Alcoholic Cardiomyopathy

Alcoholic cardiomyopathy
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Alcoholic cardiomyopathy Authors Ihsan M Rafie, MRCP Wilson S Colucci, MD Disclosures Last literature review version 19.3: Fri Sep 30 00:00:00 GMT 2011 | This topic last updated: Wed Oct 06 00:00:00 GMT 2010 (More) INTRODUCTION Low to moderate levels of alcohol intake are associated with reduced cardiovascular risk, primarily the risks of coronary heart disease and ischemic stroke although the mechanism of benefit has not been established [1]. 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 (figure 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 (28 units) but for women it is higher at 21 units [2-4] (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 a leading cause of secondary, nonischemic dilated cardiomyopathy [5,6]. 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".)
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INTRODUCTION ETIOLOGY OF MYOCARDIAL DAMAGE Possible role of ACE gene polymorphism Development of cardiomyopathy Arrhythmias PATHOLOGY CLINICAL PRESENTATION Symptoms Physical examination DIAGNOSIS Echocardiography Laboratory tests Endomyocardial biopsy Differential diagnosis TREATMENT PROGNOSIS SUMMARY REFERENCES
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Section Editor Deputy Editor William J McKenna, Susan B Yeon, MD, MD JD, FACC
FIGURES Alcohol consumption mortality Arrhythmias alcoholic CMP Survival alcoholic cardiomyop TABLES Units of alcohol Classification CV function
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ETIOLOGY OF MYOCARDIAL DAMAGE The exact pathogenesis responsible for alcoholic cardiomyopathy is not fully understood. It was once thought that alcohol causes cardiomyopathy through dietary deficiencies, but it is now clear that malnutrition is not a leading factor [7,8]. There are several proposed mechanisms by which alcohol consumption may directly or indirectly cause myocardial damage and cardiomyopathy: Ethanol induced apoptosis (programmed cell death) leading to myocytes loss [9]. Loss of cardiac cells will result in inotropic incompetence followed in the early stage by hypertrophy and later by left ventricular dilation. As the disease progresses, the left ventricular wall thickness may become normalized or reduced. Established alcoholic cardiomyopathy is characterized by pronounced left ventricular (LV) dilatation, increased LV mass, thin (or normal thickness) LV walls, diastolic dysfunction (asymptomatic phase) and systolic impairment (symptomatic phase) [10-12]. An acute and transient toxic effect on cardiac performance, resulting in impaired contraction of the myocardium [13,14]. This effect on myocardial function can become permanent with chronic alcohol consumption. The best known toxin is acetaldehyde, a metabolite of alcohol produced in the liver by alcohol dehydrogenase. Acetaldehyde is thought to cause myocardial depression through an incompletely understood process that probably involves mitochondrial dysfunction, oxidative damage, and impaired Ca2+ homeostasis [7,8,15-18]. (See "Pathogenesis of alcoholic liver disease", section on 'Alcohol metabolism'.) Defects in myofibrillar protein turnover occur during both acute and chronic alcohol consumption; and oxygen free radical-mediated damage to lipids and protein may also be involved [15]. Reduced amounts of heat shock proteins may result in poor assembly and protection of proteins [7]. The net effect of these changes in energetics,
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activation contributed to progressive decrease in heart function. The use of angiotensin receptor blocker irbesartan preserved myocardial contraction and relaxation (systolic and diastolic). Alcoholinduced hypertension observed in humans, which is associated with RAS activation, may also contribute to the development of cardiomyopathy. Patients who have more than two drinks per day have a 1.5 to 2-fold increase in the incidence of hypertension compared to nondrinkers [22]; this effect is dose-related and is most prominent when intake exceeds five drinks per day [23]. (See "Cardiovascular benefits and risks of moderate alcohol consumption", section on 'Hypertension'.) Nutritional deficiency, particularly that of thiamine. Beriberi heart disease, even though classified as alcoholic heart disease, is distinct from alcoholic cardiomyopathy and should not be regarded as such. In contrast to alcoholic cardiomyopathy, beriberi heart disease is rapidly