Cerebral infarction and mitral annulus calcification

Abstract

The role of the heart in an embolic stroke has been given much attention through previous patholoical and epidemiological studies. We have examined patients having embolic stroke by two dimensional echocardiography in order ot investigate the pathological changes of the heart and the presence of intracardiac thrombi. One hundred thirty eight infarcted patients were examined by echocardiography. They were admitted within 48 hours after onset and were diagnosed as having cerebral infarction by both physical and neuroradiological findings. The short axial view and long axial view were taken in addition to M-mode scanning. The left ventriculography and/or coronary angiography were performed, if necessary, for diagnosis.
The abnormalities found other than rheumatic heart diseases were hypertrophic type cardiomyopathy in 10, congestive type cardiomyopathy in 2, mitral valve prolapse in 3 and mitral annulus calcification in 4 cases. Rheumatic heart diseases have been well recognized as embolic sources in stroke patients. But mitral annulus calcification (MAC) has not been given much attention as an embolic source, although several descriptions on the pathologic anatomy of MAC have appeared over that past seven decades.
The echocardiography in the 4 cases of MAC showed a dense, linear echo behind the mitral valve that moved anteriorly with systole, similar to the motion of the posterior left ventricular wall. On scanning from the left ventricle to the left atrium this dense band of echoes stopped abruptly at the junction between the left ventricle and left atrium. It was difficult to differentiate this band of echoes from the posterior mitral valve leaflet and from the posterior wall of the left ventricle. Two-dimensional echocardiography provided a more exact display of anatomic relationships than the M-mode thechnique.
The ages of patients with MAC were 69, 73, 80 and 81 years respectively. Two of them were females. Calcifications of mitral annulus were demonstrated by the plain chest X-P or fluoroscopy in 2 cases. All cases showed left ventricular dilatation on chest X-P. Three cases showed atrial fibrillations and the other one had ventricular premature contractions on ECG. Intracardiac thrombi were not found in any cases by echocardiography. Two autopsied cases had no intracardiac thrombi. The internal carotid artery occlusion was confirmed in two cases, and the latter 2 cases had stenotic lesions on internal carotid arteries. On CT scan, 2 cases had low density areas on the territory of middle cerebral artery and 1 on the territory of both anterior and middle cerebral arteries. One case had no abnormal CT findings.
Our data suggest that two-dimensional echocardiography is necessary for investigating cardiac abnormalities including MAC in infarcted patients. The concomitant lesions of internal carotid artery and MAC have to be paid more attension in order to estimate MAC as an embolic source in cerebral infarction.