 3 of the action potential. The gain of function of this channel results in short QT syndrome type 3. while the loss of the function of this channel results in long QT syndrome type 7 and Andersen syndrome. 2) ITo1 and ITo2 responsible for early repolarization - phase 1 of the action potential, 3) IKr - Potassium Channel - Gene KCNH2/KCNE2. This channel is responsible for the output of potassium in the beginning of phase 3 of the action potential. The gain of function of this channel results in short QT syndrome type 1. 4) IKs potassium channel gene KCNQ1/KCNE1. This channel is responsible for the output of potassium in the middle of phase 3 of the action potential. The gain of function of this channel results in short QT syndrome type 2. The loss of function of the KCNQ1 gene (the alpha subunit which forms pores in the cell membrane) and the KCNE1 gene (which encodes the protein which forms the slow component of the IKs channel) causes long QT syndrome type 1.</p>
      <p>
        <bold>9.2. Long QT syndrome</bold>
      </p>
      <p>The long QT syndrome is the prototype of canalopathies. Reported for more than 50 years, initially as autosomal recessive syndrome of Jervell and Lange-Nielsen128 (congenital deafness, increased QTc interval and syncope or sudden death) and subsequently autosomal dominant Romano-Ward syndrome (deafness without prolonged QTc ), the LQTS showed an inherited trait of sudden death in patients without structural heart disease. Currently, there are several types of known LQTS, mutations in certain genes that cause distinct changes in ventricular depolarization and repolarization (<xref ref-type="table" rid="tab13-body2">Table 13</xref>).</p>
      <table-wrap id="tab13-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt13-en.jpg"/></table-wrap>
      <p>Different mutations in the same gene may result in loss or gain of function and, consequently, different syndromes. LQTS: long QT syndrome, AD: autosomal dominant, AR: autosomal recessive.</p>
      <p>The typical clinical features of LQTS include syncope or sudden death associated with QTc interval prolongation and ventricular tachyarrhythmia presence and torsades de pointes. Classically, there are triggers of syncope in LQTS, adrenergic activity in LQTS 1 and sudden awakening or auditory stimulus in LQTS 2. However, there is a wide variety of presentations, the carrier of the mutation may be asymptomatic since, with no increase in QTc, even have syncope or sudden death in the first days of life. Therefore, we developed diagnostic criteria for scoring changes on 3 main criteria: clinical history, family history and electrocardiographic variation<sup>129</sup> (<xref ref-type="table" rid="tab14-body2">table 14</xref>).</p>
      <table-wrap id="tab14-body2">
        <graphic xlink:href="1678-4170-abc-100-1suppl2-0001-3S002-gt14-en.jpg"/></table-wrap>
      <p>
        <bold>9.2.1. Genetic alterations of the long QT syndrome (LQTS)</bold>
      </p>
      <p>The genetic alterations are known in approximately 60% of clinical cases of LQTS. They are currently 7 known genes responsible for these syndromes. However, hundreds of mutations have been described, which is the cardiac canalopathy with the highest number of mutations described<sup>130</sup>.</p>
      <p>The most common mutation occurs in the gene KCNQ1, responsible for LQTS 1 (40-50%) and the syndrome of Jervell-Lange-Nielsen type 1. This mutation causes a loss of function of the potassium current IKs, which plays an important role in cellular repolarization and QT interval adaptation to heart rate. The KCNE1 gene, whose mutation causes LQTS5, is much less frequent (2-3%) and is also responsible for the function IKs <sup>123, 131, 132</sup>.</p>
      <p>The KCNH2 gene (HERG) encoding the alpha subunit of potassium channels rapid and KCNE2, which encodes the beta subunit are responsible for the rapid entry of potassium during the third potential action<sup>131, 133</sup>. The loss of function of the alpha subunit represents 40% of the genotyped LQTS and is responsible for LQTS 2<sup>134</sup>.</p>
      <p>The LQTS 3 represents approximately 10% of all diagnosed mutations in LQTS occurs by changes in the SCN5A gene, which produces a gain of function sodium continuous input during the plateau phase, facilitating premature depolarizations of the cardiac cell. Hundreds of other mutations have been described. However, clinical applications of these mutations to identify treatment and monitoring of patients and relatives of LQTS are restricted to known forms<sup>125</sup>.</p>
      <p>
        <bold>9.2.2. Risk Stratification in LQTS</bold>
      </p>
      <p>Genetic analysis has been widely used in risk stratification and specific therapeutic interventions in patients with prolonged QT interval, as well as their families, to identify patients with normal QT interval.</p>
      <p>The recommendation of strategies for risk stratification and treatment for medical conditions are infrequent, and therefore the data obtained on the disease cohort studies, some with large number of participants, with follow along, others with more limited or Following narrower limits the level Evidence for the recommendations to B.</p>
      <p>The most robust risk marker identified is a previous episode of aborted sudden cardiac death and its most common cause, are episodes of polymorphic ventricular tachycardia, or not degenerating into ventricular fibrillation. Patients who experience this condition are 12.9 times greater risk of new episodes of sudden death. Prior Syncope is also a risk marker extremely disadvantageous<sup>135</sup>.</p>
