997-83 Improvement of Cardiac Function in Acute Murine Coxsackievirus B 3 Myocarditis by Interferon 2α

Coxsackievirus B3 infection in male DBA/2 mice induces severe myocarditis with infiltration of leukocytes in the myocardium and a deterioration of cardiac function. Increase of cardiac virus concentration by the administration of immunosuppressive drugs has lead to an aggravation of the disease. In order to reduce replicating virus in the heart 600000 units interferon 2α were intraperitoneally injected on days 2–7 of the infection. On day 9, left ventricular systolic pressure, left ventricular end-diastolic pressure as well as +dp/dtmax and -dp/dtmax as parameters for left ventricular systolic and diastolic function were measured by open chest puncture of the left ventricle. Then the hearts were removed for histology and determination of cardiac virus concentration. Cardiac virus titers decreased in the interferon treated mice (log 5.80 vs. 6.22). Hemodynamic parameters of the left ventricle improved in the CVB 3 infected group receiving interferon as compared to untreated infected mice. Left ventricular systolic pressure rose (84 vs. 71 mmHg; p l 0.05) and left ventricular enddiastolic pressure decreased significantly (1.39 vs. 2.51 mmHg; p l 0.05). +dp/dtmax (4456 vs. 4375 mmHg/s) and -dp/dtmax (2843 vs. 2540 mmHg/s) were higher in the animals receiving interferon. Hemodynamic improvement was paralleled by a reduction of myocarditic lesions in the treated group (2.78 vs. 3.28 on a scale of 0–4; p l 0.05). Thus, the administration of interferon 2 α improves cardiac inflammation and function in acute coxsackievirus B 3 induced myocarditis, most likely by reducing viral replication in the heart. This finding underlines the importance of the virus for mediating cardiac damage in the acute phase of the disease.