A progression from viral
myocarditis to
dilated cardiomyopathy has long been hypothesized, but the actual extent of this progression has been uncertain. However, a causal link between viral
myocarditis and
dilated cardiomyopathy has become more evident than before with the tremendous developments in the molecular analyses of autopsy and endomyocardial biopsy specimens, new techniques of viral gene amplification, and modern immunology. The persistence of
viral RNA in the myocardium beyond 90 days after inoculation, confirmed by the method of polymerase chain reaction, has given us new insights into the pathogenesis of
dilated cardiomyopathy. Moreover, new knowledge of T-cell-mediated immune responses in murine viral
myocarditis has contributed a great deal to the understanding of the mechanisms of ongoing disease processes. Apoptotic cell death may provide the third concept to explain the pathogenesis of
dilated cardiomyopathy, in addition to persistent
viral RNA in the heart tissue and an immune system-mediated mechanism. Beneficial effects of alpha1-adrenergic blocking agents,
carteolol,
verapamil, and
ACE inhibitors have been shown clinically and experimentally in the treatment of viral
myocarditis and
dilated cardiomyopathy.
Antiviral agents should be more extensively investigated for clinical use. The rather discouraging results obtained to date with
immunosuppressive agents in the treatment of viral
myocarditis indicated the importance of sparing
neutralizing antibody production, which may be controlled by B cells, and raised the possibility of promising developments in immunomodulating
therapy.