      <p>For asymptomatic patients were identified as risk factors: QTc&gt; 500 ms for patients with LQTS 1 and 2 male patients in LQTS 3, regardless of the QT interval. Mutations involving a gene segment encoding the pore of the channel are also linked with poor prognosis. So once again it is clear the value of genotyping in patients with this syndrome. The presence of sudden death in the family was not a marker of increased risk of events<sup>136</sup>.</p>
      <p>
        <bold>9.2.3. Recommendations</bold>
      </p>
      <p>Restriction of physical activity: although in LQTS 2:03 episodes of ventricular arrhythmia are not related to effort, it is recommended that all affected patients avoid physical exertion competitive. This recommendation is particularly important in the case of swimming for LQTS1. In 2 patients with LQTS should avoid acoustic stimuli especially during sleep, such as alarm clock and telephone. Obviously, drugs known to prolong the QT interval should not be used, as well as drugs which reduce the plasma levels of potassium and magnesium (interventions Class I).</p>
      <p>All patients with prolonged QT interval should receive beta-blockers, although the protection is incomplete for patients with LQTS 2 and 3 (intervention Class I). For patients with mutation, but with normal QT interval, also recommended the prophylactic use of beta-blockers (IIa)<sup>137, 138</sup>.</p>
      <p>The pacemaker has been considered an adjuvant therapy, always in conjunction with beta-blocker <sup>139, 140</sup>. It is effective in preventing recurrence of torsades de pointes, although its role is not well defined. The mechanisms involved are suppression of pauses preceding and the precipitate torsades de pointes, and by shortening of the QT interval. In general, is indicated for the prevention of severe bradycardia or pauses resulting from the use of beta-blockers in patients who cannot tolerate adequate doses, who remain symptomatic despite its correct usage or when there is evidence of pause-dependent arrhythmias. Certain genotypes of LQTS may benefit more than others with pacemaker implantation. The effect of bradycardia on transmural dispersion of repolarization was more pronounced in LQTS3 and LQTS2 and inexpressive in LQTS1. The correct programming of the pacemaker is important in preventing arrhythmias in LQTS. The stimulation at higher frequencies shorten the QT interval and reduces the dispersion of ventricular repolarization. The minimum frequency limit should be set to 70 to 80 bpm and can be increased in situations of higher risk, such as in surgical procedures and post-partum period. The occurrence of atrioventricular functional in some patients (especially children with very prolonged QT) immediately before the start of torsades de pointes causes the DDD pacing mode most widely used. There is no consensus on the best programming on the frequency response and time delay atrioventricular. Some of the programming features that enable drops low heart rate should be turned off, as hysteresis and sleep function.</p>
      <p>The implantable cardioverter-defibrillator is recommended for all survivors of sudden death with good functional status and life expectancy of greater than 1 year (Class I recommendation). Patients may present syncope despite beta-blocker therapy may also benefit from defibrillator (IIa). The defibrillator may be considered in patients at high risk for sudden death, such as LQTS 2 and 3, even asymptomatic (Class IIb recommendation)<sup>141, 142</sup>.</p>
      <p>The sympathetic denervation may be considered for patients with syncope or polymorphic ventricular tachycardia that are already on beta-blockers (IIb)<sup>143, 144</sup>.</p>
      <p>
        <bold>9.3. Short QT syndrome</bold>
      </p>
      <p>In this disease there is a shortening of repolarization, favoring the genesis of ventricular arrhythmias by reentry. Characterized by a short QT interval QTc &lt;320 ms with peaked T waves, which can have increased amplitude, with its ascending phase and normal phase descending rapidly<sup>125, </sup><sup>127,145,146</sup>. As clinical parameters for diagnosis are still unclear, genetic analysis is useful to confirm the diagnosis in suspected cases. Mutations in three genes were described KCNH2, KCNQ1 and KCNJ2 all resulting in a gain of function channel IKr, IKs and IK1, respectively, and determining the short QT syndrome type 1, 2 and 3. As the number of patients with a confirmed diagnosis is low, is not yet determined whether any specific type of mutation determines a worse prognosis. Risk factors for the occurrence of arrhythmias are not known.</p>
      <p>Treatment for this condition is still a matter of controversy. In patients with mutations in the KCNH2 gene, showed the use of quinidine prolong refractoriness and suppress arrhythmia induction during electrophysiological study <sup>146</sup> for the other mutations, their utility has not been established. The disease seems to have high lethality, however, there may be a diagnostic bias only in serious cases. The use of the defibrillator may be considered, however, one must keep in mind the downside of the possibility of inappropriate shocks for the phenomenon of double counting (QRS complexes and T waves)<sup>147, 148</sup>.</p>
      <p>
