eMedicine Specialties > Cardiology > Myocardial Disease and Cardiomyopathies

Cardiomyopathy, Alcoholic

Author: Eric D Popjes, MD, Assistant Professor, Department of Medicine, Division of Cardiology, Penn State Milton S Hershey Medical Center
Coauthor(s): Frank E Silvestry, MD, Director, PENN Cardiac Care at Radnor; Assistant Professor, Department of Medicine, Division of Cardiovascular Disease, University of Pennsylvania Health System
Contributor Information and Disclosures

Updated: Mar 13, 2008

Introduction

Background

For nearly 150 years, alcohol consumption has been associated with a variety of cardiovascular diseases. Observations during the second half of the 19th century described cardiac enlargement seen at autopsy and heart failure symptoms in persons who had consumed excessive amounts of alcohol.

During the first half of the 20th century, the concept of beriberi heart disease (ie, thiamine deficiency) was present throughout the medical literature, and the idea that alcohol had any direct effect on the myocardium was doubted. Epidemics of heart failure in persons who had consumed beer contaminated with arsenic in the 1900s and cobalt in the 1960s also obscured the observation that alcohol could exhibit a direct toxic effect. In the 1950s, evidence began to emerge that supported the idea of a direct toxic myocardial effect of alcohol, and research during the last 25 years has been particularly productive in characterizing the disease entity of alcoholic cardiomyopathy (AC).

Alcohol use has also been shown to have numerous effects on the cardiovascular system other than heart failure. It has been associated with arrhythmia (eg, atrial fibrillation, atrial flutter, other supraventricular arrhythmia, premature ventricular contractions), sudden death, hypertension, and stroke. In addition, the literature reports alcohol withdrawal being associated with takotsubo, or stress-induced, cardiomyopathy. On the other hand, numerous studies have demonstrated that light-to-moderate alcohol consumption (ie, 1-2 drinks per d or 3-9 drinks per wk) decreases the risk of cardiac events such as myocardial infarction. The focus of this review is on the effects of alcohol on the myocardium and its role as a cause of heart failure due to dilated cardiomyopathy (DC).

Pathophysiology

The mechanism of the cardiac damage produced by alcohol remains unclear. Over many years, several theories have arisen based on clinical and scientific data obtained in both human and animal studies. Original theories regarding the mechanism focused on nutritional deficiencies (eg, thiamine deficiency), secondary exposures (eg, tobacco, cobalt, arsenic), and other comorbidities (eg, hypertension). However, although these mechanisms may continue to play a role in selected patients, most evidence in the literature indicates that the effects of alcohol on the myocardium are independent of these factors and that the effect is a direct toxic result of ethanol or its metabolites.

Some studies have suggested a genetic vulnerability to the myocardial effects of alcohol consumption. Individuals with certain mitochondrial DNA mutations and angiotensin-converting enzyme genotypes (DD genotype) may be particularly susceptible to the damaging effects of alcohol. Exactly how these genetic variables may create this higher risk is not known.

To identify the causative agent, investigators administered ethanol to rats pretreated with inhibitors of ethanol metabolism. Use of ethanol alone or ethanol with an alcohol dehydrogenase inhibitor resulted in a 25% decrease in protein synthesis. When the rats were given an inhibitor of acetaldehyde dehydrogenase to increase levels of the ethanol metabolite acetaldehyde, an 80% decrease in protein synthesis occurred. Based on these data, acute ethanol-induced injury appears to be mediated by both ethanol and acetaldehyde; the latter may play a more important role.

Acetaldehyde is a potent oxidant and, as such, increases oxidative stress, leading to the formation of oxygen radicals with subsequent endothelial and tissue dysfunction. Acetaldehyde may also result in impairment of mitochondrial phosphorylation. The mitochondria play an essential role in cellular metabolism, and disruption of their function can have profound effects on the entire cell. The myocyte mitochondria in the hearts of persons exposed to alcohol are clearly abnormal in structure, and many believe that this may be an important factor in the development of alcoholic cardiomyopathy (AC).

A study in a rat model using an alcohol dehydrogenase transgene that results in elevated levels of acetaldehyde demonstrated a change in calcium metabolism at the intracellular level and a decrease in peak shortening and shortening velocity. This was interpreted by the authors as suggesting that acetaldehyde plays a key role in the cardiac dysfunction seen after alcohol intake. Others have suggested that an acute decrease in mitochondrial glutathione content may play a role in mitochondrial damage and implicate oxidative stress as a contributer in this process.

