Caso 4/2005 - Infarto fatal do miocárdio em mulher de 88 anos de idade (Instituto do Coração do Hospital das Clínicas - FMUSP, São Paulo)
São Paulo, SP
Mulher de 88 anos de idade procurou atendimento médico (29/12/2003) com queixa de dor epigástrica de 4 horas de duração acompanhada de vômitos.
A paciente sabia ser portadora de hipertensão arterial de longa data. Há dois anos havia sofrido acidente vascular cerebral, sem seqüelas motoras. Há três meses surgiu dispnéia desencadeada por esforços moderados e edema de membros inferiores. Negava síncope.
O exame físico (3/10/2003) revelou freqüência cardíaca 68 bpm, pressão arterial 180x80 mmHg. O exame dos pulmões foi normal. O exame do coração revelou bulhas normofonéticas e sopro sistólico leve em área mitral. O exame do abdome foi normal e havia edema ++/4 em membros inferiores.
A paciente fazia uso de losartan 50 mg, hidroclorotiazida 50 mg e ácido acetilsalicílico 100 mg diários.
O eletrocardiograma (30/09/2003) revelou dissociação atrioventricular com ritmo juncional, freqüência de 50 bpm, duração de QRS de 80 mseg, com baixa voltagem no plano frontal (
Os exames laboratoriais revelaram hemoglobina 15 g/dl, hematócrito 45%, potássio de 5,8 mEq/l (sangue hemolisado) e sódio 138 mEq/l.
Foi feito o diagnóstico de doença do nó sinusal e prosseguiu a avaliação laboratorial, incluindo monitorização eletrocardiográfica ambulatorial.
A monitoração eletrocardiográfica ambulatorial de 24 horas de duração pelo sistema Holter (18/11/2003) revelou ritmo predominante sinusal, três extra-sístoles ventriculares em taquicardia ventricular e uma extra-sístole ventricular isolada. Havia freqüentes extra-sístoles atriais (645/h), das quais 570 isoladas, 36 pareadas e um episódio de taquicardia atrial com três batimentos. Foram diagnosticadas várias pausas sinusais de 4,3 seg em vigília, entre 20 e 21 horas (
Na evolução apresentou (29/12/2003) dor epigástrica de 4 horas de duração acompanhada de vômitos.
O exame físico (19/12/2003) revelou freqüência cardíaca 80 bpm, pressão arterial 180x100 mmHg, estertores crepitantes em bases de ambos hemitórax. O restante do exame físico não revelou dados positivos.
O eletrocardiograma (29/12/2003) demonstrou ritmo sinusal, freqüência de 72 bpm; área eletricamente negativa ântero-septal e supradesnivelamento de segmento ST de V1 a V3 e infradesnivelado em derivações II, III, aVF, V5 e V6. As alterações persistiram após o uso de 5 mg de dinitrato de isossorbida administrado por via sublingual (
Os exames laboratoriais revelaram 1 mg/dl de creatinina, 43 mg/dl de uréia, 139 mEq/l de sódio, 5,8 mEq/l de potássio, 49,4 ng/ml de CKMB e 7,8 ng/ml de troponina.
Foi feito o diagnóstico de infarto do miocárdio e foram administrados 200 mg de ácido acetilsalicílico por via oral e nitroglicerina por via endovenosa. Houve controle da pressão arterial e a paciente foi encaminhada para a cinecoronariografia para reperfusão coronária mecânica por angioplastia.
A cineangiografia, realizada 60 minutos após a chegada da paciente ao hospital, não revelou obstruções em coronárias, apesar da presença de área discinética em paredes ântero-lateral e apical de ventrículo esquerdo. Apresentou parada cardiorrespiratória em assistolia, sem resposta às manobras de ressuscitação e faleceu (30/12/2003).
O eletrocardiograma de 29/12/2003 (
A ventriculografia esquerda revela câmara com dimensões normais, exibindo área discinética restrita à parede ântero-lateral, correspondendo a território habitualmente irrigado por ramo diagonal da artéria coronária esquerda, com contração normal nas demais paredes musculares, inclusive no ápex. Observa-se regurgitação mitral de grau moderado.
O caso em questão refere-se a uma mulher de 88 anos com antecedente de hipertensão arterial sistêmica de longa data, acidente vascular cerebral há dois anos e diagnóstico recente de doença do nó sinusal. Internada na unidade de emergência por quadro clínico, eletrocardiográfico e laboratorial, de infarto agudo do miocárdio (IAM) de parede ântero-septal em Killip II com coronárias normais à cineangiocoronariografia, evoluiu para assistolia e óbito no primeiro dia pós-infarto.
O infarto do miocárdio com coronárias normais constitui uma entidade conhecida há mais de sessenta anos, antes mesmo do surgimento da arteriografia coronariana. À medida que o cateterismo cardíaco tornou-se uma ferramenta diagnóstica/terapêutica nas síndromes coronarianas agudas, ficou evidente que uma parcela dos pacientes poderia sofrer infarto agudo do miocárdio com coronárias normais.
A prevalência de infarto do miocárdio com coronárias normais parece estar aumentada no sexo feminino e em não-brancos. O estudo GUSTO 1 mostrou que 10,2% das mulheres e 6,8% dos homens com infarto do miocárdio com supradesnivelamento de ST tinham coronárias normais ou com lesões não-obstrutivas1.
Várias hipóteses foram sugeridas para explicar essa entidade, incluindo vasoespasmo, ponte miocárdica, distúrbios da coagulação adquiridos ou congênitos, agentes tóxicos, embolização, doenças do tecido conjuntivo, doenças infiltrativas, estados de desproporção entre oferta e consumo de oxigênio, entre outros2.
Em um estudo envolvendo 91 pacientes com infarto do miocárdio e coronárias normais extensamente investigados quanto à etiologia, Da Costa e cols.2 encontraram espasmo coronário em 15,5% dos pacientes, distúrbios congênitos da coagulação ou secundários ao uso de contraceptivos em 12,8%, doença do colágeno em 2,2% e embolização em 2,2%; dois terços dos pacientes permaneceram sem causa bem definida mesmo após extensa investigação.
A paciente em questão enquadra-se bem no perfil dos pacientes com infarto do miocárdio com supradesnivelamento de ST com coronárias normais, que apresentam com menor freqüência diabetes mellitus, dislipidemia, antecedente familiar de doença arterial coronariana e obesidade quando comparados com os pacientes em que se encontram obstruções significativas2.
O achado de coronárias normais no cateterismo cardíaco não exclui a presença de aterosclerose, uma vez que esses pacientes podem apresentar reserva de fluxo coronariano diminuída, disfunção endotelial coronariana e placas identificáveis pela ultra-sonografia endovascular. Tais achados são indicativos de aterosclerose inicial e correlacionam-se com maior taxa de eventos3.
Na paciente em questão a hipótese de vasoespasmo fica menos provável, tendo em vista a persistência do quadro clínico após administração de nitrato sublingual.
Os antecedentes, quadro clínico e laboratorial fornecidos são pouco compatíveis com muitas das etiologias citadas de infarto do miocárdio com coronárias normais. Tampouco demonstrou ponte miocárdica. Na faixa etária da paciente existe a remota probabilidade da ocorrência de infarto do miocárdio com supradesnivelamento de ST como primeira manifestação de doença do colágeno. Adicionalmente, não há relato de uso de drogas com potencial de causar infarto do miocárdio.
A hipótese de distúrbio da coagulação deve ser considerada tendo em vista passado de acidente vascular cerebral da paciente.
