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Abstract
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.