The formation of fatty acid ethyl esters during the metabolism of alcohol and specific genetic defects in fatty acid ethyl ester synthase (which metabolizes these esters and may predispose individuals to these toxic effects) have also been proposed to result in further impairment of mitochondrial phosphorylation. Acetaldehyde has also been associated with coronary vasospasm and the release of troponin T in the acute setting. The latter effect can be blocked by the administration of propranolol, implicating beta-adrenergic stimulation as an effect of acetaldehyde.

Other proposed mechanisms of injury include a direct inhibition of calcium-myofilament interaction, free radical induced lipopigment accumulation within the myocyte and inhibition of protein synthesis, an inflammatory or myocarditislike response (possibly secondary to antibodies formed against protein-acetaldehyde adducts), reduced receptor expression, abnormal membrane structure, disruption of zinc homeostasis, and an increase in myocardial superoxide dismutase activity resulting in an antioxidant imbalance.

Alcohol has been shown to have a negative effect on net protein synthesis. Many studies have shown this result, and it remains a topic of ongoing investigation and speculation. The exact manner in which alcohol produces this effect is not known, but the effect is consistent, observed throughout the heart, and may be exaggerated under stressful conditions.

Excessive intake of alcohol may result in increased systemic blood pressure in a dose-response relationship, and this may contribute to chronic myocardial dysfunction. Patients who drink more than 2 drinks per day have a 1.5- to 2-fold increase in hypertension compared to persons who do not drink alcohol, and this effect is most prominent when the daily intake of alcohol exceeds 5 drinks. Because hypertension may directly contribute to left ventricular (LV) dysfunction, this may be a confounding comorbidity in those who abuse alcohol, and it should be differentiated from pure forms of AC.

Sex

Based on currently available data, certain aspects of alcoholic cardiomyopathy (AC) are affected by the patient's sex. Several authors have reported that although AC is a disease that affects males more often (ie, due to a higher rate of alcohol abuse in men), females may be more sensitive to alcohol's cardiotoxic effects.

  • In 1997, Fernandez-Sola and colleagues evaluated 10 women and 26 men with alcohol abuse and reported a similar prevalence of cardiomyopathy between the sexes, but a lower total lifetime alcohol dose in women.1
  • In 1995, Urbano-Marquez described similar results in a group of 50 women and 100 men with alcohol abuse and 50 women who did not abuse alcohol (ie, controls). They reported a lifetime dose of alcohol in women that was 60% of that in men, but an equal incidence of cardiomyopathy and myopathy.2
  • Based on their work with a rat model, Jankala and colleagues have suggested a link between lower levels of p53 mRNA expression and female susceptibility to the development of AC.3

Age

  • Long-term alcohol use has been implicated as the etiology of LV dysfunction in as many as one third of cases of DC.
  • Alcoholic cardiomyopathy is a disease that primarily affects persons of at least middle age and is observed less commonly in those younger than 40 years, although preclinical cardiac abnormalities have been demonstrated in persons with chronic alcohol abuse. This is believed to be due primarily to the fact that alcohol must be consumed excessively for at least 10 years to have a clinically relevant effect on the myocardium.

Clinical

History

  • Similar to the pathological findings, the symptoms of alcoholic cardiomyopathy (AC) are essentially the same as those associated with other forms of DC.
    • Dyspnea, orthopnea, and paroxysmal nocturnal dyspnea are the hallmark complaints, but chest discomfort, fatigue, palpitations, dizziness, syncope, anorexia, and many others are not uncommon.
    • Onset of symptoms is usually insidious, but acute decompensations are also observed, especially in patients with asymptomatic LV dysfunction who develop atrial fibrillation or other tachyarrhythmia and, because of this, are unable to increase their cardiac output.
  • Ask any patient presenting with new heart failure of unclear etiology about their alcohol history, with attention to daily, maximal, and lifetime intake and the duration of that intake. Several important studies have clearly shown a dose-dependent effect.
    • Urbano-Marquez et al reported on 48 men with alcohol abuse with a mean daily intake of 243 g of alcohol and showed (1) an inverse relationship between total lifetime intake and ejection fraction and fractional shortening and (2) a direct relationship between total lifetime intake and LV mass. In those who consumed 70 g of ethanol (or the equivalent of 7 oz of whiskey, 20 oz of wine, or 72 oz of beer [ie, six 12-oz cans]) per day for 20 years, 36% had an abnormal ejection fraction. Age and nutritional status appeared to play little or no role.4
    • In 1986, Richardson et al evaluated 38 patients with nonischemic dilated cardiomyopathy (DC). Of these persons, 18 were classified as heavy drinkers (ie, 80 g/d or lifetime dose of 250 kg) and 20 were classified as abstinent or light drinkers. Those classified as heavy drinkers all were men who predominantly drank beer. They concluded that continuous, rather than episodic, drinking was the major risk factor for the development of heart failure and that this effect was unrelated to the hypertensive effect of alcohol.5
    • Other studies and reviews have also quoted quantities similar to those mentioned above, and the type of beverage consumed appeared to be irrelevant.

