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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">j7dssV5MZGLZZ8LHzFpkqJg</article-id>
      <article-id pub-id-type="other">00016</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2013000400016</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(13)10000400016</article-id>
      <article-id pub-id-type="doi">10.5935/abc.20130082</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Relato de Caso</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>S&#237;ndrome de baloniza&#231;&#227;o apical durante coronariografia diagn&#243;stica</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Dores</surname>
            <given-names>Helder</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Raposo</surname>
            <given-names>Lu&#237;s</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Ferreira</surname>
            <given-names>Jorge</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Andrade</surname>
            <given-names>Maria Jo&#227;o</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Almeida</surname>
            <given-names>Manuel</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Mendes</surname>
            <given-names>Miguel</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <addr-line>
          <named-content content-type="city">Lisboa</named-content>
          <named-content content-type="state"/>
        </addr-line>
        <institution content-type="orgname">Centro Hospitalar de Lisboa Ocidental</institution>
        <institution content-type="orgdiv1">Hospital de Santa Cruz </institution>
        <institution content-type="orgdiv2">Servi&#231;o de Cardiologia</institution>
        <country country="PT">Portugal</country>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>04</month>
        <year>2013</year>
      </pub-date>
      <volume>100</volume>
      <issue>4</issue>
      <fpage>e47</fpage>
      <lpage>e50</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>06</day>
        <month>05</month>
        <year>2013</year>
      </pub-date>
    </article-meta>
  </front>
  <body><p><bold>RELATO DE CASO</bold></p><p><bold>S&#237;ndrome de baloniza&#231;&#227;o apical durante coronariografia diagn&#243;stica</bold></p><p><bold>Helder Dores; Lu&#237;s Raposo; Jorge Ferreira; Maria Jo&#227;o Andrade; Manuel Almeida; Miguel Mendes</bold></p><p>Servi&#231;o de Cardiologia - Hospital de Santa Cruz, Centro Hospitalar de Lisboa Ocidental - Lisboa</p><p><xref ref-type="corresp" rid="end">Correspond&#234;ncia</xref></p><p><bold>Palavras-chave:</bold> Oclus&#227;o Coron&#225;ria/diagn&#243;stico, Cardiomiopatia de Takotsubo/diagn&#243;stico, Angiografia Coron&#225;ria, Cateterismo Card&#237;aco, Meios de Contraste. </p><p><bold>Introdu&#231;&#227;o</bold></p><p>As situa&#231;&#245;es de instabilidade hemodin&#226;mica durante a realiza&#231;&#227;o de coronariografia s&#227;o mais comuns em doentes com doen&#231;a coron&#225;ria grave, sobretudo na presen&#231;a de s&#237;ndromes coron&#225;rias agudas. Raramente podem ocorrer em contexto eletivo, mesmo na aus&#234;ncia de doen&#231;a coron&#225;ria, devido &#224; emboliza&#231;&#227;o gasosa inadvertida e ao aumento da vasorreatividade coron&#225;ria<sup>1,2</sup>.</p><p>O vasospasmo coron&#225;rio tem sido implicado como um dos poss&#237;veis mecanismos fisiopatol&#243;gicos envolvidos na miocardiopatia de <italic>Tako-tsubo</italic> (MCT), embora estejam descritos poucos casos na literatura que comprovem esta associa&#231;&#227;o<sup>3</sup>.