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Alcoholic cardiomyopathy

Authors
Ihsan M Rafie, MRCP
Wilson S Colucci, MD
Section Editor
William J McKenna, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC

INTRODUCTION

Long-term excess alcohol consumption is a leading cause of secondary dilated cardiomyopathy [1,2] (table 1). However, recovery of cardiac function can occur if the disease is diagnosed early and further alcohol intake is reduced or halted. (See "Causes of dilated cardiomyopathy".)

This topic will discuss the pathogenesis, diagnosis, and treatment of alcoholic cardiomyopathy. The general and cardiovascular risks and benefits of alcohol consumption are discussed separately. (See "Overview of the risks and benefits of alcohol consumption" and "Cardiovascular benefits and risks of moderate alcohol consumption".)

DEFINITION

Alcoholic cardiomyopathy is a type of acquired dilated cardiomyopathy associated with long-term heavy alcohol consumption (commonly defined as >80 g per day over a period of at least five years) (table 1). Like other types of dilated cardiomyopathy, alcoholic cardiomyopathy is characterized by a dilated left ventricle (LV), increased LV mass, and LV systolic dysfunction (generally detected as reduced LV ejection fraction). (See 'Diagnosis' below.)

PREVALENCE

The reported prevalence of alcoholic cardiomyopathy among series of patients with heart failure or dilated cardiomyopathy has varied widely (eg, from 4 to 40 percent or more), depending upon the characteristics of the study population and the threshold alcohol consumption used to identify alcoholic cardiomyopathy [3].

The prevalence of alcoholic cardiomyopathy appears to be similar among alcoholic men and women, with women developing the condition at a lower total dose of ethanol [4,5]. In one series of 50 asymptomatic alcoholic women and 100 asymptomatic alcoholic men, approximately one-third of each group had evidence of left ventricle (LV) dysfunction [4]. LV systolic dysfunction correlated with the total lifetime dose of ethanol [4]. However, when patients were matched for LV ejection fraction, women consumed a lower total dose of ethanol adjusted for body weight compared with men. Thus, women appear to have increased sensitivity to cardiac toxicity; a similar predisposition has been identified for alcoholic liver disease and alcoholic myopathy. A proposed mechanism for this sex difference is excess accumulation of ethanol metabolites in women due to lower gastric metabolism of ethanol and higher rates of ethanol metabolism in the liver [6]. (See "Pathogenesis of alcoholic liver disease", section on 'Gastric metabolism of alcohol'.)

                         

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Literature review current through: Nov 2016. | This topic last updated: Tue Mar 24 00:00:00 GMT+00:00 2015.
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