        <bold>9.4. Brugada Syndrome</bold>
      </p>
      <p>This syndrome is characterized by the occurrence of syncope or sudden death caused by polymorphic ventricular tachycardia in structurally normal hearts. His most peculiar aspect is the occurrence of ST-J point in right precordial leads V1 to V3, although this phenomenon has already been described in inferior leads<sup>149</sup>. Perhaps influenced by gender 90% of cases occur in men. Until now, only been identified in the SCN5A gene mutations that are present in about<sup>123</sup> 1/3 of affected<sup>123, </sup><sup>150</sup>. Clinically, the disease manifests with syncope or sudden death, mainly in the third or fourth decades of life. Fever is a trigger for arrhythmias.</p>
      <p>Risk stratification in individuals with ST-J point that occurs spontaneously have a worse prognosis compared to those in the typical pattern was only observed after infusion of flecainide, procainamide or ajmaline. The occurrence of syncope associated with the occurrence of spontaneous elevation, increased risk of sudden death six times. The presence of sudden death in the family has not proved useful for risk stratification as well as the detection of gene mutation SCN5A.<sup>151, 152</sup></p>
      <p>The use of programmed ventricular stimulation for risk stratification is controversial. In the series of Brugada et al <sup>152</sup>, the absence of inducible arrhythmias during electrophysiological study had a negative predictive value of 93% at 3 years for clinical events. However, the number of patients and cols.136 Priori, electrophysiological studies had low accuracy for predicting events. Currently, the use of programmed ventricular stimulation is Class IIb indication for risk stratification in asymptomatic patients.<sup>153, 154</sup></p>
      <p>As therapeutic recommendations, the use of defibrillator is indicated for Class I patients recovered from sudden death. It is Class IIa indication for patients with ST spontaneous point that J expressed or syncope who had previously documented ventricular tachycardia.</p>
      <p>The infusion of isoproterenol can be useful in the treatment of thunderstorm (Class IIa) as well as the use of quinidine for that situation (Class IIb)</p>
      <p>
        <bold>9.5. Catecholaminergic polymorphic ventricular tachycardia</bold>
      </p>
      <p>The disease is characterized by episodes of polymorphic ventricular tachycardia, triggered during stress or emotions in children and young adults who have hearts structurally normal<sup>155, 156</sup>. The ECG at rest is normal, except for a relative bradycardia for age and frequent presence of wave U. It manifests clinically as syncope triggered by physical or emotional stressful situations<sup>155, 156</sup>. Two mutations were described in RyR2 and CASQ2 genes that encode the ryanodine receptor, protein responsible for calcium release from the sarcoplasmic reticulum, and calsequestrin protein which binds to calcium in the sarcoplasmic reticulum. The genetic analysis does not contribute to risk stratification, but it is important to identify carriers of the mutation that has not yet manifested symptoms.</p>
      <p>The typical manifestation is the occurrence of arrhythmias during exercise, most often when they reach 120-130 beats per minute, starting with isolated ventricular premature beats, progressing to episodes of non-sustained ventricular tachycardia and sustained, if effort is maintained (Figure 3 ).</p>
      <p>The use of beta-blockers is very effective in reducing symptoms, and indication Class I to patients with clinical manifestations, IIa Child carriers of the mutation, but that did not exhibit symptoms, and Class IIb for adults in the same situation<sup>157, 158</sup>.</p>
      <p>The defibrillator use in Class I indication is retrieved from Class IIa and sudden death in patients who remain with sustained ventricular tachycardia or syncope despite beta-blocker therapy.</p>
      <p>It has been recently suggested treatment with cardiac denervation friendly left as a therapeutic alternative for patients who cannot make use of beta-blockers. The mechanism of action of this therapy seems very attractive for these patients, since it reduces cardiac catecholaminergic stimulation, which in theory would reduce the triggering stimulus arrhythmia. Some authors have reported promising initial experiments, but there is little evidence that this alternative is incorporated routine, currently only recommended in cases of failure or contraindication of beta-blockers.</p>
      <p>The recommendations regarding the release for sports activities take into account the type of activity and the diagnosis established from the pre-participation evaluation and any additional tests that may be necessary. Sports are categorized into static and dynamic according to <xref ref-type="table" rid="tab15-body2">table 15</xref>. The recommendations are summarized in <xref ref-type="table" rid="en_a01tab16-body2">Tables 16</xref>, <xref ref-type="table" rid="en_a01tab17-body2">17</xref> and <xref ref-type="table" rid="en_a01tab18-body2">18</xref>.</p>
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      <p>
        <bold>10. Basic life support in the athlete</bold>
      </p>
      <p>
        <bold>10.1. Sudden death in athletes</bold>
      </p>