Physical

  • Physical examination findings are nonspecific and are not unique compared with findings of dilated cardiomyopathy from other causes.
  • Elevated systemic blood pressure may reflect excessive intake of alcohol, but not alcoholic cardiomyopathy per se.
  • Frequently, a relative decrease occurs in systolic blood pressure because of reduced cardiac output and increased diastolic blood pressure due to peripheral vasoconstriction, resulting in a decrease in the pulse pressure.
  • Cardiac percussion and palpation reveal evidence of an enlarged heart with a laterally displaced and diffuse point of maximal impulse.
  • Auscultation can help reveal the apical murmur of mitral regurgitation and the lower parasternal murmur of tricuspid regurgitation secondary to papillary muscle displacement and dysfunction. Third and fourth heart sounds can be heard, and they signify systolic and diastolic dysfunction. Pulmonary rales signify pulmonary congestion secondary to elevated left atrial and LV end-diastolic pressures. Jugular venous distention, peripheral edema, and hepatomegaly are evidence of elevated right heart pressures and right ventricular dysfunction.
  • Other findings may include cool extremities with decreased pulses and generalized cachexia, muscle atrophy, and weakness due to chronic heart failure and/or a direct effect of chronic alcohol consumption.
  • See Histological Findings.

Causes

See Pathophysiology and Histological Findings.

More on Cardiomyopathy, Alcoholic

Overview: Cardiomyopathy, Alcoholic
Differential Diagnoses & Workup: Cardiomyopathy, Alcoholic
Treatment & Medication: Cardiomyopathy, Alcoholic
Follow-up: Cardiomyopathy, Alcoholic
References
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Further Reading

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Keywords

alcoholism, alcohol consumption, alcohol abuse, ethanol consumption, ethanol abuse, ethanol toxicity, alcohol toxicity, cardiovascular disease, CVD, cardiac enlargement, cardiac failure, heart failure, alcoholic cardiomyopathy, AC, arrhythmia, atrial fibrillation, atrial flutter, supraventricular arrhythmia, premature ventricular contractions, sudden death, hypertension, stroke, dilated cardiomyopathy, DC, acute ethanol-induced injury, beriberi heart disease, thiamine deficiency, acetaldehyde, myocarditis

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Contributor Information and Disclosures

Author

Eric D Popjes, MD, Assistant Professor, Department of Medicine, Division of Cardiology, Penn State Milton S Hershey Medical Center
Eric D Popjes, MD is a member of the following medical societies: American College of Cardiology, Heart Failure Society of America, and International Society for Heart and Lung Transplantation
Disclosure: Nothing to disclose.

Coauthor(s)

Frank E Silvestry, MD, Director, PENN Cardiac Care at Radnor; Assistant Professor, Department of Medicine, Division of Cardiovascular Disease, University of Pennsylvania Health System
Frank E Silvestry, MD is a member of the following medical societies: American College of Cardiology, American Medical Association, and American Society of Echocardiography
Disclosure: Nothing to disclose.

Medical Editor

Gary E Sander, MD, PhD, Professor, Department of Internal Medicine, Division of Cardiology, Tulane University Health Sciences Center
Gary E Sander, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Hypertension, Heart Failure Society of America, Louisiana State Medical Society, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Frank M Sheridan, MD, Cardiology, Providence Everett Medical Center
Frank M Sheridan, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Patrice Delafontaine, MD, FACC, FAHA, FACP, FESC, Sidney W and Marilyn S Lassen Professor of Cardiovascular Medicine, Chief, Section of Cardiology, Director, Cardiovascular Center of Excellence, Tulane University; Professor of Physiology, Chair, Department of Medicine, Tulane University School of Medicine
Patrice Delafontaine, MD, FACC, FAHA, FACP, FESC is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American College of Cardiology, American College of Physicians, American Diabetes Association, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Medical Association, American Society for Clinical Investigation, Association of American Physicians, Association of Professors of Cardiology, Association of Professors of Medicine, Endocrine Society, European Society of Cardiology, Louisiana State Medical Society, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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