Alcoholic cardiomyopathy

INTRODUCTION

Low to moderate levels of alcohol intake have been shown to reduce cardiovascular risk, primarily the risks of coronary heart disease and ischemic stroke. However, with further increases in alcohol intake, the harmful effects of alcohol consumption outweigh the benefits, resulting in a J-shaped relationship between alcohol intake and survival (graph 1). (See "Cardiovascular benefits and risks of moderate alcohol consumption".)

The recommended maximum alcohol consumption for women and men in the United States is 7 drinks (14 units) and 14 drinks (28 units) per week, respectively. In the United Kingdom, the limit for men is the same but for women is higher at 21 units [1-3] (table 1).

Similar to the abuse of alcohol and the development of liver disease, the association between chronic alcohol consumption and alcoholic heart disease in humans is well recognized. Both acute and chronic consumption of excessive amounts of alcohol have a deleterious effect on myocardial structure and function.

Long-term excess alcohol consumption is the leading cause of secondary, nonischemic dilated cardiomyopathy [4,5]. However, recovery of cardiac function can occur if the disease is diagnosed early and further alcohol intake halted. (See "Causes of dilated cardiomyopathy".)

ETIOLOGY OF MYOCARDIAL DAMAGE

The exact pathogenesis responsible for alcoholic cardiomyopathy is not fully understood. There are three proposed mechanisms by which alcohol consumption may directly or indirectly cause myocardial damage and cardiomyopathy:
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