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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">GLt8LtkK3C9DyVTNMnRZfRt</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2012000200014</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(12)09800214</article-id>
      <article-id pub-id-type="doi">10.1590/S0066-782X2012000200014</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Correla&#231;&#227;o Cl&#237;nico-Radiogr&#225;fica</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Caso 2/2012: rec&#233;m-nascido de 11 dias com coarcta&#231;&#227;o da aorta acentuada em choque cardiog&#234;nico</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Atik</surname>
            <given-names>Edmar</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">SP</named-content>
        </addr-line>
        <institution content-type="orgname">Hospital S&#237;rio-Liban&#234;s</institution>
        <country country="BR">Brasil</country>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>02</month>
        <year>2012</year>
      </pub-date>
      <volume>98</volume>
      <issue>2</issue>
      <fpage>e22</fpage>
      <lpage>e23</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>27</day>
        <month>02</month>
        <year>2012</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <p>
      <bold>CORRELA&#199;&#195;O CL&#205;NICO-RADIOGR&#193;FICA</bold>
    </p>
    <p>
      <bold>Caso 2/2012 - rec&#233;m-nascido de 11 dias com coarcta&#231;&#227;o da aorta acentuada em choque cardiog&#234;nico</bold>
    </p>
    <p>
      <bold>Edmar Atik</bold>
    </p>
    <p>Hospital S&#237;rio-Liban&#234;s, S&#227;o Paulo, SP, Brasil</p>
    <p>
      <xref ref-type="corresp" rid="end">Correspond&#234;ncia</xref>
    </p>
    <p><bold>Palavras-chave:</bold> Cardiopatias cong&#234;nitas, coarta&#231;&#227;o a&#243;rtica, insufici&#234;ncia card&#237;aca, choque cardiog&#234;nico</p>
    <p><bold>Dados cl&#237;nicos:</bold> Cansa&#231;o discreto era notado desde o nascimento com evidente agravamento de h&#225; dois dias, raz&#227;o da interna&#231;&#227;o de emerg&#234;ncia. Nasceu com 2700 g de peso, ap&#243;s gesta&#231;&#227;o e parto normais. </p>
    <p>Exame f&#237;sico: mal estado geral, taquidispneico, p&#225;lido, pulsos finos, principalmente nos membros inferiores. Peso: 2500 g, Altura: 48 cm PAMSD: 80/40 mm Hg, PAMID: 40 mm Hg, FC: 166 bpm, FR: 100 rpm. A aorta n&#227;o era palpada na f&#250;rcula.</p>
    <p>No prec&#243;rdio, havia discretas impuls&#245;es sist&#243;licas na borda esternal esquerda e o <italic>ictus cordis</italic> n&#227;o era palpado. As bulhas card&#237;acas eram hiperfon&#233;ticas e n&#227;o foram auscultados sopros card&#237;acos. O f&#237;gado era palpado a 4 cm do rebordo costal direito e os pulm&#245;es eram limpos, sem ru&#237;dos advent&#237;cios.</p>
    <p>
      <bold>Exames Complementares:</bold>
    </p>
    <p><bold>Eletrocardiograma</bold> mostrava ritmo sinusal, sinais de exclusiva sobrecarga ventricular direita (morfologia Rs em V1 e rS em V6) e com altera&#231;&#245;es da repolariza&#231;&#227;o ventricular. AQRS: -170&#186;, AP: +60&#186;, AT: indeterminado (<xref ref-type="fig" rid="a14fig01m">Figura 1</xref>). </p>
    <p content-type="asset">
      <fig id="a14fig01m">
        <graphic xlink:href="1678-4170-abc-98-02-0e22-00014-gf01.jpg"/></fig>
    </p>
