Alcohol-induced cardiomyopathy

INTRODUCTION — Long-term excess alcohol consumption is a leading cause of secondary dilated cardiomyopathy (table 1) [1,2]. 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 alcohol-induced 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 AND PREVALENCE — Alcohol-induced cardiomyopathy is a type of acquired dilated cardiomyopathy caused by long-term heavy alcohol consumption. Diagnostic criteria are discussed below. (See 'Diagnostic criteria' below.)

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

The prevalence of alcohol-induced cardiomyopathy appears to be similar among males and females with alcohol use disorder; however, there is a higher disease burden in males, with a series recording the sex ratio of hospital admission with the condition at almost 9:1 [4]. The main age group affected is from 45 to 59 years old, followed by 60 to 74 years old. Females develop the condition at a lower total dose of ethanol [5,6]. In one series of 50 asymptomatic females with alcohol use disorder and 100 asymptomatic males with alcohol use disorder, approximately one-third of each group had evidence of left ventricle (LV) dysfunction [5]. LV systolic dysfunction correlated with the total lifetime dose of ethanol [5]. However, when patients were matched for LV ejection fraction (LVEF), females consumed a lower total dose of ethanol adjusted for body weight compared with males. Thus, females appear to have increased sensitivity to cardiac toxicity; a similar predisposition has been identified for alcohol-induced liver disease and myopathy. A proposed mechanism for this sex difference is excess accumulation of ethanol metabolites in females due to lower gastric metabolism of ethanol and higher rates of ethanol metabolism in the liver [7]. (See "Pathogenesis of alcohol-associated liver disease", section on 'Gastric metabolism of alcohol'.)

Relation to alcohol consumption — At higher levels of alcohol intake, LV dysfunction and alcohol-induced cardiomyopathy are related to both the mean daily alcohol intake and the duration of drinking [8-11]. Alcohol intoxication can produce acute asymptomatic cardiac dysfunction even when ingested by healthy individuals in quantities typical of social drinking [12]. Likewise, in non-alcohol-dependent subjects, habitual binge-drinking is associated with transient myocardial changes detectable by magnetic resonance imaging (MRI), elevated serum markers for myocardial injury, changes in microindices of myocardial dysfunction, and coronary vasoconstriction [13].

Most patients in whom alcohol-induced cardiomyopathy develops have been drinking more than 80 to 90 g of ethanol per day for more than five years (some studies quoted an average of 15 years) [1,8-10,14,15]. 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 a specific type of beverage (such as wine) is not protective.

The U-shaped relationship between alcohol intake and HF is similar to that observed for alcohol consumption and survival (figure 1). (See "Overview of the risks and benefits of alcohol consumption" and "Cardiovascular benefits and risks of moderate alcohol consumption".)

Relation to liver cirrhosis — There is evidence of a rough correlation between LV dysfunction and cirrhosis. In one series, cirrhosis was found in 43 percent of 30 persons with alcohol use disorder with cardiomyopathy compared with only 6 percent of 30 persons with alcohol use disorder without cardiomyopathy [16]. Fifty percent of 20 persons with alcohol use disorder with cirrhosis had evidence of dilated cardiomyopathy. Cardiac function was normal in a control group of patients with cirrhosis but without alcohol use disorder.

Of note, other studies have identified the separate condition of cirrhotic cardiomyopathy in patients with cirrhosis related to alcohol use disorder or cirrhosis not related to alcohol use disorder. (See 'Cirrhotic cardiomyopathy' below.)

PATHOGENESIS — The pathogenesis of alcohol-induced cardiomyopathy is not fully understood. The toxic effect of acute alcohol binge on cardiac performance is transient, but chronic consumption may result in permanent impairment of myocardial contractility due to the effects of ethanol and its metabolites. The best-known toxic metabolite 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 calcium ion homeostasis [17-23]. (See "Pathogenesis of alcohol-associated liver disease", section on 'Alcohol metabolism'.)

There are several proposed mechanisms by which ethanol consumption may directly or indirectly (via metabolites) cause myocardial damage and cardiomyopathy [24-28]:

●Ethanol exposure may cause oxidative stress within the myocardium either directly by stimulating the generation of free radicals or indirectly by activating other systems, such as the renin-angiotensin system (RAS) [19,26,27].

