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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">ySHzH3cgmXQVFfBgkPgtjDq</article-id>
      <article-id pub-id-type="other">00013</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2008000300013</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(08)09000313</article-id>
      <article-id pub-id-type="doi">10.1590/S0066-782X2008000300013</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Relato de Caso</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Cardiomiopatia de takotsubo como causa de disfun&#231;&#227;o ventricular transit&#243;ria</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Alves</surname>
            <given-names>Angele A.</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Kowatsch</surname>
            <given-names>Ingrid</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Tsutsui</surname>
            <given-names>Jeane Mike</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Nicolau</surname>
            <given-names>Jos&#233; C.</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Lima</surname>
            <given-names>Marta F.</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Mathias Junior</surname>
            <given-names>Wilson</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">S&#227;o Paulo</named-content>
        </addr-line>
        <institution content-type="orgname">Universidade de S&#227;o Paulo</institution>
        <institution content-type="orgdiv1">Instituto do Cora&#231;&#227;o </institution>
        <country country="BR">Brazil</country>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>03</month>
        <year>2008</year>
      </pub-date>
      <volume>90</volume>
      <issue>3</issue>
      <fpage>e17</fpage>
      <lpage>e20</lpage>
      <history>
        <date date-type="rev-recd">
          <day>09</day>
          <month>05</month>
          <year>2007</year>
        </date>
        <date date-type="received">
          <day>06</day>
          <month>03</month>
          <year>2007</year>
        </date>
        <date date-type="accepted">
          <day>09</day>
          <month>05</month>
          <year>2007</year>
        </date>
      </history>
      <permissions>
        <license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/4.0/" xml:lang="en">
          <license-p>This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.</license-p>
        </license>
      </permissions>
      <abstract>
        <p>Relato do caso de mulher de 74 anos, com hipertens&#227;o arterial sist&#234;mica e insufici&#234;ncia vascular perif&#233;rica, que apresentou sintomas de s&#237;ndrome coronariana aguda. A angiografia coronariana demonstrou art&#233;rias sem obstru&#231;&#245;es significativas. A ventriculografia e a ecocardiografia demonstraram acinesia dos segmentos m&#233;dios e apicais, e hipercinesia dos segmentos basais do ventr&#237;culo esquerdo. A paciente evoluiu com recupera&#231;&#227;o completa da fun&#231;&#227;o global e motilidade segmentar em ecocardiografia realizada duas semanas ap&#243;s o in&#237;cio dos sintomas. Esse padr&#227;o incomum e revers&#237;vel de disfun&#231;&#227;o sist&#243;lica e comprometimento segmentar dando ao ventr&#237;culo esquerdo forma semelhante a um takotsubo &#233; hoje conhecido como cardiomiopatia do estresse.</p>
      </abstract>
      <kwd-group xml:lang="pt" kwd-group-type="author-generated">
        <kwd>Estresse psicol&#243;gico</kwd>
        <kwd>disfun&#231;&#227;o ventricular</kwd>
        <kwd>catecolaminas</kwd>
        <kwd>cardiomiopatias</kwd>
      </kwd-group>
      <pub-date publication-format="electronic" date-type="pub">
        <day>26</day>
        <month>03</month>