    <p><bold>Radiografia de T&#243;rax</bold> mostra &#225;rea card&#237;aca acentuadamente aumentada &#224; custa do arco ventricular esquerdo e trama vascular pulmonar congesta (<xref ref-type="fig" rid="a14fig02m">Figura 2</xref>).</p>
    <p content-type="asset">
      <fig id="a14fig02m">
        <graphic xlink:href="1678-4170-abc-98-02-0e22-00014-gf02.jpg"/></fig>
    </p>
    <p><bold>Ecocardiograma</bold> salienta os elementos decisivos para o diagn&#243;stico de coarcta&#231;&#227;o da aorta em regi&#227;o &#237;stmica com gradiente de press&#227;o de 40 mm Hg e com canal arterial de pequena dimens&#227;o (<xref ref-type="fig" rid="a14fig01m">Figura 1</xref>).</p>
    <p>
      <bold>Diagn&#243;stico cl&#237;nico: Coarcta&#231;&#227;o da aorta em insufici&#234;ncia card&#237;aca acentuada</bold>
    </p>
    <p><bold>Racioc&#237;nio cl&#237;nico:</bold> Os elementos cl&#237;nicos orientaram ao diagn&#243;stico de coarcta&#231;&#227;o da aorta em face da diferen&#231;a dos pulsos perif&#233;ricos, que embora fosse discreta, era explicada pela acentuada insufici&#234;ncia card&#237;aca. Corroborava para o diagn&#243;stico a sobrecarga de ventr&#237;culo direito no eletrocardiograma e a cardiomegalia acentuada na radiografia de t&#243;rax. Ali&#225;s, esta imagem era compat&#237;vel com o diagn&#243;stico de cardiopatia cong&#234;nita acianog&#234;nica com insufici&#234;ncia card&#237;aca por obstru&#231;&#227;o do cora&#231;&#227;o esquerdo dada tamb&#233;m a congest&#227;o pulmonar, ao lado da cardiomegalia.</p>
    <p><bold>Diagn&#243;stico diferencial:</bold> outras cardiopatias obstrutivas &#224; esquerda n&#227;o se acompanham de grande cardiomegalia como ocorre na estenose mitral e no <italic>cor triatriatum</italic>. As cardiopatias com sobrecarga de volume do cora&#231;&#227;o esquerdo, como a insufici&#234;ncia mitral, tamb&#233;m poderiam se exteriorizar de forma semelhante, mas com aumento mais pronunciado do &#225;trio esquerdo. As cardiopatias com sobrecarga de volume e as com desvio de sangue da esquerda para a direita se acompanham de trama arterial pulmonar aumentada. </p>
    <p><bold>Conduta e Evolu&#231;&#227;o:</bold> Ap&#243;s intuba&#231;&#227;o endotraqueal e ventila&#231;&#227;o mec&#226;nica com FiO2 a 40% e introdu&#231;&#227;o endovenosa de drogas vasoativas (dobutamina = 20 mcg/Kg/min) e vasodilatadoras (prostaglandina E1 = 0,08 mcg/Kg/min) al&#233;m de furosemida, houve melhora da condi&#231;&#227;o cl&#237;nica. </p>
    <p>O &#225;cido l&#225;tico diminuiu de 120 para 20 mg/dL, a acidose metab&#243;lica de -23 mmol/L se normalizou e com aumento da diurese e diminui&#231;&#227;o da cardiomegalia. Tr&#234;s dias ap&#243;s, p&#244;de ser operado em melhores condi&#231;&#245;es, apesar da maior eleva&#231;&#227;o dos n&#237;veis de creatinina, de 1,3 para 2,6,mg/dL e da ureia, de 48 para 73 mg/dL. &#192; opera&#231;&#227;o, foi realizada coarctectomia em estreitamento acentuado na regi&#227;o &#237;stmica com anastomose t&#233;rmino-terminal e ligadura de grande canal arterial. </p>
    <p>A evolu&#231;&#227;o foi favor&#225;vel, com n&#237;tida regress&#227;o do quadro da insufici&#234;ncia card&#237;aca com extuba&#231;&#227;o endotraqueal no primeiro dia p&#243;s-operat&#243;rio, diminui&#231;&#227;o progressiva da dobutamina em tr&#234;s dias e dos sinais da insufici&#234;ncia renal, da hipertens&#227;o arterial paradoxal (tratada com nitroprussiato de s&#243;dio e anlodipina) e alta ap&#243;s 15 dias com digoxina. Na evolu&#231;&#227;o, nove meses ap&#243;s, notou-se ganho de peso normal (9 Kg), aus&#234;ncia de sopros e de sinais de insufici&#234;ncia card&#237;aca e normaliza&#231;&#227;o dos pulsos arteriais e da &#225;rea card&#237;aca. O ecocardiograma revelava gradiente de press&#227;o na aorta de 28 mm Hg, fun&#231;&#227;o ventricular de 82% e cavidades card&#237;acas de dimens&#245;es normais. </p>