Por se tratar de paciente idosa, com queixas prévias sugestivas de insuficiência cardíaca, baixa voltagem ao eletrocardiograma, Holter de 24 horas sugestivo de doença estrutural do sistema de condução e infarto agudo do miocárdio com coronárias normais, a amiloidose senil é uma hipótese diagnóstica.
Tanto a prevalência quanto a gravidade da doença arterial coronariana aumentam com a idade em ambos os sexos. Estudos de necropsia mostram que mais da metade da população acima de sessenta anos tem doença arterial coronariana. Aos oitenta anos, 20% a 30% dos pacientes apresentam sintomas, muitas vezes equivalentes isquêmicos, como a dispnéia ao esforço presente nesse caso4.
Nesse contexto, a hipótese de embolização a partir de placa aterosclerótica não detectada pelo cateterismo com recanalização espontânea merece consideração especial.
Exceto pelo fato de que a paciente pudesse apresentar doença infiltrativa, o diagnóstico de doença do nó sinusal parece não estar relacionado ao infarto do miocárdio, uma vez que a degeneração do tecido de condução é responsável por aproximadamente metade dos casos de doença do nó sinusal nessa faixa etária5. Tampouco a hipótese de aterosclerose é reforçada pela presença de doença do nó sinusal, uma vez que a isquemia ainda tem papel controverso na etiologia da doença.
Cabe ressaltar, no entanto, que, em pacientes com insuficiência coronariana documentada, há relatos de piora da classe funcional da angina desencadeada pela bradicardia secundária à doença do nó sinusal, bem como a piora da dispnéia aos esforços. No idoso, a causa mais freqüente da doença do nó sinusal está relacionada à perda celular e infiltração de colágeno na região do nó sinusal e por todo o átrio. Essas modificações são mais acentuadas na região do nó sinusal, chegando a ocorrer destruição de até 90% das células aos 75 anos5.
Foi feito diagnóstico de doença do nó sinusal durante a avaliação ambulatorial da paciente com base no eletrocardiograma de repouso que mostrava um ritmo de escape juncional e Holter com presença de várias pausas sinusais superiores a 3 segundos, alternadas com episódios de taquiarritmias.
De fato, essa doença é definida de acordo com critérios eletrocardiográficos, uma vez que sinais clínicos e sintomas podem não estar presentes. Tonturas, pré-síncope ou síncope são as causas que geralmente levam o paciente ao médico, porém sintomas como dispnéia aos esforços, piora da angina ou palpitações podem também estar presentes5.
A doença do nó sinusal abrange qualquer disfunção do nó e inclui bradicardia sinusal inapropriada caracterizada pela freqüência cardíaca inferior a 60 bpm que não aumenta apropriadamente com o exercício, pausa sinusal maior que 3 segundos, bloqueio sino-atrial e a síndrome braditaquiarritmia definida por bradicardia sinusal ou juncional alternada com taquicardia atrial ou fibrilação atrial paroxística. As manifestações eletrocardiográficas podem ocorrer com ou sem sintomas.
A causa mais comum é a doença degenerativa idiopática. As doenças intrínsecas do sistema de condução, como hipertensão arterial sistêmica, doenças infiltrativas (amiloidose), doenças do colágeno e processos inflamatórios, também podem ser possíveis causas5. Efeitos de drogas que deprimem a função do nó sinusal, como antiarrítmicos, betabloqueadores, lítio e amitriptilina, além de distúrbios endócrinos, como hipotireoidismo, devem também ser lembrados como causas extrínsecas de doença do nó sinusal.
No presente caso, por se tratar de uma senhora idosa hipertensa sem história prévia de uso de medicações depressoras do nó sinusal, as causas intrínsecas, dentre elas a doença degenerativa, cuja incidência aumenta com a idade, é a causa mais provável. Na história da paciente não havia relato de sintomas claramente relacionados à arritmia documentada, uma vez que a paciente negava síncope e no relatório do Holter não há referência a sintomas causados pelas arritmias apresentadas, nem mesmo pelas pausas sinusais que ocorreram em vigília. Uma vez que o tratamento da doença do nó sinusal é guiado pelos sintomas, não havia, nesse caso, indicação absoluta de colocação de marcapasso. Implante de marcapasso, uso de medicamentos ou uma combinação de ambos são opções terapêuticas para tratamento da doença do nó sinusal.
O marcapasso é indicado quando há disfunção do nó sinusal documentada relacionada à bradicardia sintomática ou disfunção cronotrópica sintomática, e em caso em que a droga que causa a disfunção do nó não pode ser interrompida ou modificada.
Nos pacientes com síndrome braditaquiarritmia, o marcapasso pode ser indicado para o tratamento da bradicardia sintomática e as drogas antiarrítmicas para o tratamento dos episódios de taquiarritmias.
Pacientes com fibrilação atrial, ou pacientes com disfunção do nó sinusal, particularmente aqueles com alternância de bradicardia e taquicardia, apresentam um risco elevado para eventos tromboembólicos, mesmo após a colocação de marcapasso6. Essa correlação poderia explicar o acidente vascular cerebral sofrido previamente pela paciente.
Tendo em vista o diagnóstico de infarto agudo do miocárdio com supradesnivelamento de segmento ST com evolução de 4 horas, a paciente foi encaminhada para reperfusão coronariana mecânica. A opção pela angioplastia em detrimento da trombólise apóia-se em estudos que demonstraram superioridade da primeira com relação à sobrevida em curto e longo prazos mesmo em populações idosas7.
Pacientes maiores de 85 anos de idade têm mortalidade três vezes superior àqueles menores de 65 anos no período pós-infarto do miocárdio8.
A evolução para morte súbita no primeiro dia pós-infarto do miocárdio abre-nos um amplo leque diagnóstico. A gama de hipóteses diagnósticas para o óbito é vasta e inclui as complicações do infarto do miocárdio – arritmias, isquêmicas e mecânicas – complicações do cateterismo, tromboembolismo pulmonar e até mesmo um novo acidente vascular cerebral.
O óbito intra-hospitalar em pacientes com infarto agudo é causado substancialmente por falência circulatória decorrente de grave disfunção do ventrículo esquerdo ou por uma das complicações do infarto agudo9.
A disfunção grave do ventrículo esquerdo com choque cardiogênico é comum após infarto agudo e sua gravidade está correlacionada à extensão do infarto. Presença de infarto do miocárdio prévio, idade avançada, sexo feminino, diabetes e infarto de parede anterior são fatores de risco para o desenvolvimento de choque cardiogênico. A mortalidade é de 80% nos infartos que evoluem para choque cardiogênico10. Nesse caso, a apresentação clínica mais comum caracteriza-se por congestão pulmonar e sinais de baixo débito cardíaco. Esse quadro não esteve presente nessa paciente em particular.
No âmbito das complicações do infarto do miocárdio, devemos pensar em uma arritmia ventricular letal como causa da morte súbita dessa paciente. Morte por taquiarritmias ventriculares no infarto agudo do miocárdio é uma das causas mais freqüentes de óbito, uma vez que representa cerca de 90% de tais casos9. Em pacientes com infarto agudo com supradesnivelamento de ST a incidência de arritmias ventriculares é maior do que em pacientes com angina instável ou infarto sem supradesnivelamento de ST. Essas arritmias podem ser causadas por uma nova agressão isquêmica ou por alterações anatômicas presentes anteriormente como áreas de necrose antigas que serviriam como circuitos de reentrada para a estimulação elétrica. É importante ressaltar que, na paciente em questão, o eletrocardiograma já demonstrara área eletricamente inativa ântero-septal e a cineangiocoronariografia revelara uma área discinética em paredes ântero-lateral e apical, o que poderia corresponder a uma área de aneurisma que serviria como substrato anatômico para as arritmias. Dados epidemiológicos demonstraram que uma nova agressão isquêmica é o mecanismo mais relacionado à ocorrência de arritmias ventriculares no cenário do infarto agudo, porém a presença de substrato pré-estabelecido é uma causa mais provável nesse caso. Vale ressaltar ainda que uma bradiarritmia fatal também se inclui entre as possíveis causas do óbito, tendo em vista o diagnóstico prévio de doença do nó sinusal.