</p><p>Apresentamos o caso de um paciente com instabilidade hemodin&#226;mica transit&#243;ria durante a realiza&#231;&#227;o de coronariografia eletiva, com evid&#234;ncia de vasospasmo multivaso e achados sugestivos de MCT. </p><p><bold>Relato do Caso</bold></p><p>Paciente do sexo masculino, 70 anos de idade, fumante antigo, sem outros fatores de risco ou antecedentes cardiovasculares conhecidos. Em maio/2004, por queixas de cansa&#231;o, realizou prova de esfor&#231;o que revelou altera&#231;&#245;es do segmento ST interpretadas como isquemia silenciosa. Subsequentemente, realizou coronariografia que n&#227;o mostrou doen&#231;a coron&#225;ria significativa, mantendo-se assintom&#225;tico do ponto de vista cardiovascular.</p><p>Em mar&#231;o/2011 reiniciou queixas de cansa&#231;o para esfor&#231;os moderados. Realizou nova prova de esfor&#231;o com capacidade funcional normal (10,7 METs), resposta tensional adequada e altera&#231;&#245;es ST sugestivas de isquemia: infradesnivelamento em rampa ascendente nas deriva&#231;&#245;es inferiores e laterais, iniciado no segundo est&#225;gio e normalizando no primeiro minuto da recupera&#231;&#227;o. A pedido do m&#233;dico assistente efetuou nova coronariografia. Na primeira inje&#231;&#227;o na coron&#225;ria esquerda (vaso dominante) observou-se fluxo lento e oclus&#227;o das art&#233;rias descendente anterior proximal e descendente posterior esquerda/circunflexa distal (<xref ref-type="fig" rid="a16fig01">Figura 1A</xref>). Seguiu-se um quadro crescente de angina, eleva&#231;&#227;o generalizada do segmento ST, bradicardia progressiva e fal&#234;ncia de bomba, sendo necess&#225;ria a administra&#231;&#227;o de atropina e dopamina.</p><p content-type="asset"><fig id="a16fig01"><graphic xlink:href="1678-4170-abc-100-04-0e47-30082-gf01.jpg"/></fig></p><p>Em virtude da possibilidade de vasospasmo e apesar da instabilidade hemodin&#226;mica, administrou-se dinitrato de isossorbida intracoron&#225;rio com normaliza&#231;&#227;o do segmento ST e estabiliza&#231;&#227;o hemodin&#226;mica. As inje&#231;&#245;es seguintes (&lt; 5 minutos ap&#243;s o in&#237;cio do quadro) revelaram restabelecimento do fluxo em toda a &#225;rvore coron&#225;ria, sem evid&#234;ncia de les&#245;es angiogr&#225;ficas significativas (<xref ref-type="fig" rid="a16fig01">Figura 1B</xref>). O ecocardiograma transtor&#225;cico mostrou acinesia com baloniza&#231;&#227;o apical (<xref ref-type="fig" rid="a16fig02">Figuras 2A</xref> e <xref ref-type="fig" rid="a16fig02">2B</xref>) e hipercinesia dos segmentos basais do ventr&#237;culo esquerdo (VE). O doente foi admitido na Unidade de Cuidados Intensivos Card&#237;acos, onde se manteve est&#225;vel. Laboratorialmente registrou-se eleva&#231;&#227;o dos biomarcadores de necrose mioc&#225;rdica - troponina I (valor de refer&#234;ncia &lt; 0,04 &#181;g/L): 1,29 (&lt; 2 h) - 5,77 (24 h) - 4,89 (36 h) - 0,23 (96 h) &#181;g/L. No quinto dia de internamento o ecocardiograma revelou normaliza&#231;&#227;o da motilidade e fun&#231;&#227;o sist&#243;lica VE, recebendo alta hospitalar (<xref ref-type="fig" rid="a16fig02">Figuras 2C</xref> e <xref ref-type="fig" rid="a16fig02">2D</xref>).</p><p><fig id="a16fig02"/>&#13;
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</p><p><fn id="a16fig02a"><p><graphic xlink:href="1678-4170-abc-100-04-0e47-30082-e01.jpg"/></p><p><fig id="a16fig02xfig02b"><graphic xlink:href="1678-4170-abc-100-04-0e47-30082-gf02.jpg"/></fig></p></fn><fn id="a16fig02b"/></p>&#13;
&#160;&#13;
&#13;
