Abstract
Animal models of congestive heart failure and dilated cardiomyopathy following encephalomyocarditis (EMC) virus infection have been developed. Differences were found between different strains of mice in the frequency of occurrence and severity of myocarditis, and even in the character of the pathological lesions. Genetic factors may play an important role in pathogenesis. Right ventricular aneurysm and arrhythmias were seen in these models. Viral myocarditis may play a pathogenetic role in right ventricular dysplasia. Auto-antibodies against heart developed and the distribution of cardiac myosin isoenzymes was altered during the course of myocarditis. Myocardial uptake of technetium-99m pyrophosphate and changes in NMR relaxation parameters have been studied in these models. Virus vaccine, passive immunization, recombinant interferon α A/D and ribavirin protected mice from developing myocarditis. Immunosuppressive agents such as prednisolone and cyclosporinwere studied, but had no beneficial effect on these models. An animal model of perimyocarditis induced by coxsackie virus B3 is also described. Because the myocardial lesions are severe and occur frequently, our animal models are considered suitable for studying pathogenetic mechanisms and for the evaluation of diagnostic methods and prevention and therapeutic interventions of viral myocarditis.
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