Outra complicação do IAM que poderia evoluir rapidamente para morte seria a ruptura cardíaca. A ruptura de parede livre ocorre em cerca de 2% a 3% dos pacientes, porém é responsável por cerca de 10% da mortalidade intra-hospitalar nos casos de infarto agudo11. Depois do choque cardiogênico e das arritmias ventriculares, representa a terceira causa mais comum de morte no pós-infarto. A ruptura de parede livre do ventrículo esquerdo é oito a dez vezes mais freqüente do que a ruptura tanto do septo ventricular quanto de músculos papilares. A ruptura ocorre nos primeiros cinco dias em cerca de 50% dos pacientes e em duas semanas após o infarto em cerca de 90%12. A ruptura da parede livre ocorre somente nos infartos transmurais. Os fatores de risco para ruptura de parede livre do ventrículo esquerdo são idade avançada (> setenta anos), sexo feminino, hipertensão arterial, primeiro infarto do miocárdio, ausência de circulação colateral12. Na ruptura aguda, os pacientes apresentam dissociação eletromecânica e morte súbita. O início súbito de dor torácica ao tossir pode anunciar o início da ruptura cardíaca. Alguns pacientes podem ter um curso subagudo como resultado de uma ruptura tamponada, com dor torácica sugestiva de pericardite, náuseas e hipotensão13.
Em um grande estudo retrospectivo realizado pós-infarto13, 6,2% dos pacientes sofreram ruptura cardíaca e, cerca de um terço, apresentou doença subaguda. Existem três tipos de ruptura da parede livre: a) a ruptura tipo I, que ocorre dentro das primeiras 24 horas pós-infarto e é uma ruptura de toda a espessura da parede; b) a ruptura tipo II, que ocorre como resultado da erosão do miocárdio no local infartado e, c) a ruptura tipo III, que ocorre mais tardiamente e é localizada nas bordas ao redor do infarto onde há miocárdio normal. A única chance de sobrevivência nesses casos é o diagnóstico imediato e cirurgia de emergência.
No caso da paciente em questão, a ruptura de parede livre do ventrículo esquerdo do tipo I ou a ruptura de um eventual aneurisma justificaria a morte súbita por rápido desenvolvimento de tamponamento cardíaco e posterior parada cardíaca por dissociação eletromecânica e assistolia, visto que ela apresentava a maioria dos fatores de risco para essa complicação.
Uma outra complicação mecânica do infarto é a insuficiência mitral aguda que ocorre com uma maior freqüência nos infartos de parede inferior por ruptura do músculo papilar póstero-medial. Tal complicação ocorre em cerca de 1% dos pacientes com infarto do miocárdio e responde por 7% dos choques cardiogênicos, representando, em algumas casuísticas, 5% da mortalidade após o infarto do miocárdio14. Em cerca de 50% dos casos o infarto é pequeno e a ruptura geralmente ocorre entre o segundo e o sétimo dias pós-infarto, embora determinados estudos demonstrem um tempo médio de ruptura de aproximadamente 13 horas15. Nesses casos, a apresentação clínica mais comum seria súbita e intensa congestão pulmonar, com desenvolvimento de edema pulmonar ou choque cardiogênico, o que não foi o caso nesta paciente.
No âmbito das complicações mecânicas relacionadas ao infarto, devemos considerar a ruptura do septo interventricular. Essa complicação responde por 5% da mortalidade peri-infarto, e sua incidência caiu drasticamente após o advento da reperfusão precoce16. Os fatores de risco são idade avançada, sexo feminino, hipertensão arterial, infarto de parede anterior, taquicardia e sinais de congestão pulmonar na internação hospitalar17. Geralmente, a ruptura acontece entre o segundo e o quinto dias pós-infarto, mas existem relatos de ocorrências nas primeiras 24 horas17. Essa complicação se manifesta com sinais de congestão pulmonar, falência biventricular e hipotensão. Tais achados não foram evidenciados na paciente em questão.
Finalmente, inclui-se no diagnóstico diferencial o óbito por complicações do cateterismo cardíaco. Entre elas destacam-se infarto do miocárdio em 0,05%, acidente vascular cerebral em 0,07%, arritmias em 0,38% e perfuração de câmaras em 0,28%. A mortalidade relacionada ao procedimento é de 0,11%18.
Assim, temos como hipóteses para o óbito: 1) complicação mecânica do infarto agudo do miocárdio – ruptura de parede livre do coração. 2) Morte súbita por arritmia ventricular.
The case of this 88-year-old woman who died during an acute myocardial infarction is a glimpse of the future of cardiovascular medicine. Demographic trends indicate that the practice of cardiology will increasingly involve the "elderly old", in their eighties and nineties. Increasingly, this segment of our patient population will consist predominantly of women. Aspects of this woman's case are all too common. She had classical coronary risk factors, including advanced age and longstanding hypertension. She had sustained a previous cerebrovascular accident, although we were not told whether this was hemorrhagic or ischemic. Nonetheless, a prior stroke substantially augments for a further cardiovascular complication.
Although typical myocardial infarction in such an individual would not be unusual, certain aspects of this particular case warrant further comment. This woman was taken urgently to the cardiac catheterization laboratory for primary angioplasty. I find this disposition of a woman within the first hours of an acute myocardial infarction very appropriate. I congratulate the emergency and invasive cardiology team for their appropriately aggressive stance. All too often, we underestimate the symptoms of ischemic heart disease in women. Studies in North American have shown a systemic under-recognition of myocardial ischemic symptoms, and less aggressive management of women than men and in older versus younger individuals. The benefits of mechanical revascularization appear evident, although the numbers of individuals randomized in clinical trials in this age stratum are understandably fewer than with younger individuals.
I am sure, however, that the invasive cardiology team was surprised to find angiographically normal-appearing coronary arteries. Dra. Ariane Macedo has already provided us with an extensive differential diagnosis of myocardial infarction with normal-appearing coronary arteries. Noteworthy possibilities include vasospasm, most typical in younger individuals. Embolic causes with lysis of the occluding thrombus by the time of angiography also bear consideration. Bland emboli could be one source of a coronary thrombus. Indeed, this woman had documented sick sinus syndrome with tachybrady syndrome. However, there is no documentation of atrial fibrillation or atrial flutter, arrhythmic conditions associated with cardiac source of emboli. Septic emboli from endocarditis, for example, also could cause acute myocardial infarction. Indeed, this woman's history and left ventriculogram were compatible with significant mitral regurgitation. However, there were no clinical signs of sepsis, rendering this possibility less likely. In North America, an additional consideration for acute myocardial infarction without typical coronary atherosclerosis would be cocaine use. That diagnosis probably does not pertain to the current case.