        <year>2008</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <p>
      <bold>RELATO DE CASO</bold>
    </p>
    <p>
      <bold>Cardiomiopatia de takotsubo como causa de disfun&#231;&#227;o ventricular transit&#243;ria</bold>
    </p>
    <p>
      <bold>Angele A. Alves; Ingrid Kowatsch; Jeane Mike Tsutsui; Jos&#233; C. Nicolau; Marta F. Lima; Wilson Mathias Junior</bold>
    </p>
    <p>Instituto do Cora&#231;&#227;o (InCor)- HCFMUSP &#150; S&#227;o Paulo, SP - Brasil</p>
    <p>
      <xref ref-type="corresp" rid="back">Correspond&#234;ncia</xref>
    </p>
    <p>
      <bold>RESUMO</bold>
    </p>
    <p>Relato do caso de mulher de 74 anos, com hipertens&#227;o arterial sist&#234;mica e insufici&#234;ncia vascular perif&#233;rica, que apresentou sintomas de s&#237;ndrome coronariana aguda. A angiografia coronariana demonstrou art&#233;rias sem obstru&#231;&#245;es significativas. A ventriculografia e a ecocardiografia demonstraram acinesia dos segmentos m&#233;dios e apicais, e hipercinesia dos segmentos basais do ventr&#237;culo esquerdo. A paciente evoluiu com recupera&#231;&#227;o completa da fun&#231;&#227;o global e motilidade segmentar em ecocardiografia realizada duas semanas ap&#243;s o in&#237;cio dos sintomas. Esse padr&#227;o incomum e revers&#237;vel de disfun&#231;&#227;o sist&#243;lica e comprometimento segmentar dando ao ventr&#237;culo esquerdo forma semelhante a um takotsubo &#233; hoje conhecido como cardiomiopatia do estresse.</p>
    <p><bold>Palavras-chave:</bold> Estresse psicol&#243;gico, disfun&#231;&#227;o ventricular, catecolaminas, cardiomiopatias.</p>
    <p>
      <bold>Introdu&#231;&#227;o</bold>
    </p>
    <p>A disfun&#231;&#227;o ventricular induzida por estresse (ou cardiomiopatia de <italic>takotsubo,</italic> palavra japonesa para designar armadilha para pegar polvo, representada por um pote com fundo arredondado e pesco&#231;o estreito) foi inicialmente descrita no Jap&#227;o em pacientes que apresentavam quadro semelhante ao infarto agudo do mioc&#225;rdio, por&#233;m com art&#233;rias coron&#225;rias normais. Posteriormente, v&#225;rios relatos foram apresentados em popula&#231;&#227;o caucasiana, com forte predomin&#226;ncia na popula&#231;&#227;o feminina e r&#225;pida recupera&#231;&#227;o do quadro. Como fatores desencadeantes foram relacionados o estresse f&#237;sico ou emocional e diversas doen&#231;as n&#227;o-card&#237;acas<sup>1-6</sup>. Aqui &#233; relatado o caso de paciente que apresentou quadro compat&#237;vel com cardiomiopatia de <italic>takotsubo,</italic> em que um fator desencadeante n&#227;o foi encontrado.</p>
    <p>
      <bold>Relato do Caso</bold>
    </p>
    <p>Paciente do sexo feminino, com 74 anos de idade, apresentando antecedentes de hipertens&#227;o arterial sist&#234;mica e insufici&#234;ncia vascular perif&#233;rica cr&#244;nica, iniciou quadro de dor precordial em opress&#227;o com irradia&#231;&#227;o para o membro superior esquerdo e sudorese, ao tomar banho. A paciente negava quadro de estresse emocional antes da dor. Foi admitida no servi&#231;o de emerg&#234;ncia tr&#234;s horas ap&#243;s o in&#237;cio dos sintomas, com hipotens&#227;o arterial sist&#234;mica (press&#227;o arterial 80 mmHg/40 mmHg) e eletrocardiograma em 12 deriva&#231;&#245;es com discreta eleva&#231;&#227;o do segmento ST nas deriva&#231;&#245;es DII, DIII, aVF, V5 e V6 e discreto infradesnivelamento do segmento ST em V1, V2 e V3 (<xref ref-type="fig" rid="fig1">fig. 1</xref>). A paciente foi submetida a angiografia coronariana em car&#225;ter de emerg&#234;ncia, que mostrou art&#233;rias coron&#225;rias sem les&#245;es obstrutivas significativas e irregularidades parietais na art&#233;ria descendente