●Acetaldehyde from ethanol activates local RAS, which has been implicated in apoptosis leading to myocyte loss and adverse remodeling at the cellular level and arterial hypertension at the systemic level [28-30]. Arterial hypertension may contribute to or worsen HF. (See "Cardiovascular benefits and risks of moderate alcohol consumption", section on 'Hypertension'.)

●Impaired mitochondrial bioenergetics may contribute, as suggested by studies showing changes in mitochondrial ultrastructure and/or function [26,27].

●Low levels of STAT3 (signal transducer and activator of transcription 3), act as a downstream target for ALDH2 (aldehyde dehydrogenase). ALDH2 provides cardioprotective effects following ethanol exposure via STAT3, which is an important pathway component for mitochondrial respiration [31]. In mice, a moderate alcohol dose stimulates ALDH2, whereas a high dose inhibits ALDH2 [30].

●Altered fatty acid metabolism and transport may contribute to myocardial dysfunction [26].

●Long-term ethanol administration decreases myocardial protein synthesis and accelerates protein catabolism and autophagy [17,26,29].

Genetic factors may predispose to alcohol-induced cardiomyopathy, though evidence is limited. As an example, DD polymorphism of the angiotensin-converting enzyme (ACE) gene may predispose to alcohol-induced cardiomyopathy. In a study in which 30 males with alcohol use disorder with symptomatic cardiomyopathy were compared with 27 males with alcohol use disorder with normal cardiac function, the DD genotype was much more common in the males with cardiomyopathy (57 versus 7 percent) [32].

The prevalence of most variants of well-characterized genes known to cause dilated cardiomyopathy were similar in patients with dilated versus alcohol-induced cardiomyopathy. However, in patients with excess alcohol consumption, patients with truncations of the large structural protein, titin, showed an 8.7 percent absolute decrease in LVEF versus patients without titin truncations [33].

Although it was once thought that alcohol caused cardiomyopathy primarily through nutritional deficiencies, it is now clear that malnutrition is not a leading factor [17,18]. Even though beriberi heart disease has been classified as an alcohol-induced heart disease, it is distinct from alcohol-induced cardiomyopathy. (See 'Beriberi' below.)

In addition to the above toxicities attributed to ethanol and its metabolites, additives to an alcoholic beverage (for example, cobalt added to beer) may exert a toxic effect on the myocardium. (See "Causes of dilated cardiomyopathy", section on 'Alcohol'.)

PATHOLOGY — The gross and microscopic findings in alcohol-induced cardiomyopathy are generally nonspecific and indistinguishable to those observed in idiopathic dilated cardiomyopathy, though the latter condition may be associated with more marked histologic abnormalities [34-37]. Findings include interstitial fibrosis, myocyte hypertrophy, and myocytolysis [38].

However, certain ultrastructural details may be suggestive of alcohol-induced cardiomyopathy. Alcohol, even in small amounts, may result in alterations of mitochondrial structure and function, and endomyocardial biopsy material from patients with chronic alcohol use disorder exhibits structural alterations of the mitochondrial reticulum [39]. In vitro animal studies show the cardiac ultrastructural changes after exposure to ethanol to be consistent and predictable [40,41].

The progression of gradually developing structural changes is related to the stage of the disease [39]:

●The early stage is characterized by spatial reorganization of the mitochondrial reticulum; junctions between mitochondria disappear and the mitochondria form separate clusters, uniformly distributed within a myocyte.

●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-induced cardiomyopathy.

Changes in enzymatic activity in the myocardium have also been observed in both early and established alcohol-induced cardiomyopathy in humans and animal models. A decrease in the activity of the majority of oxidation-reduction mitochondrial enzymes, normal or increased activity of malate dehydrogenase, increased fatty acid uptake, and increased activity of lysosomal and microsomal enzymes are seen [42]. However, these alterations in activity are nearly identical to those seen in patients with idiopathic dilated cardiomyopathy [43].