      <p>Although rare, sudden death (SD) in sports is an event that causes public outcry, especially when it involves high-performance athletes. Statistics from different countries show that its prevalence varies from 0.28 to 1 per 100,000 athletes<sup>159, 160</sup>. Different structural and arrhythmogenic variations are responsible for cases of sudden cardiac arrest in athletes, however, the most common is hypertrophic cardiomyopathy, accounting for 25-36% of cases<sup>159, 160</sup>. Vigorous exercise linked to heart disease seems to be the hidden trigger that triggers the arrhythmia responsible for cardiopulmonary arrest (CPA).</p>
      <p>Guidelines nacionais3 internacionais161 and advise the pre-participation cardiovascular screening, which is, in general, in a detailed history, physical examination and 12-lead electrocardiogram. Such a screening would be able to detect approximately 90% of athletes who had a fatal event, although there are reports of the sportsmen SD victims who did not have any structural or condu&#231;&#227;o162 isolation, screening is not able to significantly decrease the number of deaths from sudden cardiac arrest in this risk group, mainly by not performing this evaluation by athletes and the possible false-negative results, necessitating the establishment and strengthening of a second pillar, basic life support.</p>
      <p>10.2. Initial care to the athlete</p>
      <p>Care for better emergency care are summarized as a set of actions taken in the first minutes that follow after a sudden event. These actions can be summarized in two pillars: the organization and planning of the emergency care team, at the places where physical activity is performed, and training of first responders in CPR and handling of automated external defibrillator (AED). Sites where physical activities, such as training centers, schools, colleges, gyms, etc.. must have an emergency response plan well organized, with professionals trained in basic life support (BLS) and communication services with fast and effective prepared to perform advanced life support in cardiology (ACLS).</p>
      <p>Effective treatment of an athlete who suffers a sudden PCR depends on a sequence of interdependent actions, so that, when linked together, form a chain effect, increasing the survival rate of victims, named by the American Heart Association, the "current survival, "comprised of the following links: fast access, early CPR, early defibrillation and early ACLS.</p>
      <p>Most sudden PCR in athletes occurs due to a tachiarrhythmia<sup>163</sup> (ventricular fibrillation) and therefore can be treated with defibrillation. The reduction in mortality in athletes surprised by such an event requires CPR training programs and handling the DEA, and rescuers equipped and trained to recognize emergencies, activate the emergency system, providing quality CPR and use the AED. There are current guidelines for sports facilities that have more than 2,500 patrons or develop physical activity programs for individuals belonging to certain risk groups, such as heart disease and the elderly, have defibrillators strategically allocated<sup>131</sup>.</p>
      <p>It is already well established that for each minute without cardiopulmonary resuscitation (CPR) survival of a victim PCR witnessed decreases from 7 to 10%. However, in the context of ventricular arrhythmias structural diseases appear to be more susceptible to small delays compared to a defibrillation<sup>129</sup> context a structurally sound heart, which possibly brings to athletes victims of a sudden PCR a more significant decline in survival while waiting for an AED, stressing the utmost importance of the third link in the chain, early defibrillation.</p>
      <p>The consequent increase in survival programs of public access to defibrillation has been well documented in numerous studies, including leases as casinos<sup>164</sup>, and airplanes<sup>165</sup> airports <sup>132</sup> however, little is known about the impact of this initiative on the specific risk group of athletes, mainly by that this is a rare event.</p>
      <p>Important risk marker, the pre-participation medical evaluation should be mandatory for practitioners of physical and sports activities, as it is able to detect cardiovascular abnormalities that predispose to sudden death. Despite different recommendations, there is a consensus that every athlete should do, necessarily, a medical history, physical examination and 12-lead ECG, complementing the research with other tests according to the degree of suspicion.</p>
      <p>Sportsmen victims of SD should be handled promptly and need immediate CPR quality, providing a vital amount of blood flow to the brain and heart. The local emergency team should be able to accomplish an ideal time between collapse and defibrillation of 3-5 minutes, thus increasing the chances of success of shock. As in most cases the post-pace defibrillation is not capable of a perfusion effective CPR should be resumed immediately after the shock.</p>
      <p>Finally, periodic medical evaluation, an effective local protocol for emergency responders and trained in BLS and able to provide quality CPR, early defibrillation and quick contact centers with qualified ACLS are the pillars of support for a common goal: reducing the number cases of sudden death in athletes and increased survival of victims.</p>
      <p>
        <bold>10.3. Special aspects of prevention of SD related to exercise and sport</bold>
      </p>
      <p>10.3.1. Doping: illicit substances in sport (<ext-link ext-link-type="uri" xlink:href="http://www.wada-ama.org"><bold>www.wada-ama.org</bold></ext-link>)</p>