However, we always query patients with acute myocardial infarction about substance abuse. Another cause of acute myocardial infarction with extensive distal wall-motion abnormalities on left ventriculogram, the Takotsubo syndrome, also can cause myocardial infarction with angiographically normal-appearing coronary arteries. Typically, the electrocardiogram shows more prominent T-wave inversion and the ST segment elevation with reciprocal ST segment depression so well described by Dr. Paulo Moffa in his discussion of the electrocardiogram. In addition, the Takotsubo syndrome usually is precipitated by a severe emotional shock. There is no evidence for this in the case at hand. Although Takotsubo syndrome affects women much more often than men, these women tend to be much younger than 88 years old. Finally, rendering the diagnosis of Takotsubo syndrome highly unlikely, the prognosis is excellent with recovery of ventricular function, rather than rapid progression to death, as in the present case. Dra. Ariane Macedo raised the possibility of infiltrative cardiomyopathy. Given the focal nature of the electrocardiographic changes, and the regionality of the extensive left ventricular dysfunction noted on the left ventriculogram by Dr. Eulogio Martinez, I consider infiltrative disease much less likely as an explanation for this patient's current clinical scenario.
In the presence of traditional coronary risk factors, I believe that the likely explanation for the acute myocardial infarction in this woman is atherosclerotic coronary artery disease. We have learned over the last decade or so that many acute myocardial infarctions result from a physical disruption of atherosclerotic plaques that do not necessarily cause a critical coronary artery stenosis. We also have learned that the coronary arteriogram vastly underestimates the extent of coronary atherosclerosis.
Traditionally thought of as a segmental disease, classical autopsy studies and contemporary intravascular ultrasound studies show the ubiquity of intimal disease in individuals with coronary atherosclerosis. The lesions usually occur much more diffusely than the coronary angiogram would suggest. The Glagov phenomenon, compensatory enlargement or outward remodeling, protects the caliber of the lumen of the coronary artery affected by atherosclerosis. It is not until the late stage of this disease that luminal encroachment visible on the angiogram occurs. A disruption with thrombosis of a plaque at a site of outward remodeling of the artery, followed by lysis or distal embolization of the thrombus into the microcirculation after fragmentation could explain the apparently normal coronary arteriogram in the face of the documented myocardial infarction in this woman. I prefer use of the cumbersome term "angiographically normal-appearing coronary arteries" to the shorter but all too often misleading term "normal coronary arteries" to describe the cinecoronariographic findings, to remind us of the limitations of luminography in gauging atherosclerosis, as disease of the artery wall that only occasionally narrows the lumen.
The other particular feature of this clinical scenario that bears comment is the cause of death. Presumably, this woman who succumbed within the first day of an acute myocardial infarction was in a monitored ward. There is no mention of a brady- or tachyarrhythmia as a primary complication of her myocardial infarction that led to her death. We are not told of a downward hemodynamic spiral preceding the terminal event that would suggest primary pump failure or cardiogenic shock in the woman with severe impairment of left ventricular function. While the case protocol is not explicit, the clinical scenario of sudden, unheralded cardiac arrest and a prolonged resuscitative effort evokes the clinical scenario now called pulseless electrical activity cardiac arrest (PEA), previously referred to as electromechanical dissociation. In patients in the acute phase of myocardial infarction, I agree with Dra. Ariane Macedo that cardiac rupture should be considered in such circumstances. Dr. Paulo Moffa described low voltage in the frontal plane on the electrocardiogram. This could indicate pericardial effusion. However, this electrocardiographic finding preceded by some time the abrupt death and could well be unrelated to a hemopericardium secondary to cardiac rupture. However, as Dra. Ariane Mcedo pointed out, this woman had many risk factors for cardiac rupture, including longstanding hypertension, female gender, advanced age, and no history of prior myocardial infarction. While myocardial ruptures typically occur later than the first day after onset of infarct symptoms, the clinical scenario strongly suggests consideration of this cause of death.
À necropsia, o principal achado foi infarto do miocárdio, parcialmente hemorrágico, que atingia a parede anterior do ventrículo esquerdo e as porções adjacentes a ela do septo e da parede anterior do ventrículo direito. Nessas duas últimas localizações, houve ruptura do miocárdio, com comunicação interventricular e extravasamento de sangue para o saco pericárdico (
As artérias coronárias apresentavam obstrução moderada por aterosclerose (máximo de 69% no ramo circunflexo da artéria coronária esquerda e de 77% na artéria coronária direita); no ramo interventricular anterior, havia trombo mural não-oclusivo que, em conjunto com a aterosclerose, determinava obstrução de 82% (
O estudo microscópico revelou a existência de fibrose da região do nó sinusal (
Havia também hipertrofia do miocárdio do ventrículo esquerdo, secundária a hipertensão arterial sistêmica; ainda relacionada com essa doença detectou-se arteriosclerose renal benigna.
A causa mais comum de infarto do miocárdio é a trombose coronariana, em geral oclusiva e secundária à ruptura de placa de aterosclerose. A placa mais propensa a romper caracteristicamente tem grande conteúdo lipídico e é responsável por obstrução grave das artérias coronárias, ao menos ao estudo histopatológico (embora possa não sê-lo ao estudo cineangiocoronariográfico). Isso não ocorreu, no entanto, no presente caso, em que não havia trombo recente, a despeito de a paciente ter morrido no primeiro dia pós-infarto. Assim sendo, duas possibilidades principais devem ser consideradas na tentativa de explicação da necrose isquêmica do miocárdio: o mais provável é que esta tenha sido decorrente de vasoespasmo, o qual em geral atinge artérias com lesões ateroscleróticas com oclusão menos acentuada, como as dessa paciente; alternativamente, o infarto pode ter sido causado por embolia do trombo encontrado no ramo interventricular anterior. O fato de que houve hemorragia na lesão demonstra que, após interrupção do fluxo sangüíneo que causou a morte das fibras miocárdicas, este foi restabelecido e reforça a possibilidade de o vasoespasmo ter acontecido, pois se a embolia tivesse levado à oclusão ela deveria ser fixa.
Em relato recente19, mostramos 14 casos de tamponamento cardíaco presentes em necropsias realizadas no Laboratório de Anatomia Patológica do Instituto do Coração entre 2000 e 2004. A média de idade dos pacientes submetidos a necropsia e que sofreram ruptura do miocárdio foi 70,1 anos, a mediana 74; predominaram os homens (55%). A ruptura ocorreu em média no dia 6,6 da evolução do infarto (mediana 4). A ruptura ocorreu no primeiro infarto em 72,2% dos casos, hipertensão arterial foi diagnosticada em 77,8% dos casos e diabetes mellitus em 27,8% dos casos.
A
A ruptura dupla foi encontrada no presente caso e em mais um da nossa casuística. É uma forma pouco comum da complicação, mas já relatada anteriormente21-25. Quando indicada nesses estudos, a proporção de dupla ruptura no total dos casos com essa complicação foi parecida com a nossa (2/18=11,1%), variando de 7,7 a 12,9%21,22,25. Entretanto, são poucos os casos descritos em que a parede livre rota tenha sido do ventrículo direito24,25.
1. Hochman JS, Tamis JE, Thompson TD et al. Sex, clinical presentation, and outcome in patients with acute coronary syndromes. Global Use of Strategies to Open Occluded Coronary Arteries in Acute Coronary Syndromes IIb Investigators. N Engl J Med 1999; 341:226-32.
2. Da Costa A, Isaaz K, Faure E, Mourot S, Cerisier A, Lamaud M. Clinical characteristics, aetiological factors and long-term prognosis of myocardial infarction with an absolutely normal coronary angiogram; a 3-year follow-up study of 91 patients. Eur Heart J 2001;22(16):1459-65.
