Chronic infections of Chagas Disease can lead to persistent tissue inflammation around the heart leading to myocardial fibrosis and cardiac remodeling. Cardiac inflammation is mainly attributed to parasitic load, immune response, fibrosis, dysautonomia and microvascular changes. Although the inflammatory response is required to control parasitic proliferation, the secretion of Th1 cytokines may lead to the destruction of the cardiac tissue. SARS-CoV-2, which binds to the ACE2 receptor, elicits the production of type 2 pneumocytes, macrophages, perivascular pericytes and cardiomyocytes. Additionally, infections lead to cytokine storms, producing cytokines and chemokines associated with an inflammatory response similar to those elicited in chronic chagas cardiomyopathy. Myocarditic cases have been associated with infection of SARS-CoV-2 and are considered to be related to viral injury and the host immune response. One of the clinical manifestations of Covid-19 is thrombotic disease caused by excessive inflammation, platelet production, endothelial dysfunction and stasis.