      <p>Some used as doping substances are able to cause deleterious effects, particularly cardiovascular system, including sudden death. Among the most commonly used substances include anabolic steroids themselves, ephedrine and amphetamine. Among the most used social drugs are cocaine, marijuana and 3,4-methylenedioxymethamphetamine MDMA, known as ecstasy.</p>
      <p>
        <italic>10.3.1.1. Anabolic steroids (AS)</italic>
      </p>
      <p>These substances cause various side effects, including unwanted cardiovascular effects. The EA may induce arterial hypertension (AH) and secondary nephrosclerosis. Testosterone may cause increased vascular response to norepinephrine and, as a consequence, promote fluid retention and increased peripheral vascular resistance leading to HA3.</p>
      <p>Another important effect is described by Tagarakis et al<sup>166</sup>, which demonstrated for the first time at the microscopic level, an adaptation of cardiac capillaries myocytes and with concomitant use of anabolic steroids and physical training. That would cause a disproportionate increase in myocardial mass in relation to cardiac capillaries. The results of this study suggest that the use of EA could develop an imbalance between supply and O2 consumption, especially during exercise.</p>
      <p>
        <italic>10.3.1.2. Ephedra</italic>
      </p>
      <p>Stimulants in general cause tachycardia and increased myocardial oxygen consumption, which may cause arrhythmias and myocardial infarction in susceptible individuals.</p>
      <p>Ephedrine can cause symptomatic ventricular tachycardia, ventricular extrass&#237;sstoles frequent atrial fibrillation and sudden death. Importantly, many so-called natural products and "derived from flora" have substances like ephedrine in its formula without being part of the bull.</p>
      <p>
        <italic>10.3.1.3. Cocaine</italic>
      </p>
      <p>Cocaine use causes widespread vasoconstriction, and its main consequence, hypertension. Although cocaine use cause intense vasoconstriction in the central nervous system, this may also impact on other organs such as the kidneys causing failure renal1. Cocaine use can cause, yet, MI, cardiac arrhythmias, congestive cardiomyopathy, myocarditis, subarachnoid hemorrhage, rupture of the aorta, hypertension, myocardial ischemia or induced by exercise and sudden cardiac death.</p>
      <p>
        <italic>10.3.1.4. Amphetamines</italic>
      </p>
      <p>It is the prototype of CNS stimulants. Have wide variety of salts and mixtures under various forms of presentation, the most used dextroamphetamine sulfate. This substance has a direct action by stimulation of adrenergic receptors in cortical level and ascending reticular activating system and an indirect action, displacing the endogenous sites of their nerve endings. Its side effects are more pronounced: general insomnia, dizziness, profuse sweating, shivering and euphoria; Cardiovascular palpitations, tachycardia, chest discomfort: neurological brain hemorrhage.</p>
      <p>
        <italic>10.3.1.5. MDMA (3,4 - methylenedioxymethamphetamine) (ecstasy)</italic>
      </p>
      <p>It is a hallucinogen similar to amphetamine. Due to its low cost and availability in tablets, its popularity and consumption have increased significantly. The ingestion of MDMA increases the release of serotonin, dopamine and norepinephrine by presynaptic neurons. Furthermore, prevents the metabolism of neurotransmitters by inhibiting monoamine oxidase. Its major cardiovascular effects are hypertension, tachycardia and arrhythmia, which can lead to SD<sup>167, 168</sup>.</p>
      <p>
        <bold>10.4. Evaluation of the athlete, organization and planning of care</bold>
      </p>
      <p>Sudden death related to exercise and sport is a dramatic event and the doctors and some measures can and should be taken to try to prevent this rare but dreaded complication of sports / exercise.</p>
      <p>We describe some preventive measures related to SD related to exercise and sport.</p>
      <p>
        <bold>10.4.1 Aspects related to the athlete</bold>
      </p>
      <p>
        <italic>10.4.1.1 - Pre-participation evaluation</italic>
      </p>
      <p>Considering that in most cases the SD associated with the sport are caused by known or undiagnosed heart, every candidate for physical activity should undergo clinical examination prior, regardless of age. This clinical examination should be preceded by a good history with particular attention to the family history of cardiovascular disease and sudden death. The pre-participation evaluation in an attempt to detect these pathologies is the most efficient way to prevent one cardiovascular event fatal3. In a recent document, the International Olympic Committee ratifies the importance of periodic medical evaluations for athletes elite2.</p>
      <p>While acknowledging that clinical examination alone can not fail to detect all heart diseases with potential to cause SD, this procedure with emphasis on the cardiovascular examination, preceded by a thorough history and past medical history and family history, is the first step to proper evaluation of the athlete.</p>
