Published: 10 April 2022
Author(s): Antonio Mirijello, Luisa Sestito, Christian Lauria, Claudia Tarli, Gabriele Angelo Vassallo, Mariangela Antonelli, Cristina d'Angelo, Anna Ferrulli, Filippo Crea, Anthony Cossari, Lorenzo Leggio, Salvatore De Cosmo, Antonio Gasbarrini, Giovanni Addolorato
Issue: June 2022
Section: Original article

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].

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