Cerebral infarction with mitral valve prolapse

Report of a case and review of literatures

Abstract

Mitral valve prolapse has now become a well-known disease for cardiologists and many authors have reported several secondary complications. They are arrhythmias, mitral regurgitation, bacterial endocarditis and sudden death. In addition, neurological disturbances such as transient ischemic cerebral attacks, partial non-progressive stroke were reported a few years ago. We recently experienced one case with mitral valve prolapse and completed stroke. The lack of clinical report in Japan as for cerebral infarction with this pathological condition merits this case report. The authors reviewed an association among transient ischemic cerebral attacks, stroke and mitral valve prolapse in the literature. And we emphasized that echocardiography was very useful for the screening of the ischemic cerebrovascular diseases secondary to the emboli originated from the heart.
A 65-year-old right-handed female was admitted to our hospital because of left-hemiplegia in February, 1980. The physical examination and chest X-ray revealed arrhythmia and cardiomegaly. Electrocardiogram showed atrial fibrillation and left ventricular hypertrophy. But she had no abnormal heart sounds and murmurs on auscultation. The neurological findings were left hemiplegia with extensor planter reflex, ocular conjugate deviation to the right side, and disturbed consciousness. Computed tomography (CT) showed no abnormal density on admission. The right carotid angiography performed on the 1st day after onset demonstrated an occlustion of the middle cerebral arterial branch and collaterals from the anterior cerebral artery. Repeated CT on the following day showed a large low density area in the territory of the anterior and the middle cerebral artery. The angiographic findings were suspected to reflect the prior recanalization of an embolic occlusion of the internal carotid artery, or that of multiple arteries retrospectively. Echocardiography was performed to study any embolic source in the heart six after onset. Two-dimensional echocardiography demonstrated mitral valve prolapse without other anatomical changes. M-mode scan also revealed pansystolic bowing or hammocking of the anterior mitral leaflet. But phonocardiography revealed no mid-systolic click or systolic murmur.
Afte admission, she slowly showed clinical improvement enough to walk with a brace. But she often complained of precordial pain and palpitation after exercise or even at rest. Therefore we performed angiocardiography to scrutinize the causes of chest pain and atrial fibrillation. Left ventriculography showed mitral valve prolapse involving both posterior and anterior mitral leaflets with regurgitation of mild degree on the 27th day after onset. The selective coronary angiography showed slight luminal irregularity without any significant occluded lesion. Her cardiac complaints were, we considered, possible secondary to idiopathic mitral valve prolapse. After the administration of aspirin and nitroglycerin, she scarcely complained of chest pain.