Chronic alcohol exposure can cause myocardial degenerative diseases, manifested as cardiac insufficiency, arrhythmia, etc. These are defined as alcoholic cardiomyopathy (ACM). Alcohol-mediated myocardial injury has previously been studied through metabolomics, and it has been proved to be involved in the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway related to the biosynthesis of unsaturated fatty acids and oxidative phosphorylation, which tentatively explored the mechanism of ACM induced by chronic drinking. To further study the myocardial damage caused by alcohol, the mouse model of ACM successfully established previously was used to perform proteomics analysis on myocardial specimens. Fifty-six differentially expressed proteins (DEPs) were identified, and they are involved in the KEGG pathway related to fatty acid biosynthesis, lipid metabolism, oxidative stress, and the development of dilated cardiomyopathy (DCM). The present study further demonstrated the underlying causes of myocardial damage caused by chronic alcohol consumption and lays the foundation for further research to clarify the underlying mechanism of ACM.