Immunologic regulator and effector functions in perimyocarditis, postmyocarditic heart muscle disease and dilated cardiomyopathy

Abstract

In acute perimyocarditis we found that OKIAI-positive cells were increased, and in dilated cardiomyopathy OKMI-positive cells were increased. No significant alteration in suppressor T cell activity was observed in our patients with either disease. The characteristic immunofluorescent pattern in carditis and postmyocarditic heart disease is the presence of antimyolemmal antibodies with intact rat and human cardiocytes in titers of 1:40-1:320 as antigens. The antimyolemmal fluorescence can be absorbed with the respective causative virus in Coxsackie B, influenza, mumps and EBV-myocarditis, indicating that the antibodies are a cross-reactive. AMLA-positive sera induce cytolysis of vital rat cardiocytes in vitro, suggesting that the antibodies are of pathogenetic relevance. Cytolytic serum activity could be absorbed out with the respective virus. Immunohistologic specimens obtained from patients with carditis demonstrate the fixation of IgG and IgM antibodies; IgG antibodies also occur in dilated cardiomyopathy and coronary artery disease. In dilated postmyocarditic heart disease both antimyolemmal fluorescence and cytolytic activity are preserved at a lower level when compared to carditis. These antibodies can also fix complement. In the acute phase of carditis circulating immune complexes can be demonstrated. Cellular effector mechanisms against vital cardiocytes were maintained or even slightly enhanced in carditis, postmyocarditic and primary dilated cardiomyopathy. In vitro NK cell activity against K 562, however, was decreased. This is compatible with a sustained target-specific cytotoxicity whereas reduced NK cell activity may indicate impairment of this effector organ.