CLINICAL MANIFESTATIONS — The patient with alcohol-induced cardiomyopathy presents with symptoms and signs like those in patients with other forms of cardiomyopathy. In addition, symptoms and signs of unhealthy alcohol use may be observed. (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Management and prognosis of asymptomatic left ventricular systolic dysfunction" and "Risky drinking and alcohol use disorder: Epidemiology, clinical features, adverse consequences, screening, and assessment", section on 'Clinical manifestations'.)

Symptoms and signs — Symptoms may develop insidiously, although, in some patients, symptoms of left-sided HF may be acute in onset. Dyspnea, orthopnea, and paroxysmal nocturnal disease are frequently observed. Angina pectoris is suggestive of concomitant coronary artery disease (CAD; or aortic stenosis), though up to one-third of patients with nonischemic cardiomyopathy have chest pain that may resemble angina or be atypical. Palpitation and syncope due to tachyarrhythmias, usually supraventricular, are occasionally present. (See 'Arrhythmias' below.)

Physical examination usually reveals signs of left and right HF including a narrow pulse pressure, often with an elevated diastolic systemic arterial pressure secondary to excessive peripheral vasoconstriction. Cardiomegaly (manifest as a laterally displaced and enlarged apical impulse), protodiastolic (S3), and presystolic (S4) gallop sounds are common. An apical systolic murmur of secondary mitral regurgitation is often found. The severity of right HF varies, but jugular venous distention, ascites, and peripheral edema are common in advanced disease. (See "Heart failure: Clinical manifestations and diagnosis in adults", section on 'Physical examination' and "Auscultation of cardiac murmurs in adults" and "Auscultation of heart sounds".)

Measurement of the jugular venous pressure may be an important distinguishing feature in determining whether ascites is due to alcohol-induced 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 [44]. 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 HF much less likely as the cause of ascites. (See "Examination of the jugular venous pulse" and "Clinical manifestations and evaluation of edema in adults".)

Initial test results — Routine laboratory tests may reveal systemic findings suggestive of alcohol abuse among patients with dilated cardiomyopathy [45]. These include higher values for mean red cell corpuscular volume and hemoglobin, a mild thrombocytopenia, and elevated serum levels of gamma-glutamyl transpeptidase and aspartate aminotransferase (AST). An AST to alanine aminotransferase (ALT) ratio >2 is highly suggestive of alcohol-induced liver disease. (See "Clinical manifestations and diagnosis of alcohol-associated fatty liver disease and cirrhosis", section on 'Laboratory tests'.)

An electrocardiogram (ECG) is generally performed in patients with suspected alcohol-induced cardiomyopathy, although findings are nonspecific. In patients with alcohol-induced cardiomyopathy, ECG findings may include arrhythmia (particularly atrial fibrillation [AF]), a prolonged corrected QT (QTc) interval, a prolonged QRS duration (which is an adverse prognostic indicator), conduction abnormalities (eg, left bundle branch block or intraventricular conduction delay), and ST and T wave changes [46]. (See 'Arrhythmias' below and 'Prognosis' below.)

A chest radiograph is not required for diagnosis of cardiomyopathy but is commonly obtained in patients with suspected HF to identify signs of pulmonary edema and to exclude other causes of dyspnea. Some patients with alcohol-induced cardiomyopathy have cardiomegaly (increased cardiothoracic ratio), but this finding has limited specificity and sensitivity for LV dilation compared with echocardiography [47].

An echocardiogram is a key test in the diagnosis of alcohol-induced cardiomyopathy, as discussed below. (See 'Echocardiography' below.)

Arrhythmias — Patients with alcohol-induced cardiomyopathy have similar rates of atrial and ventricular arrhythmias to patients with idiopathic dilated cardiomyopathy. The most common manifestation is paroxysmal atrial arrhythmias, especially AF, but ventricular arrhythmias may also occur [48-51]. In a study comparing 94 patients with alcohol-induced cardiomyopathy with 188 patients with idiopathic dilated cardiomyopathy, AF was common in both groups (34 and 24 percent, respectively) [52]. Mild prolongation of the QTc interval on the surface ECG (QTc), a risk factor for ventricular arrhythmias, is found in a proportion of patients with alcohol use disorder compared with persons without alcohol use disorder [53]. Hypomagnesemia and hypokalemia, which occur with increased frequency in patients with alcohol use disorder, may be contributing factors [54-56]. Abstinence appears to reduce the frequency of arrhythmic events (figure 2) [54].

