Chagas' disease, due to a chronic and persistent infection with the parasite Trypanosoma cruzi, is the cause of one of the most prevalent forms of congestive cardiomyopathy in South and Central America. In common with other congestive cardiomyopathies due to acquired and hereditary etiologies seen worldwide, chagasic cardiomyopathy is characterized by cardiomegaly, ventricular chamber remodeling, myocellular necrosis, and multifocal areas of interstitial and replacement fibrosis. The microscopic presence of the parasite in the late stages of the disease is rare. This review examines some of the evidence for the role of a dysfunctional microvasculature as a pathophysiological mechanism for myocardial damage in chagasic cardiomyopathy. Perturbations of the interstitial connective tissue matrix in Chagas' disease also are described in regard to the remodeling characteristic of the affected ventricle. Similar abnormalities of the microvasculature and matrix have been reported in other congestive cardiomyopathies, thereby suggesting that common pathophysiologic mechanisms may lead to ventricular damage even when the initiating etiologic agent is different. Preventive treatment or palliation of Chagas' cardiomyopathy and other congestive cardiomyopathies may result from a better understanding of these secondary pathogenetic events.
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Cardiology and Cardiovascular Medicine