anterior. A ventriculografia revelou anormalidades na motilidade parietal com acinesia dos segmentos m&#233;dios e apicais e hipercinesia basal, resultando em dilata&#231;&#227;o aneurism&#225;tica do ventr&#237;culo sugestivo de cardiomiopatia de <italic>takotsubo</italic> (<xref ref-type="fig" rid="fig2">fig. 2</xref>). No ecocardiograma transtor&#225;cico em repouso tamb&#233;m foi evidenciada presen&#231;a de acinesia dos segmentos m&#233;dio-apicais e hipercinesia dos segmentos basais do ventr&#237;culo esquerdo (<xref ref-type="fig" rid="fig3">fig. 3</xref>). A curva enzim&#225;tica apresentou dosagem de troponina card&#237;aca I igual a 9,29 ng/ml e 6,39 ng/ml ap&#243;s 14 horas e 38 horas do quadro de dor precordial, respectivamente, sendo o valor normal de troponina card&#237;aca em nossa institui&#231;&#227;o de &lt; 2,0 ng/ml. Os respectivos valores de creatina cinase fra&#231;&#227;o MB (massa) foram de 21,2 ng/ml e 11,3 ng/ml (valor normal, &lt; 4,0 ng/ml). A paciente evoluiu com estabilidade cl&#237;nica, sem recorr&#234;ncia dos sintomas, e recebeu alta hospitalar. Foi realizada nova ecocardiografia duas semanas ap&#243;s o in&#237;cio dos sintomas, que demonstrou recupera&#231;&#227;o completa da fun&#231;&#227;o sist&#243;lica e da motilidade segmentar do ventr&#237;culo esquerdo (<xref ref-type="fig" rid="fig4">fig. 4</xref>).</p>
    <fig id="fig1">
      <graphic xlink:href="1678-4170-abc-90-03-0e17-00013-gf01.jpg"/></fig>
    <fig id="fig2">
      <graphic xlink:href="1678-4170-abc-90-03-0e17-00013-gf02.jpg"/></fig>
    <fig id="fig3">
      <graphic xlink:href="1678-4170-abc-90-03-0e17-00013-gf03.jpg"/></fig>
    <fig id="fig4">
      <graphic xlink:href="1678-4170-abc-90-03-0e17-00013-gf04.jpg"/></fig>
    <p>
      <bold>Discuss&#227;o</bold>
    </p>
    <p>Numerosos relatos t&#234;m descrito pacientes com disfun&#231;&#227;o ventricular esquerda revers&#237;vel e sintomas similares &#224;queles do infarto agudo do mioc&#225;rdio, geralmente ap&#243;s estresse emocional ou concomitante a v&#225;rias afec&#231;&#245;es, incluindo pneumot&#243;rax, hemorragia subaracn&#243;idea e feocromocitoma, entre outras, sem estenose das art&#233;rias coron&#225;rias<sup>1-8</sup>. Na paciente em quest&#227;o n&#227;o foi identificado um estressor emocional evidente, mas o quadro cl&#237;nico de s&#237;ndrome coronariana aguda, o padr&#227;o coronariogr&#225;fico, o aspecto ventriculogr&#225;fico da disfun&#231;&#227;o mioc&#225;rdica segmentar com dilata&#231;&#227;o aneurism&#225;tica e a reversibilidade da disfun&#231;&#227;o ventricular remetem ao diagn&#243;stico da cardiomiopatia de <italic>takotsubo</italic>.</p>
    <p>Na literatura, a cardiomiopatia de <italic>takotsubo</italic> ou cardiomiopatia do estresse, corresponde a cerca de 1% dos infartos agudos do mioc&#225;rdio e acomete mais freq&#252;entemente mulheres com mais de 60 anos de idade<sup>4</sup>. Os sintomas iniciais assemelham-se aos do infarto agudo do mioc&#225;rdio, sendo geralmente identificado um estressor emocional ou f&#237;sico precipitante. As art&#233;rias coron&#225;rias s&#227;o normais, com padr&#227;o de disfun&#231;&#227;o ventricular assemelhando-se a um <italic>takotsubo</italic> pela ventriculografia, sendo a disfun&#231;&#227;o sist&#243;lica card&#237;aca completamente revers&#237;vel dentro de poucas semanas. Essa altera&#231;&#227;o geralmente apresenta bom progn&#243;stico, uma vez terminada a fase aguda. A despeito de relatos fatais, como por rotura ventricular, o bom progn&#243;stico dessa afec&#231;&#227;o &#233; confirmado pelo r&#225;pido decl&#237;nio dos n&#237;veis de pept&#237;deo natriur&#233;tico atrial, em rela&#231;&#227;o aos n&#237;veis do infarto agudo do mioc&#225;rdio, correlacionando com a r&#225;pida melhora da fun&#231;&#227;o sist&#243;lica ventricular<sup>9</sup>. Sua caracter&#237;stica inclui forte predomin&#226;ncia no sexo feminino e o manuseio consiste principalmente em terapia de suporte e sintom&#225;tica.</p>
