LEFT-VENTRICULAR HEMODYNAMICS IN MURINE VIRAL MYOCARDITIS

In susceptible DBA/2, mice infection with coxsackievirus B3 leads to s evere inflammatory and necrotic lesions in the heart. There is a tempo ral discrepancy of peak concentrations of replicative virus in the hea rt and maximal cardiac inflammation. Aims of this study were, first, t o determine whether haemodynamic changes occur in coxsackievirus BS-in duced murine myocarditis and, second, the time frame in which those al terations may be apparent. By puncture of the left ventricle, pressure s and the first derivative dp/dt as parameters of left ventricular fun ction could be obtained on several days of the infection. Haematoxylin -eosin stains of cross-sections of the heart showed the course of infl ammatory lesions in the heart; a plaque forming assay assessed virus t itres in the heart. Cardiac concentrations of replicative replicative virus peaked on day 3, inflammatory lesions in the heart were maximal on day 7. Left ventricular function was almost preserved until day 5 o f the infection, then dropped significantly until day IO. The study su ggests that either a cumulative virus-mediated destruction of the myof ibres or virally triggered immune reactions to heart cells lead to imp airment of left ventricular function.