eMedicine Specialties > Cardiology > Myocardial Disease and Cardiomyopathies

Cardiomyopathy, Alcoholic: Differential Diagnoses & Workup

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

Differential Diagnoses

Other Problems to Be Considered

Causes of dilated cardiomyopathy (DC) commonly sought during a workup for heart failure are as follows:

Coronary artery disease and ischemia
Long-standing hypertension
Infections (eg, viral [HIV], bacterial, parasitic)
Collagen vascular disease and vasculitides
Infiltrative disease (eg, amyloidosis, sarcoidosis, hemochromatosis)
Metabolic disease (eg, nutritional abnormalities, thyroid disease, diabetes, uremia)
Toxicities (eg, heavy metals, chemotherapeutic agents, cocaine, alcohol)
Muscular dystrophies and late-stage hypertrophic cardiomyopathy
Postpartum
Idiopathic

For many years, people who abused alcohol and had cirrhosis were believed to be spared from the cardiotoxic effects of alcohol; conversely, those with cardiomyopathy were believed to be spared from cirrhosis. However, recent data have shown that this almost certainly is not the case.

Estruch et al evaluated (1) 30 men with alcohol abuse and cardiomyopathy, (2) 30 men with alcohol abuse without cardiomyopathy, (3) 20 persons with alcohol abuse and cirrhosis who were actively drinking, (4) 15 persons with alcohol abuse and cirrhosis who abstained from alcohol, and (5) 15 persons without alcohol abuse with cirrhosis of other etiologies. Of the patients in group 1, 43% had evidence of cirrhosis. In group 2, 6% had evidence of cirrhosis. In group 3, 50% had evidence of DC. Cardiac evaluation of all patients in group 5 yielded normal results.6

Estruch et al concluded that (1) those who abuse alcohol and have cardiomyopathy have a higher incidence of cirrhosis compared to those who do not have cardiac dysfunction, (2) those with cirrhosis have a high incidence of cardiac dysfunction, and (3) those who drink but have liver disease and have abstained from alcohol have a low incidence of cardiac disease.6

Workup

Laboratory Studies

  • Results from serum chemistry evaluations have not been shown to be useful for distinguishing patients with alcoholic cardiomyopathy (AC) from those with other forms of dilated cardiomyopathy (DC).
    • Results from an evaluation of mean cell volume, aspartate aminotransferase levels, alanine aminotransferase levels, lactate dehydrogenase (LDH) levels, and gamma-glutamyltransferase levels have been shown to be similar in persons with AC compared to persons with other forms of DC. However, results from tissue assays have been shown to be potentially helpful in distinguishing AC from other forms of DC.
    • Richardson et al showed an elevation of creatine kinase, LDH, malic dehydrogenase, and alpha-hydroxybutyric dehydrogenase levels in endomyocardial biopsy specimens taken from 38 patients with DC.

Imaging Studies

  • Chest radiographs usually show evidence of cardiac enlargement, pulmonary congestion, and pleural effusions.
  • Results from resting and stress nuclear imaging techniques (eg, stress testing with thallium and sestamibi imaging, multiple gated acquisition (MUGA) scan, positron emission tomography scan) may be useful for evaluating cardiac size and function and for screening for coronary disease.
  • Echocardiography is perhaps the most useful initial diagnostic tool in the evaluation of patients with heart failure.
    • Because of the ease and speed of the test and its noninvasive nature, it is the study of choice in the initial and follow-up evaluation of most forms of cardiomyopathy.
    • In addition, it provides information not only overall heart size and function, but on valvular structure and function, wall motion and thickness, and pericardial disease.
    • Echocardiographic findings in persons with AC are similar to those in persons with idiopathic DC.
    • Echocardiographic findings in persons with AC are as follows:
      • Four-chamber dilatation
      • Globally decreased ventricular function
      • Mitral and tricuspid regurgitation
      • Pulmonary hypertension
      • Evidence of diastolic dysfunction: These changes can be seen even in the absence of systolic dysfunction but seem to be more prevalent in patients with coexisting systolic dysfunction. The progression of diastolic dysfunction in asymptomatic individuals may be related to the duration of alcoholism.
      • Intracardiac thrombi (atrial or ventricular)
      • LV hypertrophy

