Depressed myocardial function in subacute experimental viral myocarditis.
A model of experimental Coxsackie virus B3 myocarditis has been developed in the weaning Syrian golden hamster. The acute infection is characterized by extensive viral replication in the myocardium, associated with transient myocytolysis and leukocytic infiltration. At 2 weeks after inoculation, there is survival without evidence of cardiac hypertrophy or failure, and minimal residual light microscopic changes. In order to evaluate myocardial function during convalescence form this form of myocarditis, muscle mechanics were studied in left ventricular trabeculae careae in 10 infected and 7 control animals, 18 days after inoculation. Maximum developed tension of the infected animals was depressed by 25%, and there was a significant decrease in the time to peak tension. Furthermore, the infected muscles required less stretch to reach that length at which maximal developed tension was produced. These data indicate that myocardial function remains depressed during early convalescence from acute Coxsackie virus B3 myocarditis and suggest that this state is associated with decreased compliance. Studies of myocardial morphology and function at longer intervals after acute experimental viral myocarditis are indicated, to further test the hypothesis that viral myocarditis might be a precursor chronic isiopathic cardiomyopathy.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D009202:Cardiomyopathies / Q000209:etiology; D003384:Coxsackievirus Infections / Q000503:physiopathology*; D006224:Cricetinae; D004195:Disease Models, Animal; D006321:Heart / Q000382:microbiology*; D066298:In Vitro Techniques; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism
D002118:Calcium