Clinical aspects of myocarditis.

The diagnosis of myocarditis is discussed with reference to endomyocardial biopsy and the possible relation of dilated cardiomyopathy to myocarditis is explored. The various degrees of immune damage to the myocardium produced by myocarditis are reviewed, and evidence for altered immunity in dilated cardiomyopathy is assessed. The rationale for immunosuppressive therapy is surveyed. Both clinical and experimental data suggest that viral myocarditis is biphasic. The initial phase is infective with myocytolysis, lymphocytic infiltration, and a humoral immune response. The second phase is associated with a persistent antigen-antibody reaction between the virus and the myocardium. Myocarditis may be acute with lymphocytic infiltration and myocytolysis; persistent active, with continuing changes including widening of the interstitium and fibrosis; healing, with persistent inflammatory cell exudate but no myocyte necrosis; and healed, with the absence of necrosis and of inflammatory cell infiltrates but widening of the interstitium and fibrosis. This state is indistinguishable from dilated cardiomyopathy. The selection of patients for treatment and the regimens of treatment are discussed. Acute myocarditis or persistent active myocarditis are indications for therapy with steroids and the immunosuppressive agent azathioprine. Benefit is unlikely when myocarditis is healed. Lymphocytic inflammatory cell infiltration alone is not sufficient indication for such therapy, because such infiltration may be found in dilated cardiomyopathy and also in toxic myocarditis due to drugs. Results of immunosuppressive therapy for acute and active myocarditis are encouraging, but a prospective randomized study is needed.