Other Tests

  • ECG findings are frequently abnormal, and these findings may be the only indication of heart disease in asymptomatic patients.
    • Palpitations, dizziness, and syncope are common complaints and are frequently caused by arrhythmias (eg, atrial fibrillation, flutter) and premature contractions.
    • In the setting of acute alcohol use or intoxication, this is called holiday heart syndrome because incidence is increased following weekends and during holiday seasons.
    • Other supraventricular tachyarrhythmias and sudden death have also been associated with alcohol use and AC, with the latter being most likely secondary to the development of ventricular fibrillation.
    • Conduction disturbances, such as degrees of atrioventricular block, left or right bundle-branch block, and hemiblocks, are also observed.
    • Criteria associated with LV hypertrophy with a repolarization abnormality, prolonged repolarization (ie, QT interval), nonspecific ST- and T-wave changes, and Q waves have also been described.

Procedures

  • In patients with DC, if additional questions remain after a history is obtained and noninvasive testing is performed, cardiac catheterization may be used to help exclude other etiologies of heart failure.
    • Although the most common cause of heart failure and is coronary artery disease, ischemic cardiomyopathy is unlikely in the absence of a clear history of prior ischemic events or angina and in the absence of Q waves on the ECG strip. In most patients, exercise or pharmacological stress testing with echocardiographic or nuclear imaging is an appropriate screening test for heart failure due to coronary artery disease.
    • In addition to the assessment of the status of the coronary arteries, cardiac catheterization may help obtain useful information regarding cardiac output, the degree of aortic or mitral valvular disease, and cardiac hemodynamics and filling pressures. Importantly however, remember that much of this information can be derived or inferred from the results of noninvasive testing.
    • In persons with AC, common findings after catheterization include nonobstructive coronary disease; elevated LV end-diastolic pressure, wedge pressure, pulmonary artery pressure, and right heart pressure; increased LV size with decreased overall function; and mild or moderate mitral regurgitation. Regional wall motion abnormalities are not uncommon, but they are usually less prominent than those observed in persons with ischemic heart disease.

Histologic Findings

The pathological and histological findings of AC are essentially indistinguishable from those of other forms of DC (see Proposed mechanisms of injury for AC). Findings from gross examination include an enlarged heart with 4-chamber dilatation and overall increased cardiac mass. Histologically, light microscopy reveals interstitial fibrosis (a finding that has been shown to be prevented by zinc supplementation in the mouse model), myocyte necrosis with hypertrophy of other myocytes, and evidence of inflammation. Electron microscopy reveals mitochondrial enlargement and disorganization, dilatation of the sarcoplasmic reticulum, fat and glycogen deposition, and dilatation of the intercalating discs.

Although the qualitative properties of AC and other forms of DC may be similar, quantitative differences may exist. Teragaki and colleagues compared 20 patients with AC and 10 patients with DC.7 They reported less myocyte hypertrophy and fibrosis in patients with AC, found a greater improvement of cardiac size with treatment or abstinence in the AC group, and noted that the cardiac index was higher in patients with AC who had less fibrosis.8 In the 1989 study by Urbano-Marquez et al, a comparison of symptomatic to asymptomatic patients revealed more extensive fibrosis in patients with symptoms.4 Others have looked at immunohistologic markers and have suggested that the presence of these markers might suggest an inflammatory process such as myocarditis, and their absence may point more toward AC or an idiopathic etiology.

Ultimately, AC is a clinical diagnosis made in a patient presenting with the constellation of findings that includes a history of excessive alcohol intake, possible physical signs of alcohol abuse (eg, parotid disease, telangiectasia or spider angiomata, mental status changes, cirrhosis), heart failure, and supportive evidence consistent with DC. Hypertension due to alcohol may be a confounding comorbidity in that it may contribute to LV dysfunction; therefore, LV dysfunction due to hypertension must be differentiated from pure AC.

Proposed mechanisms of injury for AC are as follows:
  • Inhibition of protein synthesis
  • Inhibition of oxidative phosphorylation
  • Fatty acid ester accumulation
  • Free radical damage
  • Inhibition of calcium-myofilament interaction
  • Inflammatory and immunological factors
  • Receptor abnormalities
  • Disruption of cell membrane structure
  • Coronary vasospasm
  • Synergy with concomitant conditions

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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