 <p>Um m&#234;s depois realizou uma resson&#226;ncia magn&#233;tica card&#237;aca que mostrou edema mioc&#225;rdico, sem evid&#234;ncia de realce tardio ou altera&#231;&#245;es da contratilidade segmentar (<xref ref-type="fig" rid="a16fig02">Figuras 2D</xref> e <xref ref-type="fig" rid="a16fig02">2F</xref>). Aos doze meses de seguimento o paciente encontra-se assintom&#225;tico, sem ocorr&#234;ncia de eventos cardiovasculares.</p>   <p><bold>Discuss&#227;o</bold></p> <p>A MCT &#233; uma entidade pouco frequente, com preval&#234;ncia estimada em 0,7-2,5% dos doentes com suspeita de s&#237;ndrome coron&#225;ria aguda<sup>4</sup>. A designa&#231;&#227;o de <italic>Tako-tsubo </italic>adv&#233;m da semelhan&#231;a morfol&#243;gica entre o aspecto do VE em s&#237;stole na ventriculografia e um objeto cer&#226;mico com esse nome usado como armadilha para polvos em comunidades piscat&#243;rias no Jap&#227;o, pa&#237;s onde esta patologia foi originalmente descrita. Embora todos os segmentos ventriculares possam ser afetados, o achado mais t&#237;pico &#233; a acinesia medioapical de todas as paredes com hipercinesia basal. Ocasionalmente pode ocorrer movimento sist&#243;lico do folheto anterior da v&#225;lvula mitral, e a fra&#231;&#227;o de eje&#231;&#227;o encontra-se diminu&#237;da na fase aguda<sup>5</sup>. Cerca de 1-5% dos casos cursam com instabilidade hemodin&#226;mica, muitas vezes com a ado&#231;&#227;o de medidas emergentes como implanta&#231;&#227;o de bal&#227;o intra-a&#243;rtico<sup>6</sup>.</p> <p>A etiopatogenia da MCT permanece mal-esclarecida, sendo a hiperestimula&#231;&#227;o do sistema nervoso simp&#225;tico um dos mecanismos propostos. Este mecanismo mediador pode justificar a associa&#231;&#227;o com situa&#231;&#245;es de estresse, havendo relatos de casos em situa&#231;&#245;es de ansiedade, estresse, precipitados pela administra&#231;&#227;o de catecolaminas e em doentes com feocromocitoma<sup>7</sup>. O atingimento do cone apical e das por&#231;&#245;es m&#233;dias do VE (sobretudo da parede anterior) est&#225; provavelmente relacionado com a maior densidade da inerva&#231;&#227;o simp&#225;tica nessas localiza&#231;&#245;es.</p> <p>O vasospasmo coron&#225;rio, que pode resultar de hiperatividade simp&#225;tica, constitui outra hip&#243;tese etiol&#243;gica. Atualmente, o &#250;nico mecanismo conhecido capaz de explicar as altera&#231;&#245;es da motilidade segmentar similares &#224;s evidenciadas na MCT &#233; o <italic>stunning</italic> mioc&#225;rdico, usualmente relacionado com oclus&#227;o coron&#225;ria transit&#243;ria. A reversibilidade das altera&#231;&#245;es contr&#225;teis, a aus&#234;ncia de les&#245;es significativas, a liberta&#231;&#227;o reduzida de enzimas card&#237;acas e a resolu&#231;&#227;o r&#225;pida das altera&#231;&#245;es eletrocardiogr&#225;ficas enquadram-se nesta possibilidade. O vasospasmo multivaso pode justificar as altera&#231;&#245;es observadas na MCT. Essas altera&#231;&#245;es segmentares, que n&#227;o correspondem &#224; distribui&#231;&#227;o segmentar da circula&#231;&#227;o coron&#225;ria, podem justificar-se pelo fato de o espasmo atingir o cone apical do VE, envolvendo a por&#231;&#227;o terminal dos tr&#234;s territ&#243;rios coron&#225;rios subsidi&#225;rios. No entanto &#233; preciso esclarecer se o vasoespasmo &#233; o "fen&#244;meno essencial", conduzindo &#224; hipoxia mioc&#225;rdica transit&#243;ria, ou se ocorre paralelamente a outros mecanismos, que ao atuarem diretamente nos cardiomi&#243;citos interferem com o acoplamento eletroqu&#237;mico da mitoc&#244;ndria. Apesar de raros, existem casos de MCT documentada durante coronariografia diagn&#243;stica com demonstra&#231;&#227;o de vasospasmo coron&#225;rio generalizado<sup>8</sup>. A pr&#243;pria circunst&#226;ncia da realiza&#231;&#227;o do exame poder&#225; instalar um quadro de estresse emocional que deflagre a MCT. Provavelmente esta patologia &#233; um modelo de somatiza&#231;&#227;o da ansiedade com descarga maci&#231;a de neurotransmissores que conduzem &#224; perturba&#231;&#227;o da vasomotricidade.