reversible after thiamine therapy, manifests predominantly as right heart failure, is associated with increased cardiac output (high output failure), and exhibits normal myocardial histology [24]. (See "High-output heart failure", section on 'Beriberi'.) Additives to an alcoholic beverage, for example cobalt, may rarely exert a toxic effect on the myocardium [25]. (See "Causes of dilated cardiomyopathy", section on 'Trace elements'.) Possible role of ACE gene polymorphism Plasma and tissue concentrations of angiotensin converting enzyme (ACE) are determined in part by the ACE gene, which is located on chromosome 17. This gene may manifest insertion (I) or deletion (D) polymorphism and therefore three genotypes (DD, II, and ID). Plasma and cardiac levels of ACE are 1.5 to 3-fold higher in patients with the DD compared to those with II genotype; they are intermediate in patients with ID genotype. The DD polymorphism has been linked to an increased risk of a
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cardiomyopathy. In a study in which 30 alcoholic men with symptomatic cardiomyopathy were compared to 27 alcoholic men with normal cardiac function, the DD genotype was much more common in the men with cardiomyopathy (57 versus 7 percent) [26]. The odds ratio for developing left ventricular dysfunction in alcoholics with the DD compared to the ID or ID genotype was 16.4. It is not surprising that there may be genetic susceptibility to alcoholic cardiomyopathy since genetic factors also can affect the likelihood of developing cirrhosis. It is likely that currently unrecognized genetic factors contribute to the susceptibility to alcoholic cardiomyopathy. (See "Pathogenesis of alcoholic liver disease", section on 'Alcohol metabolism'.) Development of cardiomyopathy The risk of developing left ventricular dysfunction and alcoholic cardiomyopathy is related to both the mean daily alcohol intake and the duration of drinking [11,27-29]. Alcohol can produce asymptomatic cardiac dysfunction even when ingested by healthy individuals in smaller quantities typical of social drinking [30]. Most patients in whom alcoholic cardiomyopathy develops have been drinking more than 80 to 90 g of ethanol per day for more than five years (some studies quoted the average of 15 years) [5,11,27,28,31,32]. This corresponds to approximately one liter of wine, eight standard sized beers, or one-half pint of hard liquor each day. The risk is based upon the absolute amount of ethanol, so consumption of one type of beverage (such as wine) is not protective. The exact prevalence of alcoholic cardiomyopathy is not well defined. In one series of 50 asymptomatic alcoholic women and 100 asymptomatic alcoholic men, approximately one-third had evidence of left ventricular dysfunction [33]. There also appears to be a rough correlation between left ventricular dysfunction and cirrhosis. In one series, cirrhosis was found in 43 percent of 30 alcoholics with cardiomyopathy compared to only 6 percent of 30 alcoholics without cardiomyopathy [34]. Fifty percent of 20 alcoholics with cirrhosis had evidence of dilated cardiomyopathy. Cardiac function was normal in a
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lifetime dose of ethanol adjusted for body weight regardless of sex [33]. However, when patients were matched for left ventricular ejection fraction, women consumed a lower total dose of ethanol adjusted for body weight compared to men. Thus, women appear to have increased sensitivity of cardiac toxicity; a similar predisposition has been identified for alcoholic liver disease and alcoholic myopathy [33]. 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 [36]. (See "Pathogenesis of alcoholic liver disease", section on 'Gastric metabolism of alcohol'.) Arrhythmias There is no significant difference in the prevalence of atrial arrhythmias and sustained or non-sustained ventricular tachycardia (VT) in patients with alcoholic cardiomyopathy in comparison to patients with idiopathic dilated cardiomyopathy (IDCM). The most common manifestation is paroxysmal atrial arrhythmias, especially atrial fibrillation, but ventricular arrhythmias may also occur [37-40]. Prolongation of the corrected QT interval on the surface ECG (QTc), a major risk factor for ventricular arrhythmias, is found in significant proportion of alcoholics compared with non-alcoholics [41]. Hypomagnesemia and hypokalemia, which occur with increased frequency in chronic alcoholics, may be contributing factors [42-44]. Abstinence