Cardiomyopathy and myocarditis--a review of new aspects in research in West Germany.
New aspects in the research of myocarditis and dilated cardiomyopathy in West Germany have evolved from molecular biology, immunobiology of the mitochondrion, immunoserology, and immunohistology. Coxsackie B3 virus inoculated into fetal human myocytes induced myocytolysis in the absence of immunologic effector mechanisms. By pretreatment with beta-interferon, the virus yield from the myocytes was reduced significantly. In myocarditis and dilated cardiomyopathy, antibodies against an organ-specific autoantigen of cardiac mitochondria, the adenine nucleotide translocator, were demonstrated. Antibody titers roughly correlated with the ejection fraction using the Elisa technique. It could also be shown that in 13% of cases in myocarditis and 31% in dilated cardiomyopathy heart-associated antimitochondrial antibodies are found, called anti-M7. Most of the patients had an interfibrillary staining pattern in the immunofluorescence test. No correlation with the severity of heart disease could be established. In dilated cardiomyopathy and myocarditis, there has recently been controversy over low suppressor T-cell activity. Whereas other groups have demonstrated a low concanavaldin-A-induced suppressor T-cell activity in both diseases, we have not been able to confirm reduced Con-A-induced or spontaneous T-suppressor cell activity in the different indicator systems used in analysis.
D000818:Animals; D000917:Antibody Formation; D001323:Autoantibodies / Q000276:immunology; D002311:Cardiomyopathy, Dilated / Q000276:immunology*; D004195:Disease Models, Animal; D005860:Germany, West; D006801:Humans; D007113:Immunity, Innate; D008214:Lymphocytes / Q000145:classification; D008929:Mitochondria, Heart / Q000276:immunology; D009205:Myocarditis / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
D001323:Autoantibodies