</p> <p>A resson&#226;ncia magn&#233;tica card&#237;aca permite a avalia&#231;&#227;o morfol&#243;gica, ajuda no diagn&#243;stico diferencial com outras entidades e constitui o exame <italic>gold-standard</italic> para estudar a fun&#231;&#227;o VE<sup>9</sup>.</p> <p>O progn&#243;stico da MCT &#233; favor&#225;vel, sendo o choque cardiog&#234;nico e as taquiarritmias as complica&#231;&#245;es mais prevalentes<sup>10</sup>.</p> <p>No caso descrito, a ocorr&#234;ncia de espasmo coron&#225;rio esteve provavelmente na g&#234;nese do epis&#243;dio. A possibilidade de emboliza&#231;&#227;o gasosa, embora dif&#237;cil de excluir, n&#227;o foi documentada angiograficamente. O ecocardiograma na fase aguda revelou contratilidade segmentar t&#237;pica da MCT, com normaliza&#231;&#227;o subsequente. Este achado pode indicar que estas altera&#231;&#245;es n&#227;o s&#227;o espec&#237;ficas desta patologia ou que a oclus&#227;o coron&#225;ria transit&#243;ria pode estar implicada na sua fisiopatologia. A eleva&#231;&#227;o da troponina, sem evid&#234;ncia de necrose mioc&#225;rdica na resson&#226;ncia magn&#233;tica, deve-se provavelmente &#224; liberta&#231;&#227;o do <italic>pool </italic>da troponina citoplasm&#225;tica, que resulta do aumento da permeabilidade celular induzida pela isquemia, eventualmente subsequente ao vasospasmo, sem haver les&#227;o irrevers&#237;vel das miofibrilas.</p> <p>A coronariografia &#233; um exame seguro, mas n&#227;o desprovido de complica&#231;&#245;es, devendo suas indica&#231;&#245;es, mesmo com intuito diagn&#243;stico, ser cuidadosamente ponderadas. A aus&#234;ncia de dor, &#224; semelhan&#231;a do eletrocardiograma de esfor&#231;o anteriormente realizado, e a aus&#234;ncia de doen&#231;a coron&#225;ria na angiografia efetuada podem constituir argumentos favor&#225;veis &#224; escolha de um teste alternativo para exclus&#227;o de doen&#231;a obstrutiva, como a angiografia por tomografia computadorizada, pelo seu elevado valor preditor negativo.</p> <p> Esta forma de apresenta&#231;&#227;o da MCT encontra-se pouco descrita na literatura<sup>3</sup>. No entanto, em situa&#231;&#245;es de instabilidade hemodin&#226;mica, durante a realiza&#231;&#227;o de coronariografias sem confirma&#231;&#227;o de doen&#231;a coron&#225;ria significativa e na aus&#234;ncia de outro motivo precipitante, a sua possibilidade deve ser considerada. </p>   <p><bold>Contribui&#231;&#227;o dos autores</bold></p> <p>Concep&#231;&#227;o e desenho da pesquisa: Dores H, Raposo L; Obten&#231;&#227;o de dados: Dores H; An&#225;lise e interpreta&#231;&#227;o dos dados: Dores H, Raposo L, Ferreira J, Andrade MJ, Almeida M; Revis&#227;o cr&#237;tica do manuscrito quanto ao conte&#250;do intelectual: Raposo L, Ferreira J, Andrade MJ, Almeida M, Mendes M.</p> <p><bold>Potencial Conflito de Interesses</bold></p> <p>Declaro n&#227;o haver conflito de interesses pertinentes.</p> <p><bold>Fontes de Financiamento</bold></p> <p>O presente estudo n&#227;o teve fontes de financiamento externas.</p> <p><bold>Vincula&#231;&#227;o Acad&#234;mica</bold></p> <p>N&#227;o h&#225; vincula&#231;&#227;o deste estudo a programas de p&#243;s-gradua&#231;&#227;o.</p>                  <p><fn id="end" fn-type="corresp"><label><bold>Correspond&#234;ncia:</bold></label><p> Helder Dores </p><p> Rua Jos&#233; Cardoso Pires, N5, 7A, Lumiar </p><p> 1750-356, Lisboa </p><p> E-mail: </p><p><email xlink:href="heldores@hotmail.com">heldores@hotmail.com</email></p></fn></p> <p>Artigo recebido em 22/05/12, revisado em 04/08/12, aceito em 29/10/12.</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>Case Report</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="en">Apical ballooning syndrome during diagnostic coronary angiography</article-title>
