S. Zakhari

Alcohol can be beneficial or harmful to the cardiovascular system, depending on the amount consumed and the characteristics of the consumer. Of the numerous cellular and molecular mechanisms that are thought to explain the beneficial effects of moderate drinking, this article discusses four, involving (1) high density lipoproteins, (2) cellular signaling, (3) platelet function in blood clot formation, and (4) stimulation of blood clot dissolution. Although light-to-moderate drinking can protect against coronary artery disease, heavy alcohol consumption can damage the cardiovascular system, resulting in maladies such as heart muscle disorders, irregular heart rhythms, high blood pressure, and strokes. This article summarizes representative epidemiological and animal studies on these cardiovascular consequences of chronic heavy alcohol consumption and reviews mechanisms that have been suggested to explain alcohol's effects.

Chronic consumption of ethanol has deleterious effects on the cardiovascular system, as manifested by an attenuation in myocardial contractility, a reduction in cardiac output, and the induction of arrhythmia. The arrhythmogenic effect of ethanol is associated with the high incidence of sudden death in alcoholics. Further, alcohol was found to potentiate arrhythmias due to nonpenetrating chest trauma, a finding of profound clinical significance. In addition, chronic ethanol consumption is closely linked to hypertension. Whether modest alcohol consumption may protect against coronary artery disease is controversial and not clearly established. Cessation of alcohol consumption occasionally results in reversal of ethanol-induced myocardial injury. However, the transition from ethanol-induced reversible injury to permanent heart damage is not well understood. Finally, the combined effects on the myocardium of alcohol and other abused drugs, such as cocaine and amphetamines, and the interaction of ethanol with chemicals such as nicotine, digitalis, and other medicaments are not well understood and may be fatal.

This paper is based upon the 'Charles Lieber Satellite Symposia' organized by Manuela G. Neuman at each of the 2009-2012 Research Society on Alcoholism (RSA) Annual Meetings. The presentations represent a broad spectrum dealing with alcoholic liver disease (ALD). In addition, a literature search (2008-2013) in the discussed area was performed in order to obtain updated data. The presentations are focused on genetic polymorphisms of ethanol metabolizing enzymes and the role of cytochrome P4502E1 (CYP2E1) in ALD. In addition, alcohol-mediated hepatocarcinogenesis, immune response to alcohol and fibrogenesis in alcoholic hepatitis as well as its co-morbidities with chronic viral hepatitis infections in the presence or absence of human deficiency virus are discussed. Finally, emphasis was led on alcohol and drug interactions as well as liver transplantation for end-stage ALD.

Shapira, Y. MD, PhD; Eilig, I. MD; LAM, A. M. MD; Paez, A.; Zakhari, S. MD; Pavlin, E. G. MD Author Information