Clinical significance and pathogenic role of anti-cardiac myosin autoantibody in dilated cardiomyopa

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In order to explore the possible roles played by the autoimmune mechanism in the progression of myocarditis into dilated cardiomyopathy (DCM) using an animal model, we investigated whether autoimmune myocarditis might develop into DCM Methods Experimental Balb/C mice (n=20) were immunized with cardiac myosin with Freun d’s complete adjuvant at days 0, 7 and 30 The control Balb/C mice (n=10) were immunized with Freund’s complete adjuvant in the same mannere Serum and my ocardium samples were collected after the first immunization at days 15, 21 and 120 The anti-myosin antibody was examined by enzyme-linked immunosorbent assay and immunoblotting Results Pathological findings demonstrated that there was myocardial necrosis or inflammatory infiltration during acute stages and fibrosis mainly in the late phase of experimental group, but the myocardial lesions were not found in the control group Autoimmunity could induce myocarditis and DCM in the absence of viral infection High titer anti-myosin IgG antibodies were found in the experimental group, but not in the control group Furthermore, the anti-myosin heavy chain (200 KD) antibody was positive in 21 of 48 patients with DCM and viral myocarditis, but only 4 of 20 patients with coronary heart disease, including 1 case and 3 c ases that reacted with heavy and light chains (27 5 KD), respectively The antibodies were not detected in healthy donors Conclusion Cardiac myosin might be an autoantigen that provokes autoimmunity and leads to the transformation of myocarditis into DCM Detection of anti-myosin heavy chain antibody might contribute to diagnosis for DCM and viral myocarditis In order to explore the possible roles played by the autoimmune mechanism in the progression of myocarditis into dilated cardiomyopathy (DCM) using an animal model, we investigate whether autoimmune myocarditis might develop into DCM Methods Experimental Balb / C mice (n = 20) were immunized with cardiac myosin with Freun d’s complete adjuvant at days 0, 7 and 30 The control Balb / C mice (n = 10) were immunized with Freund’s complete adjuvant in the same mannere Serum and my ocardium samples were collected after the first immunization at days 15 , 21 and 120 The anti-myosin antibody was examined by enzyme-linked immunosorbent assay and immunoblotting Results Pathological findings demonstrated that there was myocardial necrosis or inflammatory infiltration during acute stages and fibrosis mainly in the late phase of experimental group, but the myocardial lesions were not found in the control group Autoimmunity could induce myocarditis and DCM in the absence of viral infection High titer anti-myosin IgG antibodies were found in the experimental group, but not in the control group Furthermore, the anti-myosin heavy chain (200 KD) antibody was positive in 21 of 48 patients with DCM and viral myocarditis, but only 4 of 20 patients with coronary heart disease, including 1 case and 3 c ases that reacted with heavy and light chains (27 5 KD), respectively The antibodies were not detected in healthy donors Conclusion Cardiac myosin might be an autoantigen that provokes autoimmunity and leads to the transformation of myocarditis into DCM Detection of anti-myosin heavy chain antibody might contribute to diagnosis for DCM and viral myocarditis
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