Alcoholic cardiomyopathy (ACM) represents one of the leading causes of non-ischemic dilated myocardial disease in Western Countries [1]. ACM significantly contributes to the global burden of cardiovascular diseases, accounting for substantial morbidity and mortality among young people, particularly men [2,3]. ACM is defined as a dilatation of ventricular chambers with impaired ejection fraction and normal or reduced wall thickness in individuals with chronic excessive alcohol use [4]. Pathophysiological mechanisms of ACM include a dose-dependent toxic effect of alcohol and its metabolites (e.g., acetaldehyde and ethyl esters) on myocytes, together with the activation of neuro-hormonal compensatory mechanisms, leading to structural myocardial alterations and clinically relevant heart failure (end-stage ACM) [5,6].
