Findings in Murine Viral Myocarditis

Acute myocarditis may not only develop into congestive heart failure, but it has also been strongly implicated in the pathogenesis of dilated cardiomyopathy. The mechanism of myocardial cell injury involved in acute myocarditis is of great clinical significance, but remained to be clarified for a long period. Because patients with acute myocarditis often show significantly increased virus titer in serum, and the myocardial histological find‐ ings of acute myocarditis are similar to those of experimental viral myocarditis, it is believed that most of human acute myocarditis is induced by virus infection. Many studies have been done on the experimental murine viral myocarditis caused by Coxsackievirus (CVB3), which is the most common pathogen of human acute myocarditis. Because maximal inflammation develops after a significant decrease in virus titer, it is thought that immunological mechanisms in addition to the direct cytolytic effects of viruses play a critical role in myocardial injury in viral myocarditis [1]. Furthermore, myocardial necrosis occurs with massive cell infiltration, strongly suggesting that cell-mediated (rather than humoral) cytotoxicity plays an important role.