Ethanol ingestion can induce a variety of metabolic changes in the heart, and recent studies have even suggested that moderate ethanol intake confers cardio-protective effects in reducing mortality due to coronary artery disease. However, in this review we explore the consequences of excessive ethanol intake or alcohol misuse. We investigate the epidemiology of alcohol misuse, and thereafter present evidence supporting the existence of a specific alcoholic heart muscle disease (AHMD). The prevalence of AHMD is described and the contributing mechanisms are discussed. These include the involvement of free radicals, defects in intermediary metabolism and the formation of acetaldehyde adducts. Special attention has been paid to ethanol-induced changes in protein turnover. Our studies show that ethanol impairs the protein synthetic pathways, affecting the contractile proteins per se, as well as the subcellular organelles as exemplified by the mitochondria. Acetaldehyde appears to be a particularly potent toxin. The experiments described in this review emphasize the need for investigative studies in intact models. The mechanisms inherent in the pathogenesis of AHMD may be applicable to other heart muscle disorders.