The Syrian hamster as a model for the dilated cardiomyopathy of Chagas' disease: a quantitative echocardiographical and histopathological analysis.

Chronic Chagas' disease cardiomyopathy (CCC) is caused by the protozoan Trypanosoma cruzi, and it affects 30% of the 16-18 million people infected in Latin America. A good rodent model that develops a dilated cardiomyopathy closely resembling human CCC after T. cruzi infection is still needed. We compared the cardiomyopathy developed by T. cruzi-infected Syrian hamsters with human Chagas' disease cardiomyopathy using quantitative methods. Female hamsters were infected with 3.5 x 10(4) (G1, n = 10) or 10(5) (G2, n = 10) T. cruzi Y strain blood trypomastigotes. Control animals (C, n = 10) were injected with saline solution. Cardiac function was assessed by echocardiography at 4, 8 and 12 months post-infection. Heart sections were submitted to histopathological/morphometric analysis 12 months post-infection. At this time, ventricular dysfunction and diffuse or multi-focal myocarditis were observed in 91% and 100% of G1 and G2 infected groups, respectively. Median interstitial collagen volumes in groups C, G1 and G2 were 1.2%, 1.9% and 3.9%, respectively, and were significantly higher in group G2 than in group C. Among infected animals, myocarditis showed a positive correlation with interstitial fibrosis. Deaths in the chronic phase (8-12 months post-infection) were more frequent among G2 than G1, and were associated with macroscopic ventricular dilation, severe myocarditis and increased fibrosis values, along with an earlier onset of ventricular dysfunction. The T. cruzi chronically infected Syrian hamster develops a cardiomyopathy which resembles human Chagas' disease cardiomyopathy, and might be an adequate tool to investigate pathogenic mechanisms of this disease and to search for novel therapeutic strategies.