appears to reduce the frequency of arrhythmic events (figure 2) [42]. Atrial fibrillation occurs in up to 60 percent of binge drinkers with or without underlying myocardial damage, and an increased risk of atrial fibrillation has been reported among men with chronic heavy alcohol consumption [38,40,45]. Most of the cases related to binge drinking occur over weekends or holidays, producing what has been termed "the holiday heart syndrome." (see "Epidemiology of and risk factors for atrial fibrillation", section on 'Alcohol'). PATHOLOGY The gross and microscopic findings in alcoholic cardiomyopathy are usually nonspecific and are generally similar to those observed in idiopathic dilated
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exhibits structural alterations of the mitochondrial reticulum [46]. The progression of gradually developing structural changes is related to the stage of the disease [46]: The early stage is characterized by spatial reorganization of the mitochondrial reticulum; intermitochondrial junctions disappear and the mitochondria form separate clusters, uniformly distributed within a muscle cell. In the second and third stages, destructive irreversible changes in the ultrastructural organization of mitochondria develop. Megamitochondria and septate mitochondria appear. A third compartment, containing granules, forms in mitochondria. Many lipofuscin granules appear due to the accumulation of lipids in mitochondria. Structural changes in the mitochondrial reticulum are considered a compensatory adaptation in response to altered myocardial function in alcohol cardiomyopathy. Changes in enzymatic activity in the myocardium have also been observed in established alcoholic cardiomyopathy. A decrease in the activity of the majority of oxidationreduction mitochondrial enzymes, normal or increased activity of malate dehydrogenase, and increased activity of lysosomal and microsomal enzymes are seen. However, these alterations in activity are nearly identical to those seen in patients with idiopathic dilated cardiomyopathy [47]. CLINICAL PRESENTATION The patient with alcoholic cardiomyopathy presents with symptoms and physical findings that are similar to those in patients with a dilated cardiomyopathy of any etiology. Symptoms Symptoms may develop insidiously, although in some patients, symptoms of left-sided congestive heart failure may be acute in onset. Dyspnea, orthopnea, and paroxysmal nocturnal disease are frequently observed. Palpitations and syncope due to
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reveals a narrow pulse pressure, often with an elevated diastolic pressure secondary to excessive peripheral vasoconstriction. Cardiomegaly, protodiastolic (S3) and presystolic (S4) gallop sounds are common. An apical systolic murmur of mitral regurgitation, due to papillary muscle dysfunction, is often found. (See "Etiology, clinical features, and evaluation of chronic mitral regurgitation" and "Auscultation of cardiac murmurs" and "Auscultation of heart sounds".) The severity of right heart failure varies, but jugular venous distention, ascites, and peripheral edema are common in advanced disease. Measurement of the jugular venous pressure may be an important distinguishing feature in determining whether ascites is due to alcoholic cardiomyopathy or cirrhosis. The jugular venous pressure is typically normal or low-normal in cirrhosis unless there is tense ascites which, via upward pressure on the diaphragm, can increase the intrathoracic pressure [48]. Thus, in the absence of tense ascites, an elevated jugular venous pressure is highly suggestive of at least a contribution from cardiac dysfunction. On the other hand, a low normal jugular venous pressure makes heart failure much less likely as the cause of ascites. (See "Clinical manifestations and diagnosis of edema in adults", section on 'Distribution of edema and central venous pressure' and "Examination of the jugular venous pulse".) DIAGNOSIS The diagnosis of alcoholic cardiomyopathy is based upon the history of heavy and prolonged alcohol intake and signs and symptoms of heart failure as described above; the diagnosis can be confirmed by invasive and noninvasive studies. (See "Evaluation of the patient with suspected heart failure".) Echocardiography Approximately one-half of asymptomatic alcoholic subjects have left ventricular hypertrophy without echocardiographic evidence of decreased myocardial contractility [49,50]. Compared to normal control subjects, chronic alcoholics in one series had increases in the thickness of the left ventricular wall (10.4 versus 8.8 mm) and interventricular septum (11.7 versus 9.6 mm) and in left ventricular mass (145 versus 101 g/m2) [50]. These abnormalities were present despite