    <p><bold>Coment&#225;rios:</bold> A coarcta&#231;&#227;o da aorta evolui de maneira desfavor&#225;vel quando se mostra de grande repercuss&#227;o j&#225; no per&#237;odo neonatal, em geral nas duas primeiras semanas de vida. O quadro inicial pode at&#233; ser confundido com o de miocardiopatia com acentuada disfun&#231;&#227;o ventricular, sem sopros card&#237;acos e sem os sinais cl&#225;ssicos da doen&#231;a. Os pulsos contrastantes entre os membros, caracter&#237;sticos da coarcta&#231;&#227;o da aorta, exteriorizam-se em presen&#231;a de fun&#231;&#227;o ventricular mais preservada, obtida ap&#243;s tratamento inicial adequado. &#201; tamb&#233;m de interesse notar a acentuada sobrecarga ventricular direita no eletrocardiograma, decorrente da hipertens&#227;o pulmonar retr&#243;grada em face da sobrecarga s&#250;bita do ventr&#237;culo esquerdo, ap&#243;s estreitamento maior do canal arterial. A fal&#234;ncia mioc&#225;rdica, no entanto, melhora ap&#243;s a dilata&#231;&#227;o do mesmo com PGE1 e mais ainda ap&#243;s a corre&#231;&#227;o cir&#250;rgica. O resultado final se torna surpreendente como o demonstrado no caso em quest&#227;o.</p>
    <p>
      <fn id="end" fn-type="corresp">
        <label>
          <bold>Correspond&#234;ncia:</bold>
        </label>
        <p> Edmar Atik </p>
        <p> InCor </p>
        <p> Av. Dr. En&#233;as Carvalho de Aguiar, 44 </p>
        <p> 05403-000 - S&#227;o Paulo, SP - Brasil </p>
        <p> E-mail: </p>
        <p>
          <email xlink:href="conatik@incor.usp.br">conatik@incor.usp.br</email>
        </p>
      </fn>
    </p>
  </body>
  <sub-article article-type="translation" id="TRen" xml:lang="en">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Clinicoradiological Session</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="en">Case 2/2012: eleven-day-old infant with marked coarctation of the aorta in cardiogenic shock</article-title>
      </title-group>
    </front-stub>
    <body>
      <p>
        <bold>CLINICORADIOLOGICAL SESSION</bold>
      </p>
      <p>
        <bold>Case 2/2012 - eleven-day-old infant with marked coarctation of the aorta in cardiogenic shock</bold>
      </p>
      <p>
        <bold>Edmar Atik</bold>
      </p>
      <p>Hospital S&#237;rio-Liban&#234;s, S&#227;o Paulo, SP, Brasil</p>
      <p>
        <xref ref-type="corresp" rid="end-body2">Correspond&#234;ncia</xref>
      </p>
      <p><bold>Keywords:</bold> Heart, defects; aortic coarctation; heart failure; shock, cardiogenic</p>
      <p><bold>Clinical data:</bold> Slight tiredness had been noticed since birth, with obvious aggravation in the last two days, which prompted the hospital admission. Weight at birth had been 2700 g after an uneventful pregnancy and normal delivery.</p>
      <p> At physical examination: poor general status, tachydyspneic, pale, weak pulses, especially in the lower limbs. Weight: 2500 g; Height: 48 cm; BP-RSL: 80/40 mm Hg, BP-RIL: 40 mm Hg, HR: 166 bpm, RR: 100 rpm. The aorta was not palpable at the sternal notch. There were mild precordial systolic impulses in the left sternal border and the apical impulse was not palpable. The heart sounds were very loud and there were no heart murmurs. The liver was palpable 4 cm from the right costal margin and the lungs were clear, with no adventitious sounds.</p>