3. Bugiardini R, Bairey Merz CN. Angina with "normal" coronary arteries: a changing philosophy. JAMA 2005;293(4):477-84.
4. Kuller L, Fisher L, McClelland R et al. Differences in prevalence of and risk factors for subclinical vascular disease among black and white participants in the Cardiovascular Health Study. Arterioscler Thromb Vasc Biol 1998;18(2):283-93.
5. Braunwald E, Zipes DP, Libby P. Heart disease: A Textbook of Cardiovascular Medicine. 7th Ed. Philadelphia: WB Saunders, 2004.
6. Andersen HR, Nielsen JC, Thomsen PE et al. Arterial thromboembolism in patients with sick sinus syndrome: Prediction from pacing mode, atrial fibrillation and echocardiographic findings. Heart 1999;81:412-8.
7. Weaver WD, Simes RJ, Betriu A et al. Comparison of primary coronary angioplasty and intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review. JAMA 1997;278(23):2093-8. Erratum in: JAMA 1998;279(23):1876.
8. Rich MW. PRICE-2 Organizing Committee; PRICE-2 Investigators. Executive summary: Second Pivotal Reseach in Cardiovascular Syndromes in the Eldery(Price II). Symposium. Acute Coronary syndromes in the elderly: Mechanisms and managements. Am J Geriatr Cardiol 2003;12:307-18.
9. Chatterjee K. Complications of acute myocardial infarction. Curr Probl Cardiol 1993;18:1-79.
10. Menon V, White H, LeJemtel T, Webb JG, Sleeper LA, Hochman JS. The Clinical profile of patients with suspect cardiogenic shock due to predominant left ventricular failure. J Am Coll Cardiol 2000;36:1071-6.
11. Becker RC, Gore JM, Lambrew C et al. A composite view of cardiac rupture in The United States: National registry of myocardial infarction. J Am Coll Cardiol 1996;27:1321-6.
12. Topol EJ, Griffin BP. Manual of Cardiovascular Medicine. 2nd Edition. Philadelphia: Lippincott Williams & Wilkins, 2004.
13. Lopez-Sendon J, Gonzalez A, Lopez de Sa E et al. Diagnosis of subacute ventricular wall rupture after acute myocardial infarction:sensivity and specificity of clinical, hemodynamic and echocardiographic criteria. J Am Coll Cardiol 1992;19:1145-53.
14. Hochman JS, Buller CE, Sleeper LA et al. Cardiogenic shock complicating acute myocardial infarction-etiologies, management and outcome: a report from the SHOCK Trial Registry. Should we emergently revascularize occluded coronaries for cardiogenic shock? J Am Coll Cardiol 2000;36:1063-70.
15. Voci P, Bilotta F, Caretta Q, Mercanti C, Marino B. Papillary muscle perfusion pattern: a hypothesis for ischemic papillary muscle dysfunction. Circulation 1991:1714-8.
16. Topaz O, Taylor AL. Interventricular septal rupture complicating acute myocardial infarction: from pathophysiologic features to the role of invasive and non invasive diagnostic modalites in current management. Am J Med 1992;93:683-8.
17. Crenshaw BS, Granger CB, Birnbaum Y et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation 2000;101:27-32.
18. Baim DS, Grossman W. Complications of cardiac catheterization. In Baim DS, Grossman W. (ed.) Cardiac Catheterization, Angiography and Intervention. Baltimore: Williams & Wilkins, 1996.
19. Favarato D, Gutierrez PS. Parada cardíaca em atividade elétrica sem pulso em homem de 49 anos, no 23º dias após infarto agudo. Arq Bras Cardiol 2005;84:492-4.
20. Okabe M, Fukuda K, Arakawa K. Postmortem evaluation of morphologic changes in the infarcted myocardium that predict ventricular septal rupture in acute anteroseptal infarction. Jpn Circ J 1999;63:485-9.
21. Figueras J, Cortadellas J, Soler-Soler J. Comparison of ventricular septal and left ventricular free wall rupture in acute myocardial infarction. Am J Cardiol 1998;81:495-7.
22. Vlodaver Z, Edwards JE. Rupture of ventricular septum or papillary muscle complicating myocardial infarction. Circulation 1977;55:815-22.
23. Mann JM, Roberts WC. Fatal rupture of both left ventricular free wall and ventricular septum (double rupture) during acute myocardial infarction: analysis of seven patients studied at necropsy. Am J Cardiol 1987;60:722-4.
24. Reiner JS, Lundergan CF, Tenner MP, Abraham AA, Ross AM. Ventricular free wall and septal rupture (double rupture): a "pseudocomplication" during post-infarction laser angioplasty. Cathet Cardiovasc Diagn 1993;30:147-9.
25. Tanaka K, Sato N, Yasutake M et al. Clinicopathological characteristics of 10 patients with rupture of both ventricular free wall and septum (double rupture) after acute myocardial infarction. J Nippon Med Sch 2003;70:21-7.
Paulo Sampaio Gutierrez InCor Av. Dr. Eneas de Carvalho Aguiar, 44 05403-000 - São Paulo, SP E-mail:
Vera Demarchi Aiello (
Case 4/2005 – Fatal myocardial infarction in a 88-year-old woman (Instituto do Coração do Hospital das Clínicas - FMUSP, São Paulo, Brasil)
São Paulo, SP - Brazil
An 88-year-old women sought medical care (12/29/03) complaining about a 4-hour duration epigastric pain, followed by vomiting.
The patient had knowledge of her longstanding hypertension, having undergone a cerebrovascular accident two years earlier, without motive sequels. Three months before, dyspnea due to moderate exercise and lower limb edema took place. She denied syncope.
Physical assessment (10/03/03) showed 68-bpm heart rate and blood pressure of 180/80 mmHg. Lung examination did not show any problems, as well as abdomen exam. However, heart examination exhibited normophonetic sounds and mild systolic murmur in the mitral area. A ++/4 edema was identified in the lower limbs.
The patient made daily use of losartan 50 mg, hydrochlorothiazide 50 mg, and acetylsalicylic acid 100 mg.
EKG (09/30/03) displayed atrioventricular dissociation with junctional rhythm, 50-bpm heart rate, 80 msec QRS, with front plan low voltage (
Hemoglobin 15 g/dl, hematocrit 45%, potassium of 5.8 mEq/l (hemolized blood) and 138 mEq/l sodium were detected at laboratorial examinations.
Sinus node disease diagnosis was achieved, followed by laboratorial assessment, including ambulatory electrocardiographic monitoring.
Holter 24-hour ambulatory electrocardiographic monitoring (11/18/03) showed prevailing sinus rhythm, 3 ventricular extra-systoles under ventricular tachycardia and a single ventricular extra-systole. Frequent atrial extra-systoles (645/h) took place, from which 570 were isolated, 36 matched, and a 3-heartbeat atrial tachycardia episode. Several under care 4.3-sec sinus pauses, between 8 pm and 9 pm, were detected (
Evolution demonstrated (12/29/03) 4-hour epigastric pain followed by vomiting.
Physical examination (12/19/03) revealed heart rate of 80 bpm, 180/100 mmHg blood pressure, crepitant rales at both hemithorax bases, with no positive data in the remaining of the test.
The EKG (12/29/03) displayed sinus rhythm, 72-bpm heart rate, electrically negative anteroseptal area, an elevated ST segment from V1 to V3, and depressed in II, III, aVF, V5, and V6 derivations. Changes remained after use of sublingual-administrated 5mg of isosorbide dinitrate (
Laboratorial tests showed 1 mg/dl of creatinine, 43 mg/dl of urea, 139 mEq/l of sodium, 5.8 mEq/l of potassium, 49.4 ng/ml of CKMB, and 7.8 ng/ml of troponin.