DIAGNOSIS

When to suspect the diagnosis — The diagnosis of alcohol-induced cardiomyopathy should be suspected in individuals with a history of heavy and prolonged alcohol use with signs of LV dilation (eg, laterally displaced and enlarged apical impulse) or symptoms or signs of HF (eg, dyspnea, fatigue). (See 'Symptoms and signs' above.)

Diagnostic criteria — Alcohol-induced cardiomyopathy is diagnosed in patients with all three of the following criteria:

●Long-term heavy alcohol consumption (commonly defined as >80 g per day over a period of at least five years).

●Features of dilated cardiomyopathy – The following two features are generally identified by echocardiography. If the echocardiogram is suboptimal, cardiovascular magnetic resonance (CMR) or computed tomography (CT) are alternative methods for identifying these features. (See 'Echocardiography' below and 'Other cardiac imaging' below.)

•LV dilation defined as LV end-diastolic volume or LV diastolic dimension (LVDD) greater than 2 standard deviations above normal (by echocardiography, an LVDD >58.4 mm in males and >52.2 mm in females [57]).

with

•LVEF below normal – While the normal range for LVEF varies among imaging modalities and populations, an LVEF <50 percent is abnormal across modalities and is an accepted threshold for dilated cardiomyopathy [58]. (See "Tests to evaluate left ventricular systolic function".)

and

•Absence of hypertensive, valvular, and ischemic heart disease and other causes of dilated cardiomyopathy sufficient to have caused the LV systolic dysfunction. CAD should be excluded. (See "Causes of dilated cardiomyopathy" and 'Evaluation for CAD' below.)

Diagnostic tests — Patients with suspected alcohol-induced cardiomyopathy should undergo echocardiography as well as evaluation for CAD.

Echocardiography — Echocardiography is generally a key diagnostic test in patients with alcohol-induced cardiomyopathy. Alcohol-induced cardiomyopathy is characterized by pronounced LV or biventricular dilation, increased LV mass, thin (or normal thickness) LV walls, diastolic dysfunction, and systolic impairment [10,58-60]. If LV size and systolic function cannot be adequately assessed, other noninvasive cardiac imaging is recommended. (See 'Other cardiac imaging' below.)

Approximately one-half of asymptomatic subjects with alcohol use disorder have a mild increase in LV wall thickness without echocardiographic evidence of decreased myocardial contractility [61,62]. Compared with normal control subjects, persons with alcohol use disorder in one series had increases in the thickness of the LV wall (10.4 versus 8.8 mm) and interventricular septum (11.7 versus 9.6 mm) and in LV mass (145 versus 101 g/m2) [62]. These abnormalities were present despite normal echocardiographic indices of myocardial contractility including ejection fraction, wall excursion, velocity, and circumferential fiber shortening. Systolic time intervals have revealed shortening of ejection time and prolongation of the preejection period.

In the 20-year analysis of 2368 healthy subjects from the Coronary Artery Risk Development in Young Adults (CARDIA) registry, chronic alcohol consumption was found to be an independent risk factor for increased indexed LV mass and end-diastolic volume regardless of sex [63]. Despite these changes, no reduction in LVEF was noted. In an echocardiographic study of 89 asymptomatic patients with alcohol use disorder and 30 healthy subjects, LV dilation was the initial manifestation of alcohol-induced cardiomyopathy [10]. LV dilation was followed by an increase in the LV myocardial mass, posterior wall thickness, and diastolic interventricular wall thickness.

Mild cardiac dysfunction is frequently detectable in patients with chronic alcohol use disorder before a reduced ejection fraction becomes clinically manifest [10,64,65]. Diastolic dysfunction usually precedes systolic dysfunction and occurs more frequently once systolic impairment becomes apparent [66]. In one study, the extent of diastolic dysfunction was related to the duration of heavy drinking, being most apparent in those with a duration of alcohol use disorder of more than 16 years [10].