      <p>
        <bold>Complementary Examinations:</bold>
      </p>
      <p><bold>Electrocardiogram:</bold> showed sinus rhythm, signs of exclusive right ventricular overload (Rs morphology in V1 and rS in V6) and alterations in ventricular repolarization. AQRS:</p>
      <p>-170&#186;, AP: +60&#186;; AT: indeterminate (<xref ref-type="fig" rid="en_a14fig01m-body2">Figure 1</xref>). </p>
      <p content-type="asset">
        <fig id="en_a14fig01m-body2">
          <graphic xlink:href="1678-4170-abc-98-02-0e22-00014-gf01-en.jpg"/></fig>
      </p>
      <p><bold>Chest X-ray:</bold> showed markedly enlarged cardiac silhouette at the expense of the left ventricular arch and congested pulmonary vascular network (<xref ref-type="fig" rid="en_a14fig02m-body2">Figure 2</xref>).</p>
      <p content-type="asset">
        <fig id="en_a14fig02m-body2">
          <graphic xlink:href="1678-4170-abc-98-02-0e22-00014-gf02-en.jpg"/></fig>
      </p>
      <p><bold>Echocardiography:</bold> disclosed the critical elements for the diagnosis of coarctation of the aorta in the isthmic region, with a pressure gradient of 40 mm Hg and small <italic>ductus arteriosus </italic>(<xref ref-type="fig" rid="en_a14fig01m-body2">Figure 1</xref>).</p>
      <p>
        <bold>Clinical diagnosis: Coarctation of the Aorta in Marked Heart Failure</bold>
      </p>
      <p><bold>Clinical Rationale:</bold> Clinical findings are consistent with the diagnosis of coarctation of the aorta, considering the difference of peripheral pulses, which albeit slight, showed severe heart failure. Right ventricular overload on electrocardiogram and marked cardiomegaly on chest x-ray supported the diagnosis. In fact, this image was compatible with the diagnosis of acyanotic congenital heart disease with heart failure due to obstruction of the left heart, also considering the lung congestion, along with cardiomegaly. </p>
      <p><bold>Differential diagnosis:</bold> other obstructive left heart diseases are not accompanied by large cardiomegaly as it occurs in mitral stenosis and <italic>cor triatriatum</italic>. Heart diseases with volume overload of the left heart, such as mitral regurgitation, could also be identified as similar, but with a more pronounced increase of the left atrium. Herat diseases with volume overload and left-to-right shunt are accompanied by pulmonary arterial enlargement. </p>
      <p><bold>Clinical conduct and Evolution:</bold> After endotracheal intubation and mechanical ventilation with FiO2 at 40% and introduction of intravenous vasoactive (dobutamine = 20 mcg/kg/min) and vasodilator (prostaglandin E1 = 0.08 mcg/kg/min) drugs, plus furosemide, there was improvement in the clinical condition. </p>
      <p>Lactic acid decreased from 120 to 20 mg/dL; the metabolic acidosis, which was -23 mmol/L decreased to normal levels, with increased diuresis and reduction of cardiomegaly. Three days later, the patient could be submitted to surgery, considering improvement in general status, despite the greater increase in creatinine levels from 1.3 to 2.6 mg/dL and urea from 48 to 73 mg/dL. During surgery, coarctectomy was performed in the accentuated narrowing in the isthmic region with termino-terminal anastomosis and ligation of a large ductus arteriosus. </p>