    <p>Embora os mecanismos da cardiomiopatia do estresse n&#227;o estejam claramente demonstrados, o vasoespasmo coronariano ou a miocardite s&#227;o causas improv&#225;veis dessa afec&#231;&#227;o. Os pacientes com essa s&#237;ndrome t&#234;m evid&#234;ncia de ativa&#231;&#227;o simp&#225;tica exacerbada, com n&#237;veis de catecolaminas maiores que aqueles do infarto agudo do mioc&#225;rdio<sup>10</sup>. Apesar de os estudos demonstrarem associa&#231;&#227;o entre ativa&#231;&#227;o simp&#225;tica e cardiomiopatia do estresse, eles n&#227;o provam uma rela&#231;&#227;o causal. N&#237;veis elevados de catecolaminas podem ocorrer por uma resposta secund&#225;ria ou ser a principal causa da doen&#231;a. Para um entendimento mais completo da patog&#234;nese dessa s&#237;ndrome ser&#227;o necess&#225;rios mais estudos. Todavia, deve ser lembrada como um diagn&#243;stico diferencial de desconforto tor&#225;cico na sala de emerg&#234;ncia e como causa de morte card&#237;aca s&#250;bita em pessoas sem doen&#231;a card&#237;aca conhecida.</p>
    <p>
      <fn id="back" fn-type="corresp">
        <p>Correspond&#234;ncia:</p>
        <p> Jeane Mike Tsutsui  </p>
        <p> Jeane Mike Tsutsui </p>
        <p> Av. Dr. En&#233;as de Carvalho Aguiar, 44 </p>
        <p> 05403-000, S&#227;o Paulo, SP &#150; Brasil </p>
        <p> E-mail: </p>
        <p><email xlink:href="jmike@cardiol.br">jmike@cardiol.br</email> / </p>
        <p>
          <email xlink:href="jeane.tsutsui@incor.usp.br">jeane.tsutsui@incor.usp.br</email>
        </p>
      </fn>
    </p>
    <p>Artigo recebido em 06/03/07; revisado recebido em 09/05/07; aceito em 09/05/07.</p>
  </body>
  <back>
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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>Case Report</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="en">Takotsubo cardiomyopathy causing transitory ventricular dysfunction</article-title>
      </title-group>
      <abstract xml:lang="en">
        <p>This is the report of a 74-year-old female patient with a history of systemic hypertension and peripheral vascular disease who presented acute coronary syndrome symptoms. Coronary angiography showed coronary arteries with no significant obstructions. Ventriculography and echocardiography showed akinesia in mid and apical segments; and hyperkinesia of left ventricle basal segments. Two weeks after the onset of symptoms, a new echocardiogram demonstrated normal global and regional systolic function. The uncommon, reversible pattern for systolic dysfunction and segmental compromising that gives left ventricle a takostubo-like shape is known today as stress cardiomyopathy.</p>
      </abstract>
      <kwd-group xml:lang="en">
        <kwd>Stress psychological</kwd>
        <kwd>ventricular dysfunction</kwd>
        <kwd>catecholamines</kwd>
        <kwd>cardiomyopathies</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>
        <bold>CASE REPORT</bold>
      </p>
      <p>
        <bold>Takotsubo cardiomyopathy causing transitory ventricular dysfunction</bold>
      </p>
      <p>
        <bold>Angele A. Alves; Ingrid Kowatsch; Jeane Mike Tsutsui; Jos&#233; C. Nicolau; Marta F. Lima; Wilson Mathias Junior</bold>
      </p>
      <p>Instituto do Cora&#231;&#227;o (InCor)- HCFMUSP &#150; S&#227;o Paulo, SP - Brazil</p>
      <p>
        <xref ref-type="corresp" rid="back-body2">Mailing address</xref>
      </p>
