The challenge of chagasic cardiomyopathy. The pathologic roles of autonomic abnormalities, autoimmune mechanisms and microvascular changes, and therapeutic implications.

The evidence provided by both human and animal studies on chronic Chagas' heart disease suggests that the cardiomyopathy occurs as a consequence of several physiopathological processes occurring after infection interacting with unidentified host factors. The development of the chronic fibrosing myocarditis is related to progressive and additive focal cellular necrosis, and associated inflammatory lymphomononuclear infiltrate and reactive and reparative myocardial fibrosis and surrounding myocyte hypertrophy. These processes may be initiated and perpetuated by alterations in the myocardial microcirculation and by autoimmune factors. The autonomic impairment and/or the chronic fibrosing myocarditis and the left ventricular dysfunction could act as factors predisposing one to an increased risk of sudden cardiac death.