      <p>Clinical examination should be accompanied ideally by a 12-lead electrocardiogram. Although there is a disagreement between the American school (this only recommends medical history and physical examination) and European School (this recommends adding the 12-lead electrocardiogram to anamnesis and clinical examination) 52, we remember that in the SBC guideline criteria for diagnostic test ordering Cardiovascular entity considers that the 12-lead electrocardiogram as a compulsory examination first visit cardiology (ECG-1-1096) 169. Moreover, it is known that numerous electrical heart diseases that can lead to SD are likely to be diagnosed by ECG at rest, including the long QT syndrome, Brugada syndrome, syndrome Lenegre-Lev syndrome and Wolf -Parkinson-White170. The European protocol that includes history, physical examination and electrocardiogram is adopted currently by the International Olympic Committee, the Italian Olympic Committee, FIFA and Football Union (UEFA) 171. Clinical examination should include a personal and family history and a specific screening for the syndrome Marfan172.</p>
      <p>A more detailed evaluation before participation in physical activities and sports available in another section of this guideline.</p>
      <p>
        <italic>10.4.1.2 For the preparation of the athlete</italic>
      </p>
      <p>Tracking the athlete has to be done holistically. Therefore, to prevent cardiovascular clinical events, preventive measures are also important basic, adequate nutrition and hydration, respecting rest periods and avoiding training and competition in the hottest times of the day. Furthermore, it is important to monitoring and observation of athletes in training and competition for qualified medical staff, preferably with experience in sports medicine and basic first aid in cases of emergency clinical situations.</p>
      <p>
        <bold>10.4.2 Issues related to training and competition venues</bold>
      </p>
      <p>
        <italic>10.4.2.1 Emergency service and medical contingency plan</italic>
      </p>
      <p>In addition to all the material needed to care for cardiac arrest should be prepared a contingency plan in medical training and competition venues, with staff trained in cardiopulmonary resuscitation, in the event of an emergency or clinical cardiovascular, optimizing the transport of athletes hospital for more complex, as the case<sup>173, 174</sup>.</p>
      <p>
        <italic>10.4.2.2 Automated External Defibrillator</italic>
      </p>
      <p>The automated external defibrillator (AED) should be available for use in less than 5 minutes in training and competition venues, clubs, arenas, stadiums, gyms and rehabilitation clinics with staff trained in cardiopulmonary resuscitation <sup>174, 175</sup>.</p>
      <p>Among young athletes cardiac arrest occur, usually after intense training sessions or during a competition. Although these events are rare (corresponding to 1% of those that occur in middle-aged or elderly), the value of a prompt service and successful resuscitation improves survival in long term<sup>176</sup>.</p>
      <p>
        <bold>11. Para-athletes or athletes with special needs.</bold>
      </p>
      <p>
        <bold>11.1. Cardiologic evaluations: pre-participation and re-evaluations</bold>
      </p>
      <p>All Paralympic athletes must undergo independent evaluation of age, sex and disability associated with, the pre-participation evaluation should include children, adolescents, adults, master / seniors, men and women, under the sole responsibility of the attending physician (Recommendation Grade: I , Evidence level: C).</p>
      <p>The evaluation should be comprehensive, taking into account the organism as a whole, emphasizing the physical and somatic; should keep in mind the interactions between physical, comorbidities, and their sequelae in physical training and sports performance (Recommendation Grade: I, Evidence level: C) (<xref ref-type="fig" rid="fig4-body2">Figure 4</xref>).</p>
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      <p>The frequency of re-evaluations should be at the discretion of the attending physician, according to the characteristics of each case, however, the frequency should have the primary aim of the sport safe (Recommendation Grade: I, Evidence level C).</p>
      <p>The evaluation of Paralympians obeys defined protocol, summarized in <xref ref-type="table" rid="tab21-body2">Table 21</xref></p>
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      <p>After the initial evaluation, according to the findings must be given specialized tests at the discretion of the attending physician, such as cardiopulmonary exercise testing (CPET), echocardiogram (ECHO), vectorcardiogram (VCG), computed tomography, magnetic resonance, ultrasound, hemoglobin electrophoresis ( research SCD) and cardiac evaluations, ophthalmic (Marfan research, glaucoma, retinal detachment) and orthopedic<sup>177, 178</sup> (Recommendation Grade: I, Evidence level C).</p>
      <p>In athletes with cerebral palsy can use the evaluation score of spasticity (QSFC Quantitative sports and functional classification), based on the condition of muscles of upper and lower limbs and trunk, for use in clinical research, clinical and physical training<sup>179</sup>.</p>
      <p>Athletes in wheelchairs and people with dentures should be thoroughly and then examined for pressure sores or scabs on the stump of the prosthesis implantation. The presence of ulceration in these places becomes temporarily ineligible athlete until they are restored local conditions of integument (Recommendation Grade: I, Evidence level C). The practice of urinary retention in wheelchairs should be ruled out, given the risk of large elevations of blood pressure and stroke. In cases of neurogenic bladder should be alert to the presence of subclinical urinary infections.</p>