      </title-group>
    </front-stub>
    <body>
      <p>
        <bold>CASE REPORT</bold>
      </p>
      <p>
        <fn id="enda-body2">
          <label>
            <bold>Apical ballooning syndrome during diagnostic coronary angiography</bold>
          </label>
          <p>
            <bold>Helder Dores; Lu&#237;s Raposo; Jorge Ferreira; Maria Jo&#227;o Andrade; Manuel Almeida; Miguel Mendes</bold>
          </p>
        </fn>
      </p>
      <p>Servi&#231;o de Cardiologia - Hospital de Santa Cruz, Centro Hospitalar de Lisboa Ocidental - Lisboa - Portugal</p>
      <p>Mailing Address</p>
      <p><bold>Keywords:</bold> Coronary Occlusion/diagnosis; Takotsubo Cardiomyopathy/diagnosis; Coronary Angiography; Cardiac catheterization; Contrast Media.</p>
      <p>
        <bold>Introduction</bold>
      </p>
      <p>Hemodynamic instability during coronary angiography is more common in patients with severe coronary disease, particularly in the acute coronary syndrome setting. Rarely, it can occur in an elective context, in the absence of coronary disease, due to inadvertent gas embolism and increased coronary vessel reactivity<sup>1,2</sup>.</p>
      <p>Coronary vasospasm has been implicated as one of the possible pathophysiological mechanisms that are involved in Takotsubo cardiomyopathy (TCM), though a few cases substantiating this association have been described in the literature<sup>3</sup>.</p>
      <p>We hereby present the case of a patient with transient hemodynamic instability with evidence of multivessel vasospasm and findings suggestive of TCM during elective coronary angiography.</p>
      <p>
        <bold>Case Report</bold>
      </p>
      <p>We present the case of a 70-year-old male patient, a long term smoker with no known risk factors and no cardiovascular history. In May 2004, he was submitted to exercise testing due to fatigue complaints. The exam revealed ST segment changes that were interpreted as silent ischemia. Subsequently, a coronary angiography did not show significant coronary disease, and the patient remained asymptomatic from the cardiovascular point of view.</p>
      <p>In March 2011, he complained of fatigue on moderate effort again. He was submitted to exercise testing with normal functional capacity (10.7 METs), adequate blood pressure response and ST changes suggesting ischemia: upsloping ST depression at lateral and inferior leads, starting on the second stage and getting back to normal on the first minute of recovery. He was submitted again to coronary angiography as requested by the attending physician. At the first injection in left coronary artery (dominant vessel), slow flow was observed with occlusion of the proximal anterior descending, left posterior descending and distal circumflex arteries (<xref ref-type="fig" rid="en_a16fig01-body2">Figure 1A</xref>). These findings were followed by increasing chest pain, generalized elevation of the ST segment, progressive bradycardia and pump failure, and atropine and dopamine had to be given.</p>
      <p content-type="asset">
        <fig id="en_a16fig01-body2">
          <graphic xlink:href="1678-4170-abc-100-04-0e47-30082-gf01-en.jpg"/></fig>
      </p>