      <p>This is the report of a 74-year-old female patient with a history of systemic hypertension and peripheral vascular disease who presented acute coronary syndrome symptoms. Coronary angiography showed coronary arteries with no significant obstructions. Ventriculography and echocardiography showed akinesia in mid and apical segments; and hyperkinesia of left ventricle basal segments. Two weeks after the onset of symptoms, a new echocardiogram demonstrated normal global and regional systolic function. The uncommon, reversible pattern for systolic dysfunction and segmental compromising that gives left ventricle a takostubo-like shape is known today as stress cardiomyopathy.</p>
      <p><bold>Key words:</bold> Stress, psychological; ventricular dysfunction; catecholamines; cardiomyopathies.</p>
      <p>
        <bold>Introduction</bold>
      </p>
      <p>Stress-induced ventricular dysfunction (also known as Takotsubo cardiomyopathy) was originally described in Japan in patients presenting a condition similar to an acute myocardial infarction (AMI), although with normal coronary arteries. Later, a number of reports were presented from Caucasian populations, with strong predominance among females, and fast recovery. Triggering factors were associated to physical or emotional stress and a number of non-cardiac conditions<sup>1-6</sup>. This report describes a patient whose condition was compatible with Takotsubo cardiomyopathy, in whom no triggering factor found.</p>
      <p>
        <bold>Case Report</bold>
      </p>
      <p>A seventy-four-year old female patient with a history of systemic hypertension and chronic peripheral vascular failure had the onset of condition with oppressive precordial pain irradiating to left upper limb and sweating while showering or bathing. The patient denied any stress condition before the pain. The patient was admitted at the emergency service 3 hours after the onset of symptoms, with systemic hypertension (BP 80/40 mmHg) and 12-lead ECG showing mild elevation of segment ST in DII, DIII, aVF, V5 and V6, and mild unlevelling of segment ST in V1, V2, and V3 (<xref ref-type="fig" rid="fig1-body2">Figure 1</xref>). An emergency coronary angiography demonstrated coronary arteries with no significant obstructive lesions and parietal irregularities in anterior descending artery. Ventriculography showed abnormalities in parietal motility, with akinesia in mid and apical segments, and baseline hyperkinesia, resulting in ventricular aneurysmal dilation, which suggested the <italic>takotsubo</italic> cardiomyopathy condition (<xref ref-type="fig" rid="fig2-body2">Figure 2</xref>). The transthoracic ECG at rest also showed akinesia of mid-apical segments and hyperkinesia of left ventricle baseline segments (<xref ref-type="fig" rid="en_13f3-body2">Figure 3</xref>). Enzyme curve showed cardiac troponin I at 9.29 and 6.39 ng/ml 14 hours and 38 hours after precordial pain, respectively. Normal value for cardiac troponin at our institution is &lt;2.0 ng/ml. Corresponding values for creatine-kinase mB fraction (mass) were 21.2 and 11.3 ng/ml (normal value &lt;4.0 ng/ml).</p>
      <p content-type="asset">
        <fig id="en_13f3-body2">
          <graphic xlink:href="1678-4170-abc-90-03-0e17-00013-gf01-en.jpg"/></fig>
      </p>
      <fig id="fig1-body2">
        <graphic xlink:href="1678-4170-abc-90-03-0e17-00013-gf02-en.jpg"/></fig>
      <fig id="fig2-body2">
        <graphic xlink:href="1678-4170-abc-90-03-0e17-00013-gf03-en.jpg"/></fig>
      <p>The patient was clinically stable, with no relapse of symptoms, and was discharged. A new echocardiography two weeks after the onset of symptoms showed full recovery of systolic function and left ventricle segmental motility (<xref ref-type="fig" rid="fig4-body2">Figure 4</xref>).</p>
