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[Cerebral embolism of cardiac origin]
R C Rey1, S M Lepera, G Kohler
1División Neurología, Hospital Ramos Mejía, Buenos Aires, Argentina.
Insights
Nonischemic dilated cardiomyopathy is a significant cause of cardiogenic brain embolism, particularly in communities affected by Chagas
Area of Science:
- Cardiology
- Neurology
- Epidemiology
Context:
- Acute ischemic stroke patients hospitalized between 1983 and 1991 were reviewed.
- Cardioembolism criteria included sudden onset deficits, CT-confirmed infarcts, identified cardiac sources, and absence of cerebrovascular disease.
Purpose:
- To identify the prevalence and sources of cardiogenic brain embolism in hospitalized acute ischemic stroke patients.
- To investigate the role of nonischemic dilated cardiomyopathy and Chagas' disease as causes of cerebral embolism.
Summary:
- Sixty-nine patients (12.8%) met criteria for cardiogenic brain embolism.
- Primary sources included nonvalvular atrial fibrillation (29.0%), rheumatic heart disease (20.3%), and nonischemic dilated cardiomyopathy (18.8%).
- Chagas' disease was implicated in 69% of nonischemic dilated cardiomyopathy cases, highlighting a regional factor.
Impact:
- Nonischemic dilated cardiomyopathy is identified as a major cause of cerebral embolism in the studied community.
- The findings underscore the importance of considering regional endemic diseases like Chagas' disease in stroke etiology.
Abstract:
We reviewed 538 charts of patients hospitalized with acute ischemic strokes between 1983 and 1991. The inclusion criteria for cardioembolism were: 1) sudden onset and maximal neurological focal deficit from the beginning, 2) brain CT showing an ischemic infarct, hemorrhagic infarct, or multiple infarcts, 3) cardioembolic sources demonstrated by echocardiography or heart catheterization, and 4) absence of stenotic-occlusive cerebrovascular disease. Sixty-nine patients (12.8%) filled the criteria for cardiogenic brain embolism. Cardiac sources were: 1) nonvalvular atrial fibrillation in 20 patients (29.0%), 2) rheumatic heart disease in 14 (20.3%), 3) nonischemic dilated cardiomyopathy in 13 (18.8%). Nine of these (69%) had cardiac involvement due to Chagas' disease, 4) ischemic heart disease in 11 (15.9%), and 5) other less common conditions such as bacterial endocarditis, mitral valve, and congenital heart malformation in 11 (15.9). Transient ischemic attacks preceding stroke occurred in 11 patients (15.9%), six patients had previous strokes, and 14 patients (20.3%) had silent infarcts. Early recurrence of embolism (three initial weeks) occurred in 5 patients (7.2%), and 28.6% of the patients had hemorrhagic transformation within this period. Taken together, our figures show that, although they are well in line with the current literature, nonischemic dilated cardiomyopathy is one of the main causes of cerebral embolism in our community. This reflects the presence of a regional factor, namely Chagas' disease.