      <p>Evolution was favorable, with a clear regression of heart failure and endotracheal extubation on the first postoperative day, progressive decrease in dobutamine doses in three days as well as signs of renal failure and paradoxical arterial hypertension (treated with sodium nitroprusside and amlodipine). The patient was discharged after 15 days on digoxin. At the evolution, nine months later, normal weight gain (9 kg) was observed, with no murmurs or signs of heart failure and normalization of arterial pulses and cardiac silhouette. The echocardiogram showed pressure gradient in the aorta of 28 mm Hg, 82% of ventricular function and normal-sized cardiac cavities. </p>
      <p><bold>Comments:</bold> coarctation of the aorta has an unfavorable evolution when it is already far-reaching in the neonatal period, usually in the first two weeks of life. The initial picture can even be mistaken by cardiomyopathy with severe ventricular dysfunction, without murmurs and without the classic signs of the disease. The contrasting pulses between limbs, characteristic of coarctation of the aorta, are demonstrated in the presence of more preserved ventricular function, obtained after appropriate initial treatment. It is also interesting to note the marked right ventricular overload on the ECG, due to retrograde pulmonary hypertension in the presence of sudden left ventricular overload, after greater narrowing of the ductus arteriosus. The myocardial failure, however, improves after myocardial dilation with PGE1 and even further after surgical correction. The final result is surprising, as demonstrated in this case.</p>
      <p>
        <fn id="end-body2" fn-type="corresp">
          <label>
            <bold>Mailing Address:</bold>
          </label>
          <p> Edmar Atik </p>
          <p> InCor </p>
          <p> Av. Dr. En&#233;as Carvalho de Aguiar, 44 </p>
          <p> 05403-000 - S&#227;o Paulo, SP - Brazil</p>
          <p> E-mail: </p>
          <p>
            <email xlink:href="conatik@incor.usp.br">conatik@incor.usp.br</email>
          </p>
        </fn>
      </p>
    </body>
  </sub-article>
  <sub-article article-type="translation" id="TRes" xml:lang="es">
    <front-stub>
      <article-categories/>
      <title-group>
        <article-title xml:lang="es">Caso 2/2012: reci&#233;n nacido de 11 d&#237;as con coartaci&#243;n de la aorta acentuada en shock cardiog&#233;nico</article-title>
      </title-group>
    </front-stub>
    <body>
      <p>
        <bold>CORRELACI&#211;N CL&#205;NICO-RADIOGR&#193;FICA</bold>
      </p>
      <p>
        <bold>Caso 2/2012 - reci&#233;n nacido de 11 d&#237;as con coartaci&#243;n de la aorta acentuada en shock cardiog&#233;nico</bold>
      </p>
      <p>
        <bold>Edmar Atik</bold>
      </p>
      <p>Hospital S&#237;rio-Liban&#234;s, S&#227;o Paulo, SP, Brasil</p>
      <p>
        <xref ref-type="corresp" rid="end-body3">Correspondencia</xref>
      </p>
      <p><bold>Palabras clave:</bold> Cardiopat&#237;as cong&#233;nitas, coartaci&#243;n a&#243;rtica, insuficiencia card&#237;aca, shock cardiog&#233;nico</p>
      <p><bold>Datos cl&#237;nicos:</bold> Cansancio discreto era notado desde el nacimiento con evidente agravamiento hac&#237;a dos d&#237;as, raz&#243;n de la internaci&#243;n de emergencia. Naci&#243; con 2700 g de peso, despu&#233;s de gestaci&#243;n y parto normales. </p>