Myocardial infarction diagnosis was performed and 200mg per oral acetylsalicylic acid and endovenous nitroglycerin were administrated. Blood pressure was controlled and the patient sent to cinecoronariography for mechanical coronary reperfusion through angioplasty.
Cineangiography, 60 minutes after the patient had arrived at the hospital, did not display coronary obstructions. Despite dyskinetic area in left ventricular anterolateral and apical walls, the patient showed asystole cardiopulmonary arrest, without response to resuscitation procedures, and died (12/30/03).
Electrocardiogram on 12/29/03 (
Left ventriculography displays normal dimension chamber, showing anterolateral wall-restricted dyskinetic area, corresponding to an often irrigated area by left coronary artery diagonal branch, with normal contraction of other muscle walls, including at apex. Mild mitral regurgitation is observed.
The case refers to an 88-year-old woman with longstanding systemic hypertension history, cerebrovascular accident two years before, and current sinus node disease diagnosis. Admitted at emergency due to clinical, electrocardiographic and laboratorial features of Killip II anteroseptal wall myocardial infarction with normal coronary arteries at coronary angiography, she evolved to asystole and death on the first post-infarction day.
Normal coronary artery myocardial infarction has been known for more than 60 years, even before coronary arteriography. As long as cardiac catheterization has become a diagnostic/therapeutic instrument in acute coronary syndromes, part of patients could clearly suffer acute myocardial infarction with normal coronary arteries.
Normal coronary artery myocardial infarction frequency appears increased among the female sex and non-Caucasian individuals. GUSTO 1 study demonstrated that 10.2% of women and 6.8% of men with ST elevating myocardial infarction had normal or non-obstructive lesion coronary arteries1.
Vasospasm, myocardial bridging, acquired or congenital coagulation disorders, toxic agents, embolization, conjunctive tissue diseases, infiltrative diseases, disproportion status between oxygen offer and consumption2, were among assumptions suggested to explain such entity.
In an etiology-concerned 91 myocardial infarction and normal coronary artery patient study, Da Costa et al.2 found coronary spasm in 15.5% of patients, coagulation or secondary congenital disorders to contraceptive use in 12.8%, collagen disease in 2.2%, and embolization in 2.2% of patients. Two-thirds of them remained without well-defined cause, even after extensive investigation.
The object individual fits well in the profile of patients with normal coronary artery, ST elevating myocardial infarction patients who show low frequency diabetes mellitus, dyslipidemia, family history of coronary artery disease and obesity when compared to those with significant obstructions2.
Normal coronary arteries found in cardiac catheterization does not exclude thee presence of atherosclerosis, as those patients may show decreased coronary flow reserve, coronary endothelial dysfunction, and recognizable plaque through endovascular ultrasound imaging. Such findings indicate initial atherosclerosis and correlate with a higher event rate3.
Vasospasm hypothesis is less probable in the patient due to unchanged clinical features after sublingual nitrate administration.
Many mentioned normal coronary artery myocardial infarction etiologies are little compatible with history, clinical and laboratorial features provided. Neither showed by myocardial bridging. In the patient's age range there is the remote probability of myocardial infarction with elevated ST as first collagen disease manifestation. Furthermore, there are no evidences of drug use causing myocardial infarction.
Coagulation disorder shall be taken into consideration due to patient's cerebrovascular accident history.
Senile amyloidosis represents diagnostic assumption due to our patient be aged, with prior heart failure suggestive complaints, low voltage at EKG, 24-hour Holter suggesting conductive system disease and normal coronary artery acute myocardial infarction.
On the other hand, both coronary artery disease prevalence and severity increase with age in both genders. Necropsy studies have demonstrated that more than half of over 60-year-old population have coronary artery disease. At 80, 20% to 30% of patients show symptoms, often ischemic equivalent, as dyspnea during exercise, which is present in this case4.
Embolization hypothesis from cardiac catheterization undetected atherosclerotic with spontaneous recanalization deserves special importance in such context.
Except for the fact that the patient could have shown infiltrative disease, sinus node disease diagnosis does not appear to be related to myocardial infarction, as conductive tissue degeneration is responsible for nearly half of sinus node disease cases in that age range5. Neither is atherosclerosis hypothesis reinforced by sinus node disease presence, as ischemia still has had controversial role in disease's etiology.
Important to mention is that among documented coronary failure patients there are accounts of angina functional class worsening unleashed by bradycardia secondary to sinus node disease, as well as worsening of dyspnea during exercise. The most frequent cause of sinus node disease among elderly individuals is related to cell loss and collagen infiltration in sinus node area and the whole atrium. Such changes are greater in sinus node area, with destruction of up to 90% of cells at 75 years of age5.
Sinus node diagnosis was carried out during ambulatory assessment of the patient based on EKG at rest showing junctional escape rhythm and Holter with presence of several sinus pauses higher than 3 seconds, alternated with tachyarrhythmia episodes.
Such disease is indeed defined in accordance with electrocardiographic criteria, since clinical signs and symptoms may not be present. Dizziness, pre-syncope and syncope are causes that usually make the patient see the physician. However, symptoms as dyspnea during exercise, angina worsening or palpitations can be also present5.
Sinus node disease comprises any node dysfunction and unsuitable sinus bradycardia characterized by heart rate lower than 60 bpm, which does not properly increase with exercise. Sinus pause longer than 3 seconds, sinus-atrial block, and brady-tachyarrhythmia defined by sinus or junctional bradycardia, alternating with atrial tachycardia or paroxystic atrial fibrillation, are also included. Electrocardiographic expressions may take place either with or without symptoms.
Idiopathic degenerative disease is the most usual cause. Basic conductive system diseases as systemic hypertension, infiltrative disease (amyloidosis), collagen disease, and inflammatory processes can also be possible causes5. Effects from sinus node function depressing drugs, such as anti-arrhythmic, beta-blockers, lithium, and amitriptyline, besides endocrine disorders as hypothyroidism, must also be regarded as external sinus node disease causes.
For being an elderly hypertensive woman without sinus node depressive drug use history, intrinsic causes, as degenerative diseases, whose incidence increases with the age, is the most probable cause. There was no account of documented arrhythmia-related symptoms as the patient denied syncope. There was also no reference in Holter report concerning symptoms caused by featured arrhythmias, not even due to sinus pauses under care. As the treatment is symptom-guided, there was no indication of pacemaker placement in this case. Pacemaker implantation, medications, or a combination of them, are therapeutic options for sinus node disease.
Pacemaker is indicated in presence of documented sinus node disease related to symptomatic bradycardia or symptomatic chronotropic dysfunction, and in cases the drug causing node dysfunction cannot be interrupted or modified.
In brady-tachyarrhythmia patients, pacemaker can be indicated for symptomatic bradycardia treatment. Anti-arrhythmic drugs are recommended for tachyarrhythmia episode therapy.
Atrial fibrillation or sinus node dysfunction patients, especially those with bradycardia and tachycardia alternation, show high risks for thromboembolic occurrences, even after pacemaker placement6. Such correlation may explain previous cerebrovascular accident undergone by the patient.
Facing the diagnosis of acute myocardial infarction with ST segment elevation and 4-hour evolution, the patient was submitted to mechanical coronary reperfusion. Studies support angioplasty option in detriment to thrombolysis based on advantages concerning short- and long-term survival among elderly populations7.
Patients over 85 years of age have mortality rate three times higher than those under 65, in post-myocardial infarction period8.
Sudden death evolution on the first post-AMI day provides us with many diagnostic options. Diagnostic death hypotheses include myocardial infarction complications (arrhythmias, ischemic and mechanical), catheterization complications, pulmonary thromboembolism, and even a new cerebrovascular accident.
