Studies on the pathogenesis of atrial myocarditis in mice infected with Coxsackie virus B3.

Coxsackie virus B3 (CB3) was inoculated intraperitoneally into BALB/c mice to determine whether atrial myocarditis is due primarily to virus multiplication in the atrial myocardium or is secondary to the effects of virus multiplication in the ventricular myocarditis. Ventricular changes were observed in 15 (71%) out of 21 mice. The lesions consisted of hyaline or granular degeneration and necrosis with or without calcium deposits of the muscle fibres and inflammatory mononuclear cell infiltration. Histopathological changes in the atrial myocardium were found in 14 (67%) out of 21 mice. The lesions in the atrial myocardium were oedema or thickening of the endocardium, degeneration and necrosis of the muscle fibres and inflammatory mononuclear cell infiltration. The incidence and degrees of intensity of the histopathological changes in the atrial myocardium were less than those of the ventricular myocardium in mice inoculated with CB3, but no difference in the nature of the histopathological changes between the atrial and ventricular myocardium were observed. A high virus titer was found in the atrial myocardium as well as in the ventricular myocardium, and virus antigen was detected in the degenerating or necrotizing muscle fibres in the atrial myocardium by immunofluorescent technique. It is clear that CB3 could produce not only ventricular myocarditis, but also atrial myocarditis. We conclude, therefore, that damage of the atrial myocardium is due to direct action of the virus.