Dilated cardiomyopathy is characterized by dilatation of the left or right ventricle, or both ventricles. The degree of myocardial dysfunction is not attributable to abnormal loading conditions. The infectious-immune theory has long been hypothesized to explain the pathogenesis of many etiologically unrecognized
dilated cardiomyopathies.
Inflammations followed by immune reactions, which may be excessive, in the myocardium, evoked by external triggers such as
viral infections and/or autoimmune
antibodies, continue insidiously, and lead to the process of cardiac remodeling with ventricular dilatation and systolic dysfunction. This ultimately results in
dilated cardiomyopathy. Hepatitis C virus-associated
heart diseases are good examples of cardiac lesions definitely induced by
viral infections in humans that progress to a chronic stage through complicated immune mechanisms. Therapeutic strategies for
myocarditis and
dilated cardiomyopathy have been obtained through analyses of the acute, subacute, and chronic phases of experimental viral
myocarditis in mice. The appropriate modulation of excessive immune reactions during
myocarditis, rather than their complete elimination, appears to be a key option in the prevention and treatment of
dilated cardiomyopathy. The clinical application of an NF-κB decoy and immune adsorption of
IgG3 cardiac
autoantibodies have been used as immunomodulating
therapies and may provide novel approaches for the treatment of refractory patients with
dilated cardiomyopathy. Conventional therapeutic agents for chronic
heart failure such as β-blockers,
angiotensin-converting enzyme inhibitors,
angiotensin receptor blockers, and
aldosterone antagonists in particular should be re-evaluated on the basis of their anti-inflammatory properties in the treatment of
dilated cardiomyopathy.