      <p>
        <bold>11.2. Cardiopulmonary exercise testing</bold>
      </p>
      <p>The basics of cardiopulmonary exercise testing protocols include: 1) reproducibility of sports act according to the principle of specificity, 2) the adequacy sport and means of locomotion athlete, 3) perform the tests with stability and security, ensuring accuracy and reproducibility of measures<sup>11</sup> (Grade Recommendation: I, Evidence level: B).</p>
      <p>Special care should be taken in relation to the type and degree of disability, the athlete's posture, at room temperature, prior to emptying, prevention of hypotension, the risk of seizures and accidents, the blood pressure measurements and the proper veiling masks. Several factors may limit performance in evaluations: 1) Clinical: intellectual and sensory disabilities (visual, tactile, auditory, epilepsy, autonomic dysreflexia, neurogenic bladder, deprivation friendly, post-polio syndrome, tachypnoea stress, malnutrition, 2) locomotion: reduced mass, muscle strength and flexibility, increased muscle tone, decreased joint mobility, motor incoordination, osteoarticular lesions secondary to sports, injuries from amputation stumps, 3) cardiovascular: any associated disorders, 4) physiological: reduction of VO2 PICO, anaerobic threshold, respiratory compensation point, early fatigue, physical inactivity, and 4) socioeconomic and cultural: social exclusion, lack of patroc&#237;nio177.</p>
      <p>According to the principle of specificity, has been used to arm ergometers players, throwers, weightlifters, swimmers and fencers, bike cycling and treadmill to other modalidades177; cyclists can use your own equipment coupled to the system 850 Mag Minoura180 (Recommendation Grade: I, Evidence level: C).</p>
      <p>The cardiopulmonary tests can be performed by several specific protocols, citing the example summarized in <xref ref-type="table" rid="tab22-body2">Table 22</xref>.</p>
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      <p>The protocol Knechtle and K&#246;plif (Institute of Sports Medicine Swiss Paraplegic Centre) for treadmill test in wheelchairs, starts at speed of 8 km / h and slope of 1%, with 0.5% increments every 2 minutes and speed constant until exaust&#227;o181, 182.</p>
      <p>Field tests can also be performed with vantagens183, 184. Variations between 48-80% have been described in the regression equations for determining the physical capacity in paraplegics and quadriplegics. These variations can be explained by the level and degree of spinal cord injury, age, gender, physical activity and weight corporal183. In our environment, the values &#8203;&#8203;for the aerobic power of Paralympic athletes have been similar (<xref ref-type="table" rid="tab23-body2">Table 23</xref>)<sup>180,185.</sup></p>
      <table-wrap id="tab23-body2">
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      <p>The pre-participation evaluation for leisure activities is similar, depending on the physical and mental stress. On many occasions, given the emotional burden involved and the lowest level of training, physical and psychological stress can be of great intensity, similar to the relative degree of competitions.</p>
      <p>
        <bold>12. Prevention of events / sudden death in sports</bold>
      </p>
      <p>The event prevention should include prevention of accidents, injuries and aggravation of preexisting comorbidities and sudden death.</p>
      <p>The goals of a protocol event prevention in sports based on pre-participation screening:</p>
      <p>Identifying predisposing conditions, ie cardiovascular diseases that can potentially cause sudden death;</p>
      <p>Set if there are steps that can be taken to reduce the risk of sudden death: What? How should they be developed?</p>
      <p>Standardize the approach to be adopted in every heart and discuss the possible disqualification of the athlete's exercise of his profession.</p>
      <p>Prevention of events and sudden death in sports and leisure is performed taking into account the early diagnosis and treatment of cardiovascular diseases, as well as the application of existing criteria and unenforceability specific to the various conditions described in Parts I and II of this document and properly applied to Paralympic athletes<sup>187</sup>. It is imperative that the resources exist venues doctors and paramedics, appropriately equipped for emergency care.</p>
      <p>In many institutions, the clinical director and / or the physician responsible for the care answerable to the respective Regional Council of Medicine compliance with those standards.</p>
      <p>Individuals newly hospitalized or sedentary longstanding need progressive training with gradual increments in the frequency and duration of sessions and the intensity of the exercises, besides the risk of injuries and physical sequelae, the appearance of these can be discouraging factor training, damaging self-image, and predisposing to cessation program (Recommendation Grade I, Evidence level C).</p>
      <p>
        <bold>12.1. Ethical Aspects</bold>
      </p>
      <p>The medical evaluation should include experts from various fields, highlighting the sport and exercise medicine, cardiology, orthopedics and physiatry.</p>
