Review articlesAlcoholic cardiomyopathyIacovoni, Attilio; De Maria, Renata; Gavazzi, AntonelloAuthor Information aDipartimento Cardiovascolare, Ospedali Riuniti, Bergamo, Italy bIstituto di Fisiologia Clinica, CNR, Dipartimento De Gasperis, Ospedale Niguarda, Milan, Italy Received 9 December, 2009 Revised 20 January, 2010 Accepted 27 January, 2010 Correspondence to Attilio Iacovoni, MD, Dipartimento Cardiovascolare, Ospedali Riuniti, Bergamo, Italy Tel: +39 035 2639322; fax: +39 035 266128; e-mail: [email protected] Journal of Cardiovascular Medicine: December 2010 - Volume 11 - Issue 12 - p 884-892 doi: 10.2459/JCM.0b013e32833833a3 Buy Metrics Abstract The myocardial depressant effects of excessive ethanol consumption have long been known. Excessive alcohol intake is reported in a wide range (3–40%) of patients with idiopathic dilated cardiomyopathy; furthermore, chronic excessive alcohol consumption may lead to progressive and chronic cardiac dysfunction and can be a possible cause of dilated cardiomyopathy, referred to as alcoholic cardiomyopathy (ACM). The pathophysiological mechanisms underlying ACM are poorly understood. Excessive alcohol consumption has been associated with left-ventricular myocyte loss in some animal models but not in all studies. In addition, heavy drinking may cause myocyte dysfunction, due to abnormalities in calcium homeostasis, and cause elevated levels of norepinephrine. Increasing doses of ethanol have been associated with a negative inotropic effect on myocytes in animal experiments. In this review, we evaluate the epidemiology, current pathophysiological mechanisms and possible role of factors that influence ACM and discuss its clinical presentation, prognosis and treatment. © 2010 Italian Federation of Cardiology. All rights reserved.