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It is frequently possible to demonstrate mild depression of cardiac function in chronic alcoholics even before a reduced ejection fraction becomes clinically manifest on the echocardiogram [11,51,52]. Diastolic dysfunction usually precedes systolic dysfunction and occurs more frequently once systolic impairment becomes apparent [53]. In addition, as noted above, left ventricular function is impaired in many asymptomatic alcoholics or those with cirrhosis [34]. In an echocardiographic study of 89 asymptomatic alcoholics and 30 healthy subjects, LV dilation was the initial manifestation of alcoholic cardiomyopathy [11]. LV dilation was followed by an increase in the LV myocardial mass, posterior wall thickness and diastolic interventricular wall thickness. The extent of diastolic dysfunction was related to the duration of heavy drinking, being most apparent in those with a duration of alcoholism for more than 16 years. Laboratory tests Routine laboratory tests, even though not diagnostic for alcoholic cardiomyopathy, may reveal findings suggestive of alcohol abuse among patients with dilated cardiomyopathy. These include higher values for mean red cell corpuscular volume and hemoglobin (MCV and MCH), a mild thrombocytopenia, and elevated serum levels of gammaglutamyl transpeptidase. Serum magnesium and zinc are often decreased, but copper level is increased [54,55]. (See "Alcohol abuse and hematologic disorders".) Endomyocardial biopsy Ultrastructural studies from a myocardial biopsy may allow distinctions between different etiologies for a dilated cardiomyopathy, including alcoholic cardiomyopathy (if performed before substantial fibrosis has occurred) and myocarditis [56]. In practice, however, endomyocardial biopsy is not usually performed when there is a clinical history strongly suggesting chronic alcoholism. (See "Endomyocardial biopsy".) Differential diagnosis The differential diagnosis includes other causes of dilated cardiomyopathy. (See "Causes of dilated cardiomyopathy".) The diagnosis of alcoholic cardiomyopathy is generally made clinically in patients with a history of heavy and prolonged alcohol
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disease in three [57]. TREATMENT The generally accepted treatment of alcoholic cardiomyopathy has been total and perpetual abstinence from alcohol consumption. A number of small studies have demonstrated that, if begun prior to the onset of fibrosis, abstinence can result in significant improvement in left ventricular function [37,58-64]. There are two factors associated with a favorable course [60]: A short duration of symptoms of heart failure before the initiation of therapy; patients with less fibrosis generally do better Abstinence from alcohol The potential efficacy of abstinence is illustrated by the following observations. In one series of 14 patients with alcoholic cardiomyopathy and severe heart failure, 9 patients were followed for 36 months [64]. The left ventricular ejection fraction in the 9 patients improved significantly at six months (mean of 37 versus 22 percent at baseline) with continued improvement at 36 months (mean of 43 percent). In an echocardiographic study of 13 patients with alcoholic cardiomyopathy, five demonstrated normalization of left ventricular ejection fraction (LVEF) to 55 percent or more and reduction of left ventricular end-diastolic dimension (LVEDd) to 5.7 cm or less after total abstinence for six months [63]. The normalization of LVEF and LVEDd was recognized after 3 to 12 weeks of abstinence. In the remaining eight patients, no improvement was observed, suggesting that the process becomes irreversible at some point, possibly once structural myocardial dilatation and fibrosis have occurred [65]. Consistent with this hypothesis was the observation that the ratio of left ventricular radius to wall thickness (R/Th) was !2.9 in all those showing reversion of cardiomyopathy, but was "2.9 in seven of eight