      <p>Due to the possibility of vasospasm and in spite of hemodynamic instability, intracoronary isosorbide dinitrate was given with ST segment normalization and hemodynamic stabilization. The following injections (&gt; 5 minutes after beginning of the symptoms) revealed reestablishment of blood flow in the coronary tree as a whole and no evidence of significant angiography lesions (<xref ref-type="fig" rid="en_a16fig01-body2">Figure 1B</xref>). Transthoracic echocardiography showed akinesis with apical ballooning (<xref ref-type="fig" rid="en_a16fig02-body2">Figures 2A</xref> and <xref ref-type="fig" rid="en_a16fig02-body2">2B</xref>) e hyperkinesis of the left ventricle (LV) inferior segments. The patient was admitted to the Coronary Unit and remained stable. Lab investigations revealed increased levels of myocardial necrosis biomarkers - troponin I (normal values &lt;0.04 &#181;g/l): 1.29 (&lt; 2 h) - 5.77 (24 h) - 4.89 (36 h) - 0.23 (96 h) &#181;g/L. On the fifth day of hospitalization, an echocardiogram revealed normalization of wall motility and LV systolic function and the patient was discharged (<xref ref-type="fig" rid="en_a16fig02-body2">Figures 2C</xref> and <xref ref-type="fig" rid="en_a16fig02-body2">2D</xref>).</p>
      <p content-type="html"><fig id="en_a16fig02-body2"><graphic xlink:href="https://minio.scielo.br/documentstore/1678-4170/j7dssV5MZGLZZ8LHzFpkqJg/81aaa848f55adb97c28dcb1b1ab35bae455c9df8.jpg"/><graphic xlink:href="1678-4170-abc-100-04-0e47-30082-gf02-en.jpg"/></fig>&#13;
&#160;&#13;
</p>
      <p>One month later, magnetic resonance imaging showed myocardial edema without evidence of late enhancement or segmental contractility changes (<xref ref-type="fig" rid="en_a16fig02-body2">Figures 2D</xref> and <xref ref-type="fig" rid="en_a16fig02-body2">2F</xref>). On follow-up, after twelve months, the patient is asymptomatic and has not presented any cardiovascular event.</p>
      <p>
        <bold>Discussion</bold>
      </p>
      <p>TCM is a low frequency entity with estimated prevalence of 0.7-2.5% of the patients with suspected acute coronary syndrome<sup>4</sup>. It is called Takotsubo syndrome due to the morphologic similarity between the LV aspect during systole at ventriculography and a ceramic object with the same name used as an octopus trap in fishing communities in Japan, where it was originally described. Although all ventricular segments can be affected, the most typical finding is the medioapical akinesis affecting all cardiac walls associated to inferior hyperkinesis. On occasion, the anterior leaflet of the mitral valve can move with systole, and the ejection fraction is reduced in the acute phase<sup>5</sup>. In approximately 1 to 5% of the cases, hemodynamic instability develops, often requiring the adoption of emergency measures such as intraaortic balloon implantation<sup>6</sup>.</p>
      <p>TCM etiopathology remains to be elucidated and one of the proposed mechanisms is the hyper stimulation of the sympathetic nervous system. This mediating mechanism may justify the association of the condition with stressful situations (cases were reported in association with anxiety, stress, administration of cathecolamines and in patients with pheochromocytoma)<sup>7</sup>. The fact that the apex and the medium LV segments (specially the anterior wall) are affected is probably related to the greater density of the sympathetic innervation in these areas.</p>
