Recent studies suggest that intracellular Trypanosoma cruzi invasion with release of intracellular myocardial antigens during T. cruzi infection is crucial to the pathogenesis of chronic chagasic myocarditis. However, in areas endemic for Chagas' disease, the incidence of clinical acute chagasic myocarditis has been reported to be low among infected individuals, while the incidence of chronic chagasic myocarditis is relatively high. Thus, either acute chagasic myocarditis rarely complicates T cruzi infection and is not important to the pathogenesis of chronic chagasic myocarditis, or acute chagasic myocarditis rarely impairs left ventricular function and therefore causes no symptoms. To investigate this question we innoculated T. cruzi from a human patient with Chagas' disease into the subconjuntivae of six rhesus monkeys (7.5 x 103 parasites each). Parasitemia was monitored and weekly two-dimensional echocardiograms (for determination of end-diastolic and fractional change in area, EDA and FCA) were obtained to quantify global left ventricular function for 10 weeks. Regional left ventricular function was assessed by visual analysis of two-dimensional echocardiograms. Extent of acute myocarditis was established at autopsy. All monkeys had the Romafna sign and detectable parasitemia in the second week. Parasitemia rose in all by the ninth week (mean = 1.8 x 105 parasites/ml); four monkeys lost weight (mean = − 12%), three died, and three were killed. Twodimensional echocardiographic EDA and FCA remained unchanged from control to the last study within 12 hr of death (EDA = 2.6 + 0.9 to 2.7 + 1.0 Cm2, FCA = 80 + 6.8 to 74 + 7.6%, NS). Furthermore, regional left ventricular function remained unchanged throughout the period of study. At autopsy two monkeys had severe acute myocarditis (one had been killed with no weight loss) with abundant intracellular T. cruzi (one nest of T. cruzi/cm2 of myocardium sectioned). Two had moderate and two mild acute myocarditis. In conclusion, acute chagasic myocarditis may be severe after T. cruzi infection, yet cause no impairment in resting left ventricular function despite intense intracellular T. cruzi invasion.