      <fig id="fig4-body2">
        <graphic xlink:href="1678-4170-abc-90-03-0e17-00013-gf04-en.jpg"/></fig>
      <p>
        <bold>Discussion</bold>
      </p>
      <p>A number of reports have described patients with reversible left ventricular dysfunction and symptoms that are similar to those in the acute myocardial infarction condition - typically after emotional stress or concurrent to a number of pathologies that include pneumothorax, subarachnoid hemorrhage, and pheochromocytoma, among others with no coronary arteries stenosis<sup>1-8</sup>. No evident emotional stressor was identified in this particular patient, but the acute coronary syndrome clinical condition, coronariography pattern, ventriculography of segmental myocardial dysfunction with aneurysmal dilation, and ventricular dysfunction reversibility as presented are recurrent to <italic>takotsubo</italic> cardiomyopathy diagnosis.</p>
      <p>In literature, <italic>takotsubo</italic> cardiomyopathy (from the Japanese, meaning an octopus trap, represented by a jar with a flattened bottom and narrow neck) or stress cardiomyopathy accounts for approximately 1% of acute myocardial infarctions, affecting mostly women, predominantly those over 60 years of age<sup>4</sup>. Early symptoms are similar to those reported in acute myocardial infarction condition, and typically associated to a triggering emotional or physical stressor. Coronary arteries are compatible with ventricular dysfunction pattern and similar to a <italic>takotsubo</italic> on ventriculography. The systolic dysfunction is fully reversible within a few weeks. Once the acute phase is over, the condition usually has good prognosis. Despite some fatal reports, such as ventricular rupture, the good prognosis for the condition is confirmed by rapid decrease of atrial natriuretic peptide levels when compared to those in acute myocardial infarction, in correlation with fast improvement of ventricular systolic function<sup>9</sup>. Strong prevalence is reported among females, and management consists primarily in support and symptomatic therapy.</p>
      <p>Although stress cardiomyopathy mechanisms have not been clearly demonstrated, coronary vasospasm or myocarditis are not unlikely causes for the pathology. Patients with the syndrome show evidence of exacerbated sympathetic activation, with catecholamines levels higher than those seen in acute myocardial infarction<sup>10</sup>. Although studies have shown an association between sympathetic activation and stress cardiomyopathy, they are no evidence of a causal relationship. High catecholamine levels may occur due to a secondary response, or be a major cause in this pathology. Further studies are necessary for better understanding of the pathogenesis of this syndrome. However, it should be kept in mind as a differential diagnosis for thoracic discomfort at the emergency room, and a cause of sudden cardiac death in those with known cardiac disease.</p>
      <p>
        <bold>References</bold>
      </p>
      <p>
        <fn id="back-body2" fn-type="corresp">
          <p>Mailing address:</p>
          <p> Jeane Mike Tsutsui</p>
          <p> Av. Dr. En&#233;as de Carvalho Aguiar, 44</p>
          <p> 05403-000, S&#227;o Paulo, SP - Brazil</p>
          <p> E-mail: </p>
          <p><email xlink:href="jmike@cardiol.br">jmike@cardiol.br</email> / </p>
          <p>
            <email xlink:href="jeane.tsutsui@incor.usp.br">jeane.tsutsui@incor.usp.br</email>
          </p>
        </fn>
      </p>
      <p>Manuscript received March 6, 2007; revised manuscript received May 9, 2007; accepted May 9, 2007.</p>
    </body>
  </sub-article>
</article>
