CAROTID-ARTERY AND HEART-DISEASE IN SUBTYPES OF CEREBRAL INFARCTION

Background and Purpose The aim of the study was to determine the preva lences of carotid artery disease and major and minor potential cardioe mbolic sources (1) in patients with cerebral infarction and age-matche d control subjects and (2) in different clinical subtypes of cerebral infarction. Methods A series of 166 consecutive patients with cerebral infarction and 59 control subjects was examined. The study protocol i ncluded clinical subtyping of the cerebral infarctions, ultrasonograph y of the carotid arteries, transthoracic echocardiography (TTE), trans esophageal echocardiography (TEE), ECG, and examination of the brain w ith computed tomography, magnetic resonance imaging, or autopsy. Resul ts Carotid artery stenosis greater than or equal to 80% or occlusion w as present in 35 (21%) patients but in no control subjects (P<.001; ch i(2) test). A major potential cardioembolic source was detected in 65 (39%) patients and 3 (5%) control subjects. Atrial fibrillation was pr esent in 35 (21%) patients and 3 (5%) control subjects at initial ECG (P<.01) and in 47 (28%) patients at repeat examination; 17 patients ha d paroxysmal atrial fibrillation. Sinus rhythm and a major potential c ardioembolic source were detected in 18 (11%) patients but in no contr ol subjects (P<.01) at TTE (all patients and control subjects examined ) or TEE (118 patients and 52 control subjects examined). The frequenc y of a minor potential cardioembolic source detectable at TTE or TEE w as similar in the patient and control groups (51% and 53%, respectivel y [NS]) and increased significantly with age. A finding of carotid art ery stenosis greater than or equal to 80% or occlusion, atrial fibrill ation, or a major cardioembolic source detected at TTE or TEE was more frequent among patients with cortical symptoms from anterior or middl e cerebral artery territories than among those with lacunar syndromes (66% versus 22%, respectively). The probable source of cerebral infarc tion was identified in most of the 166 patients: cardiac embolism in 2 8% of cases (n=46), carotid artery disease in 8% (n=14), both cardiac embolism and carotid artery disease in 7% (n=11), and lacunar infarcti on in 23% (n=38). In 57 (34%) of the patients no unequivocal cause of the cerebral infarction was found. Conclusions The prevalences of caro tid artery and heart disease differ significantly between clinical sub types of cerebral infarction. The cause of cerebral infarction remains uncertain in one third of patients. Because a minor potential cardioe mbolic source occurs in about 50% of both patients and control subject s, this findings is of questionable value as a risk factor for stroke in the elderly.