      <p>Examen f&#237;sico: mal estado general, taquidisneico, p&#225;lido, pulsos finos, principalmente en los miembros inferiores. Peso: 2500 g, Altura: 48 cm PAMSD: 80/40 mm Hg, PAMID: 40 mm Hg, FC: 166 lpm, FR: 100 rpm. La aorta no era palpada en la f&#250;rcula.</p>
      <p>En el precordio, hab&#237;a discretos pulsos sist&#243;licos en el borde esternal izquierdo y el <italic>ictus cordis</italic> no era palpado. Los ruidos card&#237;acos eran hiperfon&#233;ticos y no fueron auscultados soplos card&#237;acos. El h&#237;gado era palpado a 4 cm del reborde costal derecho y los pulmones eran limpios, sin ruidos adventicios.</p>
      <p>
        <bold>Ex&#225;menes Complementarios:</bold>
      </p>
      <p><bold>Electrocardiograma</bold> mostraba ritmo sinusal, se&#241;ales de exclusiva sobrecarga ventricular derecha (morfolog&#237;a Rs en V1 y rS en V6) y con alteraciones de la repolarizaci&#243;n ventricular. AQRS: -170&#186;, AP: +60&#186;, AT: indeterminado (<xref ref-type="fig" rid="es_a14fig01m-body3">Figura 1</xref>). </p>
      <p content-type="asset">
        <fig id="es_a14fig01m-body3">
          <graphic xlink:href="1678-4170-abc-98-02-0e22-00014-gf01-es.jpg"/></fig>
      </p>
      <p><bold>Radiograf&#237;a de T&#243;rax</bold> muestra &#225;rea card&#237;aca acentuadamente aumentada a costa del arco ventricular izquierdo y trama vascular pulmonar congestionada (<xref ref-type="fig" rid="es_a14fig02m-body3">Figura 2</xref>).</p>
      <p content-type="asset">
        <fig id="es_a14fig02m-body3">
          <graphic xlink:href="1678-4170-abc-98-02-0e22-00014-gf02-es.jpg"/></fig>
      </p>
      <p><bold>Ecocardiograma</bold> destaca los elementos decisivos para el diagn&#243;stico de coartaci&#243;n de la aorta en regi&#243;n &#237;stmica con gradiente de presi&#243;n de 40 mm Hg y con canal arterial de peque&#241;a dimensi&#243;n (<xref ref-type="fig" rid="es_a14fig01m-body3">Figura 1</xref>).</p>
      <p>
        <bold>Diagn&#243;stico cl&#237;nico: Coartaci&#243;n de la aorta en insuficiencia card&#237;aca acentuada</bold>
      </p>
      <p><bold>Razonamiento cl&#237;nico:</bold> Los elementos cl&#237;nicos orientaron al diagn&#243;stico de coartaci&#243;n de la aorta enfrente a la diferencia de los pulsos perif&#233;ricos, que aunque fuese discreta, presentaba acentuada insuficiencia card&#237;aca. Corroboraba el diagn&#243;stico la sobrecarga de ventr&#237;culo derecho en el electrocardiograma y la cardiomegalia acentuada en la radiograf&#237;a de t&#243;rax. Es decir, esta imagen era compatible con el diagn&#243;stico de cardiopat&#237;a cong&#233;nita acianog&#233;nica con insuficiencia card&#237;aca por obstrucci&#243;n del coraz&#243;n izquierdo dada tambi&#233;n la congesti&#243;n pulmonar, al lado de la cardiomegalia.</p>
      <p><bold>Diagn&#243;stico diferencial:</bold> otras cardiopat&#237;as obstructivas a la izquierda no se acompa&#241;an de gran cardiomegalia como ocurre en la estenosis mitral y en el <italic>cor triatriatum</italic>. Las cardiopat&#237;as con sobrecarga de volumen del coraz&#243;n izquierdo, como la insuficiencia mitral, tambi&#233;n podr&#237;an exteriorizarse de forma semejante, pero con aumento m&#225;s pronunciado del atrio izquierdo. Las cardiopat&#237;as con sobrecarga de volumen y las con desv&#237;o de sangre de la izquierda a la derecha se acompa&#241;an de trama arterial pulmonar aumentada. </p>
