Abstract： Objective To explore the role of homocysteine in the pathogenesis of alcoholic cardiomyopathy. Methods A total of 69 male Wistar rats were randomly assigned into two groups: alcoholfed group and the control. Cardiac function was assessed by pulse Doppler. Plasma Hcy levels were examined using automatic biochemical instrument (chemiluminescence). The protein expression of MMP-9 was evaluated using immunohistochemical method, and collagen fiber of myocardium was quantitative analyzed by Masson stain. Results After heavy drinking, the LVEDd of alcohol-fed group were larger than the control group [( 7. 0 ± 0. 6) mm vs ( 5.0 ± 0. 4 ) mm, P ＜ 0. 05], the LVEF and FS were lower in the 4thmonth(52%±8% vs 78%±4%,31%±3% vs 47%±2%,P ＜0.05), the data changed more significantly (P ＜0. 01 ) in the 6th month. The level of plasma Hcy from alcohol-fed group was significantly higher from the 2nd month than that before the experiment [( 18. 1 ± 3. 1 ) μ mol/L vs ( 9. 8 ± 2. 1 )μ mol/L,P ＜ 0. 01], and it was higher in 4th month than that in 2nd month [(26. 3 ± 4. 0) μmol/L vs (18. 1 ±3. 1) μ mol/L,P＜0.05], it was highest in 6 months. After 4-month and 6-month drinking, the expression of MMP-9 protein from alcohol group was higher than before the experiment (0. 161%±0. 019%,0. 263%±0. 014% vs 0. 050% ± 0. 008%, P ＜ 0. 0l ). Masson staining showed myocardial collagen of alcohol group was more after 4-month and 6-month drinking than those before the experiment ( 10. 23% ±1.20% vs 0. 50%±0. 09%; 22. 41% ± 2. 57% vs 0. 50% ± 0. 09%, P ＜ 0. 01 ). Plasma Hcy and cardiac tissue MMP-9 is a significant positive correlation ( r = 0. 848, P ＜ 0. 01 ). Conclusion Long-term and large drink liquor can lead to plasma Hcy levels significantly increased, and participate cardiac remodeling and the pathogenesis of ACM through increasing the expression of myocardial tissue MMP-9 protein.