However, at the end of the acute phase, when few amastigote nests areobserved, areas of intense inflammatory infiltrate in the myocardium, characteristicof the chronic Chagas cardiomyopathy, also induced changes in the costamericdistribution of vinculin, suggesting that disturbances in thevinculin-talin-integrin-ECM interface may be responsible for the change inmechanotransduction in the chronic phase of Chagas disease.11 This evidence concerns the gene VCL and Chagas disease.