In-hospital death in acute myocardial infarction patients is caused largely circulatory failure due to severe left ventricular dysfunction or one of acute myocardial infarction complications9.
Severe left ventricular dysfunction with cardiogenic shock is usual after acute myocardila infarction. Such severity is correlated with infarction extension. Risk factors for cardiogenic shock development are presence of previous myocardial infarction, old age, female gender, diabetes, and anterior wall infarction. Mortality rate is 80% in infarctions evolving to cardiogenic shock10. In this case, the most common practice characterizes for pulmonary congestion and low cardiac outcome signs. This patient did not show such features.
Concerning myocardial infarction complications, lethal ventricular arrhythmia must be considered as sudden death cause of this patient. Death due to ventricular tachyarrhythmias in AMI is one of the most frequent death causes, as it represents 90% of those cases9. In patients with ST elevation acute myocardial infarction, ventricular arrhythmias incidence is greater than in those with unstable angina or non-ST elevation infarction. Those may be caused by a new ischemic attack or due to previous anatomic changes as old necrosis areas, which served as reentry circuits for electrical stimulation. Regarding this patient, it is important to emphasize that EKG already shows an electrically inactive anteroseptal area and coronary angiography demonstrated dyskinetic area in anterolateral and apical walls, which may correspond to an aneurism area as anatomic substrate for arrhythmias. Epidemiological data demonstrate new ischemic attack as the highest related mechanism to ventricular arrhythmias in acute myocardial infarction. However, presence of pre-established substrate is a more probable cause in this case. Fatal bradyarrhythmia is also included as possible death causes concerning previous sinus node disease diagnosis.
Another fast evolving to death AMI complication would be cardiac rupture. Free wall rupture takes place in about 2 to 3% of patients. However, it is responsible for approximately 10% of in-hospital mortality due to acute myocardial infarction11. It is the third most common post-infarction death cause after cardiogenic shock and ventricular arrhythmias. Left ventricular free wall rupture is 8 to 10 times more frequent than ventricular septum and papillary muscle rupture. It takes place on the first five days in about 50% of patients, and 90% in two post-infarction weeks12. Free wall rupture only occurs in transmural infarction. Old age (>70 years old), female gender, hypertension, first myocardial infarction, and absence of collateral circulation12 are risk factors for left ventricular free wall rupture. In acute rupture, patients show electromechanical dissociation and sudden death. Sudden thoracic pain when coughing may reveal the beginning of cardiac rupture. Some patients may have subacute pattern as result from tamponed rupture with suggestive thoracic pain from pericarditis, nausea, and hypotension13.
In a large post-infarction retrospective study13, approximately 6.2% of patients had cardiac rupture and about a third showed subacute disease. There are three types of free wall rupture: a) type I rupture, which happens within the first 24 post-infarction hours and it is a full wall thickness rupture; b) type II rupture occurs as a result from myocardial erosion in infarcted area; and c) type III rupture, which takes place later and it is located on edges around the infarction where normal myocardium is present. The only chance for survival in those cases is immediate diagnosis and emergency surgery.
In this patient case, type I left ventricular free wall rupture or a possible aneurism rupture would justify sudden death due to cardiac tamponade development, and further cardiac arrest due to electromechanical dissociation and asystole, as she showed most risk factors for that complication.
Another mechanical complication of infarction is acute mitral failure occurring more often in inferior wall infarction due to rupture of posteromedial papillary muscle. Such complication takes places in approximately 1% of myocardial infarction patients and is responsible for 7% of cardiogenic shocks. In some cases, it represents 5% of post-myocardial infarction mortality14. In approximately 50% of cases, infarction is small and rupture usually takes place between the second and seventh post-infarction day, although some studies show a mean rupture time of about 13 hours15. In those cases, the most frequent clinical presentation would be sudden and intensive pulmonary congestion with pulmonary edema or cardiogenic shock development, which did not occur with this patient.
In the extent of infarction-related mechanical complications, we must consider interventricular septum rupture. Such complication is responsible for 5% of peri-infarction mortality. Furthermore, its incidence has considerably decreased after the beginning of early reperfusion16. Risk factors are old age, female sex, hypertension, anterior wall infarction, tachycardia, and pulmonary congestion signs at hospital admission17. Rupture usually occurs between the second and fifth post-infarction day. However, occurrences within the first 24 hours have been observed17. It reveals signs of pulmonary congestion, biventricular failure, and hypotension. Such findings were not verified in our patient.
Finally, death due cardiac catheterization complications is included in differential diagnosis. Myocardial infarction in 0.05%, cerebrovascular accident in 0.07%, arrhythmias in 0.38%, and chamber perforation in 0.28% distinguish among them. Procedure-related mortality is 0.11%18.
So we have 1) mechanical complication of acute myocardial infarction – heart free wall rupture; 2) Sudden death due to ventricular arrhythmia, as death hypothesis.
The case of this 88-year-old woman who died during an acute myocardial infarction is a glimpse of the future of cardiovascular medicine. Demographic trends indicate that the practice of cardiology will increasingly involve the "elderly old", in their eighties and nineties. Increasingly, this segment of our patient population will consist predominantly of women. Aspects of this woman's case are all too common. She had classical coronary risk factors, including advanced age and longstanding hypertension. She had sustained a previous cerebrovascular accident, although we were not told whether this was hemorrhagic or ischemic. Nonetheless, a prior stroke substantially augments for a further cardiovascular complication.
Although typical myocardial infarction in such an individual would not be unusual, certain aspects of this particular case warrant further comment. This woman was taken urgently to the cardiac catheterization laboratory for primary angioplasty. I find this disposition of a woman within the first hours of an acute myocardial infarction very appropriate. I congratulate the emergency and invasive cardiology team for their appropriately aggressive stance. All too often, we underestimate the symptoms of ischemic heart disease in women. Studies in North American have shown a systemic under-recognition of myocardial ischemic symptoms, and less aggressive management of women than men and in older versus younger individuals. The benefits of mechanical revascularization appear evident, although the numbers of individuals randomized in clinical trials in this age stratum are understandably fewer than with younger individuals.
I am sure, however, that the invasive cardiology team was surprised to find angiographically normal-appearing coronary arteries. Dr. Ariane Macedo has already provided us with an extensive differential diagnosis of myocardial infarction with normal-appearing coronary arteries. Noteworthy possibilities include vasospasm, most typical in younger individuals. Embolic causes with lysis of the occluding thrombus by the time of angiography also bear consideration. Bland emboli could be one source of a coronary thrombus. Indeed, this woman had documented sick sinus syndrome with tachybrady syndrome. However, there is no documentation of atrial fibrillation or atrial flutter, arrhythmic conditions associated with cardiac source of emboli. Septic emboli from endocarditis, for example, also could cause acute myocardial infarction. Indeed, this woman's history and left ventriculogram were compatible with significant mitral regurgitation. However, there were no clinical signs of sepsis, rendering this possibility less likely. In North America, an additional consideration for acute myocardial infarction without typical coronary atherosclerosis would be cocaine use. That diagnosis probably does not pertain to the current case.
