title: Alcoholic cardiomyopathy: is it dose-dependent?
abstract: Alcohol is a known myocardial depressant. In a dose-dependent fashion, one can show progressive decline in left ventricular systolic function. This observation has been used to implicate alcohol as a major cause of up to 30% of all dilated cardiomyopathies. However, it is not well recognized that there appears to be a biphasic cardiovascular effect based on the chronic dose of alcohol ingested. At low to moderate doses, studies suggest that alcohol has a favorable impact on cardiovascular outcomes. In other words, patients who have one to two glasses of alcohol per day have fewer myocardial infarctions and an improved survival. Large trials, such as the Physician Health Study, indicate that this benefit may be over wide ranges of doses, from one to seven glasses per week. When this is looked at in higher-risk diabetic patients, the benefit of low to moderate doses of alcohol persists. Together, this information suggests that low to moderate doses of alcohol improve cardiovascular risk, and this benefit may exceed the risk of hypertension or heart failure. It is equally important to recognize the serious down side to alcohol ingestion. At chronic high-dose intake of alcohol, there is a direct relationship to elevated blood pressure. Also, prolonged exposure to alcohol increases the likelihood of developing congestive heart failure. Combining the negative cardiovascular effects with potential danger to other organs, such as the liver, underscores the risk for high-dose alcohol. Therefore, there is a biphasic dose response to alcohol. At low to moderate doses, patients experience an overall cardiovascular benefit; it is only when a critical threshold is reached by high-dose alcohol that one observes the toxic effects. Patients on low to moderate ingestion of alcohol should be reassured, but those on high doses should be strongly encouraged to abstain due to potential toxic effects of alcohol.
authors.affiliation: Department of Medicine, UMDNJ-New Jersey Medical School, Newark, NJ, USA.
authors.forename: William K
authors.initials: WK
authors.lastname: Lee
authors.forename: Timothy J
authors.initials: TJ
authors.lastname: Regan
mesh_terms: D002310:Cardiomyopathy, Alcoholic / Q000453:epidemiology / Q000209:etiology*; D002311:Cardiomyopathy, Dilated / Q000139:chemically induced / Q000453:epidemiology; D002492:Central Nervous System Depressants / Q000008:administration & dosage* / Q000009:adverse effects*; D002986:Clinical Trials as Topic; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000008:administration & dosage* / Q000009:adverse effects*; D006321:Heart / Q000187:drug effects; D006801:Humans; D015994:Incidence; D012307:Risk Factors; D013997:Time Factors; D014481:United States / Q000453:epidemiology; D018487:Ventricular Dysfunction, Left / Q000139:chemically induced
chemical_list: D002492:Central Nervous System Depressants; D000431:Ethanol