      <p><bold>Conducta y Evoluci&#243;n:</bold> Despu&#233;s de intubaci&#243;n endotraqueal y ventilaci&#243;n mec&#225;nica con FiO2 a 40% e introducci&#243;n endovenosa de drogas vasoactivas (dobutamina = 20 mcg/Kg/min) y vasodilatadoras (prostaglandina E1 = 0,08 mcg/Kg/min) adem&#225;s de furosemida, hubo mejora de la condici&#243;n cl&#237;nica. </p>
      <p>El &#225;cido l&#225;ctico disminuy&#243; de 120 a 20 mg/dL, la acidosis metab&#243;lica de -23 mmol/L se normaliz&#243; y con aumento de la diuresis y disminuci&#243;n de la cardiomegalia. Tres d&#237;as despu&#233;s, pudo ser operado en mejores condiciones, a pesar de la mayor elevaci&#243;n de los niveles de creatinina, de 1,3 para 2,6,mg/dL y de la urea, de 48 a 73 mg/dL. En la operaci&#243;n, fue realizada coartectom&#237;a en estrechamiento acentuado en la regi&#243;n &#237;stmica con anastomosis t&#233;rmino-terminal y ligadura de gran canal arterial. </p>
      <p>La evoluci&#243;n fue favorable, con n&#237;tida regresi&#243;n del cuadro de la insuficiencia card&#237;aca con extubaci&#243;n endotraqueal el primer d&#237;a postoperatorio, disminuci&#243;n progresiva de la dobutamina en tres d&#237;as y de las se&#241;ales de la insuficiencia renal, de la hipertensi&#243;n arterial paradoxal (tratada con nitroprusiato de sodio y anlodipina) y alta despu&#233;s de 15 d&#237;as con digoxina. En la evoluci&#243;n, nueve meses despu&#233;s, se not&#243; aumento de peso normal (9 Kg), ausencia de soplos y de se&#241;ales de insuficiencia card&#237;aca y normalizaci&#243;n de los pulsos arteriales y del &#225;rea card&#237;aca. El ecocardiograma revelaba gradiente de presi&#243;n en la aorta de 28 mm Hg, funci&#243;n ventricular de 82% y cavidades card&#237;acas de dimensiones normales. </p>
      <p><bold>Comentarios:</bold> La coartaci&#243;n de la aorta evoluciona de manera desfavorable cuando se muestra de gran repercusi&#243;n ya en el per&#237;odo neonatal, en general en las dos primeras semanas de vida. El cuadro inicial puede hasta ser confundido con el de miocardiopat&#237;a con acentuada disfunci&#243;n ventricular, sin soplos card&#237;acos y sin las se&#241;ales cl&#225;sicas de la enfermedad. Los pulsos contrastantes entre los miembros, caracter&#237;sticos de la coartaci&#243;n de la aorta, se exteriorizan en presencia de funci&#243;n ventricular m&#225;s preservada, obtenida despu&#233;s de tratamiento inicial adecuado. Es tambi&#233;n de inter&#233;s notar la acentuada sobrecarga ventricular derecha en el electrocardiograma, resultante de la hipertensi&#243;n pulmonar retr&#243;grada frente a la sobrecarga s&#250;bita do ventr&#237;culo izquierdo, despu&#233;s de estrechamiento mayor del canal arterial. La insuficiencia mioc&#225;rdica, mientras tanto, mejora despu&#233;s de la dilataci&#243;n del mismo con PGE1 y m&#225;s aun despu&#233;s de la correcci&#243;n quir&#250;rgica. El resultado final se vuelve sorprendente como lo demostrado en el caso en cuesti&#243;n.</p>
      <p>
        <fn id="end-body3" fn-type="corresp">
          <label>
            <bold>Correspondencia:</bold>
          </label>
          <p> Edmar Atik </p>
          <p> InCor </p>
          <p> Av. Dr. En&#233;as Carvalho de Aguiar, 44 </p>
          <p> 05403-000 - S&#227;o Paulo, SP - Brasil</p>
          <p> E-mail: </p>
          <p>
            <email xlink:href="conatik@incor.usp.br">conatik@incor.usp.br</email>
          </p>
        </fn>
      </p>
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  </sub-article>
</article>
