Cardiological Evaluation of Patients with a Cerebral Ischemic Event: the Relation between Heart and Brain Cardiological Evaluation of Patients with a Cerebral Ischemic Event: the Relation between Heart and Brain

Using both precordial and transesophageal echocardiography, we studied 72 consecutive patients with a recent unequivocal transient ischemic attack or nondisabling stroke to determioe the relative value of the two techniques for detecting potential intracardiac sources of cerebral emboli. Group 1 (n=53) patients had no clinical abnormalities, and group 2 (n=19) patients had abnormal cardiac findings on clinical examination. In group 1, precordial echocardiography detected an abnormality in only one patient (aortic valve thickening) but transesophageal echocardiography defined morphologic abnormalities in five patients (one with a left atrial appendage mass lesion, one with aortic dissection, one with mitral valve prolapse, one with a mitral leaflet mass lesion, and one with aortic valve thickening). In group 2, both precordial and transesophageal echocardiographic smdies were normal in 13 patients, while both were abnormal in the remaining six patients. Five of these six patients had pathologic left atrial and/or left ventricular dilatation, but only transesophageal echocardiography defined a left atrial appendage thrombus in two of the six. The sixth patient had mitral chordal rupture, seen on both precordial and transesophageal echocardiography. In addition, in 32 of the 72 patients transesophageal echocardiography identified widespread thoracic aortic atherosclerotic plaques not visualized by precordial echocardiography. We conclude that transesophageal echocardiography significantly increases the yield in visualizing potential intracardiac sources of emboli compared with precordial echocardiography. However, the precise clinical value of the former in the management of such patients requires further study as the number of abnormal transesophageal echocardiographic findings is not high and a causative relation with transient ischemic attacks cannot be proven. (Stroke 1990; 21: 560-565).