      <p>Coronary vasospasm, which can result from sympathetic hyperactivity, is another proposed etiology. Currently, the only known mechanism that can explain the segmental motility changes similar to the ones evidenced in TCM is myocardial stunning, usually related to transient coronary occlusion. This hypothesis can explain the reversibility of contractile changes, the absence of significant damage, the reduced cardiac enzymes release and the rapid recovery of electrocardiographic changes. Multivessel vasospasm may justify changes observed on TCM. The segmental alterations, which do not correlate to the segmental distribution of coronary circulation, may be explained by LV apex spasm involving the terminal portion of the three subsidiary coronary territories. However, it is important to clarify if vasospasm is the "essential phenomenon", leading to transient myocardial hypoxia, or if it occurs in parallel to other mechanisms that, on acting directly on cardiomyocytes, interfere with the electrochemical coupling of the mitochondrias. Though rare, there are documented cases of TCM during diagnostic coronary angiography showing generalized coronary vasospasm<sup>8</sup>. The exam circumstances themselves may lead to emotional stress and TCM. This condition is probably a model of anxiety somatization with massive neurotransmitter discharge causing vasomotricity disturbance.</p>
      <p>Cardiac resonance magnetic imaging allows morphologic evaluation, helps in differential diagnosis and is the gold standard for studying LV function<sup>9</sup>.</p>
      <p>The prognosis for TCM is favorable. Cardiogenic shock and tachyarrhythmia are the most prevalent complications<sup>10</sup>.</p>
      <p>In the case above described, coronary vasospasm was probably the cause of the episode. Although not possible to exclude, gas embolism was not angiographically documented. Acute phase echocardiogram revealed segmental contractility typical of TCM, with subsequent normalization. This finding can indicate that the changes are not specific for this condition or, alternatively, that its pathophysiology can include transient coronary occlusion. Troponin elevation, without evidence of myocardial necrosis on magnetic resonance, is probably related to cytoplasmic troponin pool release, resulting in increased cellular permeability induced by ischemia, eventually following vasospasm, without irreversible myofibril damage.</p>
      <p>Coronary angiography is a safe exam, but is not devoid of complications and the indications for its use, even for diagnostic purposes, must be carefully weighted. The absence of pain (similar to the exercise testing previously performed) and the absence of coronary disease on angiography may favor the selection of an alternative test for obstructive disease exclusion, such as computed tomography angiography, which has high negative predictive value.</p>
      <p>This presentation of TCM is not widely described in literature<sup>3</sup>. However, its possibility must be considered when hemodynamic instability develops during coronary angiography in the absence of confirmed coronary disease and other triggering factor. </p>
      <p>
        <bold>Author contributions</bold>
      </p>
      <p>Conception and design of the research: Dores H, Raposo L; Acquisition of data: Dores H; Analysis and interpretation of the data: Dores H, Raposo L, Ferreira J, Andrade MJ, Almeida M; Critical revision of the manuscript for intellectual content: Raposo L, Ferreira J, Andrade MJ, Almeida M, Mendes M.</p>
      <p>
        <bold>Potential Conflict of Interest</bold>
      </p>
      <p>No potential conflict of interest relevant to this article was reported.</p>
      <p>
        <bold>Sources of Funding</bold>
      </p>
      <p>There were no external funding sources for this study.</p>
      <p>
        <bold>Study Association</bold>
      </p>
      <p>This study is not associated with any post-graduation program.</p>
      <p>
        <bold>References</bold>
      </p>
    </body>
  </sub-article>
</article>