      <p>When it comes to athletes with disabilities, it is important to emphasize that it is the exclusive competence of the physician directing the training, diagnose any diseases and sequelae, order tests, prescribe treatment and athletes away from sports, being forbidden to assign medical functions or delegate its exclusive competence for professionals not qualified to practice medicine. (Federal Medical Council, Resolution No. 1236/87). Moreover, the implementation of the training will be conducted by physical education teachers and therapists. The interaction between physicians, physical education teachers, physiotherapists, physiologists, nutritionists and psychologists is critical to the success of the program. The training prescription should be made in prescription doctor, aiming mode, frequency and duration of sessions, training intensity and other observations, at the discretion of the attending physician. This conduct is ratified by the Federal Medical Opinion 4141/2003: "For all the above, it is for the doctor, after diagnosing the disease, prescribe the appropriate treatment to the patient and even the prescription of physical activity in the face of pathology diagnosis or prevention of various pathologies."</p>
      <p>In many institutions, the clinical director and / or the physician responsible for the care of these standards by responding to the respective Regional Council of Medicine.</p>
      <p>The relationship between doctor and other professionals practicing in health care should be based on mutual respect, freedom and independence of each professional, always seeking the interest and welfare of the patient (Code of Medical Ethics 08/01 / 1988 Article 18). The interaction between doctors and para-medical physical education teachers, physical therapists, nutritionists, psychologists and coaches is critical to the success of the training program and should be encouraged at every moment.</p>
      <p>
        <bold>12.2. Recommendations</bold>
      </p>
      <p>Nowadays, given the paucity of reports in the literature, the criteria for answering Paralympians are based generally on expert consensus (Evidence level C).</p>
      <p>The determination of eligibility sports must follow the protocol of the International Paralympic Committee Classification Code and International Olympic Committee and Standards188 Brasileiro189. Thus, the para-athlete may be eligible and ineligible to a modality to another. The eligibility criteria are defined for each sport Paralympic sport by federations internacional190.</p>
      <p>The recommendations for the care of Para-athletes are listed in <xref ref-type="table" rid="tab24-body2">Table 24</xref>.</p>
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      <p>
        <bold>13. Appendix</bold>
      </p>
      <p>
        <bold>13.1. Elaboration of aptness or release reports to exercise and practice sports<sup>173</sup></bold>
      </p>
      <p>The medical report to release for amateur and competitive physical activities is a part of the medical act and a patient right. It should be objective, clarifying as to the kind of physical activity allowed and preferably suggesting the physical training intensity. In cases in which there are restrictions to the practice of a modality, those should be clearly mentioned in the document. Any and every information concerning the clinical profile, physical examination and complementary exams should be in the medical report when required and authorized by the patient.</p>
      <p>With basis in evidence-based medicine the individual risk stratification is more appropriate, considering clinical condition and physical aptness, gender, age and conditions under which this practice will be performed. For most situations it is possible to compare the risk of a given individual with that expected for their fellows of same age and thus characterize the risk as much smaller, smaller, similar, bigger or much bigger. Specifically, it may also be convenient to characterize the practice as therapeutic, recreational or competitive. In addition, environmental factors, notably climatic, may be relevant.</p>
      <p>As to the issuing of the report, this should characterize or specify any clinical restriction, be it of locomotor or cardiorespiratory nature. Ideally, the conclusive statement should attain to the limits of what was actually examined or evaluated, avoiding generic and poorly funded sentences as "apt to sports practice", being probably more adequate to use something like "formal clinical contraindications to the practice of recreational or competitive physical exercise were not found".</p>
      <p>When the decision is for the professional disqualification, the part most interested in the information should be the athlete or their legal representative (when under 18), even when the athlete is part of a team and his/her evaluation was offered by the club or association to which they are associated. In these cases it would be prudent that the report be signed by the physician responsible and at least two other physicians that follow the decision, besides the athlete himself/herself, in at least two copies, one of them filed in the athlete's medical records. Special care must be taken to keep the athlete's integrity, keeping the secret required in each case.</p>
      <p>
        <bold>14. References</bold>
      </p>
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