However, we always query patients with acute myocardial infarction about substance abuse. Another cause of acute myocardial infarction with extensive distal wall-motion abnormalities on left ventriculogram, the Takotsubo syndrome, also can cause myocardial infarction with angiographically normal-appearing coronary arteries. Typically, the electrocardiogram shows more prominent T-wave inversion and the ST segment elevation with reciprocal ST segment depression so well described by Dr. Paulo Moffa in his discussion of the electrocardiogram. In addition, the Takotsubo syndrome usually is precipitated by a severe emotional shock. There is no evidence for this in the case at hand. Although Takotsubo syndrome affects women much more often than men, these women tend to be much younger than 88 years old. Finally, rendering the diagnosis of Takotsubo syndrome highly unlikely, the prognosis is excellent with recovery of ventricular function, rather than rapid progression to death, as in the present case. Dr. Ariane Macedo raised the possibility of infiltrative cardiomyopathy. Given the focal nature of the electrocardiographic changes, and the regionality of the extensive left ventricular dysfunction noted on the left ventriculogram by Dr. Eulogio Martinez, I consider infiltrative disease much less likely as an explanation for this patient's current clinical scenario.
In the presence of traditional coronary risk factors, I believe that the likely explanation for the acute myocardial infarction in this woman is atherosclerotic coronary artery disease. We have learned over the last decade or so that many acute myocardial infarctions result from a physical disruption of atherosclerotic plaques that do not necessarily cause a critical coronary artery stenosis. We also have learned that the coronary arteriogram vastly underestimates the extent of coronary atherosclerosis.
Traditionally thought of as a segmental disease, classical autopsy studies and contemporary intravascular ultrasound studies show the ubiquity of intimal disease in individuals with coronary atherosclerosis. The lesions usually occur much more diffusely than the coronary angiogram would suggest. The Glagov phenomenon, compensatory enlargement or outward remodeling, protects the caliber of the lumen of the coronary artery affected by atherosclerosis. It is not until the late stage of this disease that luminal encroachment visible on the angiogram occurs. A disruption with thrombosis of a plaque at a site of outward remodeling of the artery, followed by lysis or distal embolization of the thrombus into the microcirculation after fragmentation could explain the apparently normal coronary arteriogram in the face of the documented myocardial infarction in this woman. I prefer use of the cumbersome term "angiographically normal-appearing coronary arteries" to the shorter but all too often misleading term "normal coronary arteries" to describe the cinecoronariographic findings, to remind us of the limitations of luminography in gauging atherosclerosis, as disease of the artery wall that only occasionally narrows the lumen.
The other particular feature of this clinical scenario that bears comment is the cause of death. Presumably, this woman who succumbed within the first day of an acute myocardial infarction was in a monitored ward. There is no mention of a brady- or tachyarrhythmia as a primary complication of her myocardial infarction that led to her death. We are not told of a downward hemodynamic spiral preceding the terminal event that would suggest primary pump failure or cardiogenic shock in the woman with severe impairment of left ventricular function. While the case protocol is not explicit, the clinical scenario of sudden, unheralded cardiac arrest and a prolonged resuscitative effort evokes the clinical scenario now called pulseless electrical activity cardiac arrest (PEA), previously referred to as electromechanical dissociation. In patients in the acute phase of myocardial infarction, I agree with Dr. Ariane Macedo that cardiac rupture should be considered in such circumstances. Dr. Paulo Moffa described low voltage in the frontal plane on the electrocardiogram. This could indicate pericardial effusion. However, this electrocardiographic finding preceded by some time the abrupt death and could well be unrelated to a hemopericardium secondary to cardiac rupture. However, as Dr. Ariane Macedo pointed out, this woman had many risk factors for cardiac rupture, including longstanding hypertension, female gender, advanced age, and no history of prior myocardial infarction. While myocardial ruptures typically occur later than the first day after onset of infarct symptoms, the clinical scenario strongly suggests consideration of this cause of death.
At necropsy, partially hemorrhagic myocardial infarction, in left ventricular anterior wall and its adjacent portions, septum and right ventricular anterior wall, was the main finding. Myocardial rupture took place in those last two locations, with interventricular communication and blood overflowing to pericardial sac (
Coronary arteries showed mild blockage due to atherosclerosis (up to 69% at left coronary circumflex branch and 77% at right coronary artery). Non-occlusive mural thrombus in anterior interventricular branch anterior established 82% obstruction (
Sinus node fibrosis (
Myocardial left ventricular hypertrophy, secondary to systemic blood pressure, was also present. Benign renal atherosclerosis was detected.
Coronary thrombosis, usually occlusive and secondary to atherosclerosis plaque rupture, is the most common myocardial infarction cause. The most prone to rupture plaque usually has high lipidic content and is responsible for severe coronary artery obstruction, at least at histopathological study (although it is not possible at the coronary angiographic one). However, it did not take place in the present case, in which recent thrombus was not present, despite the patient had died on the first post-infarction day. Two possibilities must be taken into consideration in trying to explain myocardial ischemic necrosis. The most likely is it has been due to vasospasm, which usually affects atherosclerotic lesion arteries with less severe occlusion, such as this patient's. Instead, infarction must have been caused by thrombus embolia found in anterior interventricular branch. Lesion hemorrhage confirms that after blood flow interruption, which caused myocardial fiber demise, it was reestablished. That reinforces the possibility of occurrence of vasospasm. If embolia had led to occlusion, it should have been fixed.
In a recent report19, we showed 14 cases of cardiac tamponade present in necropsies carried out at Laboratório de Anatomia Patológica (Pathological Anatomy Laboratory) of Instituto do Coração between 2000 and 2004. Mean age of necropsy-submitted patients who suffered myocardial rupture was 70.1 years old and median 74, with prevalence of men (55%). Rupture took place, in average, on day 6.6 from infarction evolution (median 4). First infarction rupture occurred in 72.2% of cases; hypertension was diagnosed in 77.8%, and diabetes mellitus in 27.8% of cases.
Dual rupture was found in the present case and in another from our series. It is an unusual form of complication, but previously reported21,25. When indicated in those studies, dual rupture proportion in total cases with that complication was similar to ours (2/18=11.1%), varying from 7.7% to 12.9%21,22,25. On the other hand, few are the cases described in which rotten free wall has been right ventricular24,25.
1. Hochman JS, Tamis JE, Thompson TD et al. Sex, clinical presentation, and outcome in patients with acute coronary syndromes. Global Use of Strategies to Open Occluded Coronary Arteries in Acute Coronary Syndromes IIb Investigators. N Engl J Med 1999; 341:226-32.
2. Da Costa A, Isaaz K, Faure E, Mourot S, Cerisier A, Lamaud M. Clinical characteristics, aetiological factors and long-term prognosis of myocardial infarction with an absolutely normal coronary angiogram; a 3-year follow-up study of 91 patients. Eur Heart J 2001;22(16):1459-65.
3. Bugiardini R, Bairey Merz CN. Angina with "normal" coronary arteries: a changing philosophy. JAMA 2005;293(4):477-84.
4. Kuller L, Fisher L, McClelland R et al. Differences in prevalence of and risk factors for subclinical vascular disease among black and white participants in the Cardiovascular Health Study. Arterioscler Thromb Vasc Biol 1998;18(2):283-93.
5. Braunwald E, Zipes DP, Libby P. Heart disease: A Textbook of Cardiovascular Medicine. 7th Ed. Philadelphia: WB Saunders, 2004.
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Paulo Sampaio Gutierrez InCor Av. Dr. Eneas de Carvalho Aguiar, 44 05403-000 - São Paulo, SP - Brazil
Vera Demarchi Aiello (
English version by Bridge Inglês Personalizado
Foi feito diagnóstico de doença do nó sinusal durante a avaliação ambulatorial da paciente com base no eletrocardiograma de repouso que mostrava um ritmo de escape juncional e Holter com presença de várias pausas sinusais superiores a 3 segundos, alternadas com episódios de taquiarritmias.