Molecular biological methods such as in situ hybridization and the polymerase chain reaction (PCR) have confirmed the pathogenetic role of enteroviruses and primarily coxsackieviruses of group B (CVB) in the induction and maintenance of inflammatory cardiomyopathy. More recently, additional viruses such as adenoviruses (ADV), various herpes viruses and increasingly parvovirus B19 (PVB19) have been identified as potential cardiotropic agents in the human heart. The different cell tropism of cardiotropic viruses implicates distinct pathogenetic principles. Whereas cardiac myocytes are target cells for infection with enteroviruses and adenoviruses with consecutive virus-induced cytolysis, PVB19-associated inflammatory cardiomyopathy is characterized by infection of intracardiac endothelial cells of small arterioles and veins, which may be associated with endothelial dysfunction, impairment of myocardial microcirculation, penetration of inflammatory cells and secondary myocyte necrosis.