In order to explore the possible roles played by the autoimmune mechanism in the progre ssion of myocarditis into dilated cardiomyopathy (DCM) using an animal model, we inve stigated whether autoimmune myocarditis might develop into DCM1 Methods Experimental Balb/C mice (n=20) were immunized with cardiac myosin with Freund'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 mannere1 Serum and myocardium samples were collected after the first immunization at days 15, 21 and 120. The anti-myo sin antibody wa s examined by enzyme-linked immuno sorbent a ssay and immunoblotting. Results Pathological findings demonstrated that there was myocardial necro sis or inflammatory infiltration during acute stage s and fibro sis mainly in the late phase of experimental group, but the myocardial lesions were not found in the control group. Autoimmunity could induce myocarditis and DCMin the absence of viral infection1 High titer anti-myosin IgG antibodies were found in the experimental group, but not in the control group. Furthermore, the anti-myo sin 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. case and 3 cases that reacted with heavy and light chains (27.5KD), 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 diagno sis for DCM and viral myocarditis.