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symptoms, and cardiothoracic ratio. Although the goal is total abstinence from alcohol, this may not be necessary as there is also an improvement in LVEF if alcohol intake is "controlled" (ie, 20 to 60 g per day). This was illustrated in a prospective study of 55 men with a cardiomyopathy who consumed "100 g alcohol per day for at least 10 years [66]. During a one year follow-up, the improvement in LVEF was the same in abstainers and those who controlled their intake. In contrast, patients who continued to drink >80 g per day had a further deterioration in LVEF. Because one cannot easily measure or control alcohol intake, however, the most prudent course is to recommend abstinence. Treatment of heart failure includes salt restriction, diuretics, beta blockers, angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor blockers, and digoxin. (See "Overview of the therapy of heart failure due to systolic dysfunction".) Even in asymptomatic left ventricular dysfunction, prophylactic pharmacotherapy, eg, beta blockers, angiotensin blockers coupled with abstinence may halt or reverse the negative remodeling of the myocardium. (See "Evaluation and management of asymptomatic left ventricular systolic dysfunction".) Patients should receive a balanced diet and any nutritional deficiencies should be corrected. Vitamin supplementation with vitamin B12 and folate are important adjuncts for these patients. Attention must be paid to electrolyte disturbances, including hypokalemia and hypomagnesemia. Arrhythmias are treated in the usual fashion. (See "Ventricular arrhythmias in heart failure and cardiomyopathy" and "Atrial fibrillation in patients with heart failure".) The role of anticoagulation in patients with heart failure is discussed separately. (See "Indications for anticoagulation in heart failure".) PROGNOSIS The four-year mortality without total alcohol abstinence is close to 50 percent, even though the rate of progression and mortality in patients with alcoholic cardiomyopathy may be significantly lower than that in
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survivals (81 versus 30 percent) than 52 patients with idiopathic cardiomyopathy of comparable severity at presentation [67]. In contrast, another study of 50 patients with alcoholic cardiomyopathy found that, after a 47 month follow-up, the cardiac death rate for those who stopped drinking was the same as that for 84 patients with an idiopathic dilated cardiomyopathy; however, mortality was higher for those with alcoholic cardiomyopathy who continued to drink (figure 3) [31]. In another study of 338 men with a dilated cardiomyopathy, 23 percent had an alcoholic cardiomyopathy; those who continued to drink had a lower seven year transplant-free survival compared to those who stopped drinking or those with an idiopathic cardiomyopathy (27 versus 45 and 53 percent) [68]. SUMMARY Alcoholic cardiomyopathy is a relatively uncommon heart condition and without abstinence is associated with poor prognosis. (See 'Prognosis' above.) The pathogenesis of alcoholic cardiomyopathy is not fully understood, but experimental data has suggested potential mechanisms including ethanol induced apoptosis, toxic effects of ethanol metabolites, and activation of the renin angiotensin system. (See 'Etiology of myocardial damage' above.) The prevalence of atrial and ventricular arrhythmias is similar in alcoholic cardiomyopathy to that in idiopathic dilated cardiomyopathy. Atrial fibrillation occurs commonly in binge drinkers with or without alcoholic cardiomyopathy. (See 'Arrhythmias' above.) Women appear to have increased sensitivity to cardiac toxicity not explained by differences in body size. This sex difference may be due to excess accumulation of ethanol metabolites in women due to lower gastric metabolism of ethanol and higher rates of ethanol metabolism in the liver. (See 'Development of cardiomyopathy' above.). Unlike virtually all other form of cardiomyopathy,
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The mainstay of therapy for alcoholic cardiomyopathy is abstinence from alcohol. Treatment of heart failure includes beta blockers, angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor blockers, digoxin, and diuretics. Vitamin B12 and folate supplements are important adjuncts for these patients. (See 'Treatment' above.)
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Lancet 1985; 1:1122.

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Alcoholic Cardiomyopathy

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Alcoholic cardiomyopathy

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37. Regan TJ. Alcoholic cardiomyopathy. Prog Cardiovasc

Lancet 1985; 1:1122.

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