In another series utilizing two-dimensional speckle tracking echocardiography involving 122 subjects, those who consumed moderate (>90 to 150 mg ethanol daily, three to five days per week for 9 to 20 years) and heavy (>150 mg ethanol daily, six to seven days per week for more than 10 years) alcohol displayed lower circumferential, longitudinal, and radial strain values (systolic) as well as early to late (E/A) filling ratios (diastolic) compared with mild drinkers (>90 mg ethanol daily, three to five days per week for five to eight years) and nondrinkers. These changes show that moderate to heavy alcohol intake can cause subclinical depression of both systolic and diastolic function, and suggest that this echocardiographic technique may be useful in identifying drinkers with asymptomatic LV dysfunction who are at risk of developing alcohol-induced cardiomyopathy [67].

Evaluation for CAD — We suggest evaluation for CAD in patients with new HF and/or dilated cardiomyopathy who are potential candidates for revascularization. Noninvasive stress testing is a reasonable first step, since this also provides information for risk stratification and prognosis. However, coronary angiography is an alternative to stress testing in high-risk patients who are potential candidates for revascularization (and is also indicated in patients with intermediate- or high-risk features on stress testing and LV dysfunction). Noninvasive coronary angiography using CMR or CT is a potential option to evaluate CAD in patients with dilated cardiomyopathy of uncertain cause. (See "Prognostic features of stress testing in patients with known or suspected coronary disease" and "Clinical utility of cardiovascular magnetic resonance imaging", section on 'Cardiomyopathy'.)

Additional tests in selected patients — Additional testing is indicated in selected patients with a nondiagnostic echocardiogram or indications for endocardial biopsy to exclude another cause of dilated cardiomyopathy.

Other cardiac imaging — If echocardiographic images are suboptimal for identification of features of dilated cardiomyopathy, other cardiac imaging to evaluate ventricular chamber sizes, wall thicknesses, and systolic function is suggested. CMR often provides superior image quality and definition compared with echocardiography, although there are no distinctive CMR features to differentiate alcohol- induced cardiomyopathy from other types of cardiomyopathy [68]. An additional benefit of CMR is its utility in identifying characteristics suggestive of other specific causes of HF and cardiomyopathy, such as ischemic heart disease, amyloidosis, and iron overload. CT is another alternative to echocardiography that can combine coronary artery and ventricular imaging. The use of other cardiac imaging to assess LV size and function (such as radionuclide ventriculography) is discussed separately. (See "Tests to evaluate left ventricular systolic function".)

Endomyocardial biopsy — Endomyocardial biopsy is not generally indicated when the diagnosis of alcohol-induced cardiomyopathy is strongly suspected, since histologic changes in alcohol-induced cardiomyopathy are similar to those seen in idiopathic dilated cardiomyopathy. However, endomyocardial biopsy is indicated in selected cases when other diagnoses (eg, amyloidosis) are suspected based upon the noninvasive evaluation and other means of confirming the diagnosis are unavailable. (See "Determining the etiology and severity of heart failure or cardiomyopathy" and 'Differential diagnosis' below and "Endomyocardial biopsy".)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of alcohol-induced cardiomyopathy includes other causes of HF such as hypertensive, valvular, and ischemic heart disease and other inherited and systemic causes of dilated cardiomyopathy, including cirrhotic cardiomyopathy and beriberi; CAD should be excluded, as described above. (See 'Evaluation for CAD' above.)

Other causes of dilated cardiomyopathy — The differential diagnosis includes other causes of dilated cardiomyopathy (table 1) which should be considered based upon history, symptoms, and signs suggestive of specific etiologies. As an example, ischemic heart disease should generally be excluded in patients with new HF and/or dilated cardiomyopathy. The importance of considering other potential causes was highlighted by a series that included seven patients with alcohol use disorder; endomyocardial biopsy revealed hemochromatosis in two, amyloidosis in one, doxorubicin-related toxicity in one, and evidence of alcohol-induced heart disease in three [69]. (See "Causes of dilated cardiomyopathy" and "Determining the etiology and severity of heart failure or cardiomyopathy".)

Cirrhotic cardiomyopathy — The differential diagnosis includes cirrhotic cardiomyopathy, another type of myocardial dysfunction that occurs in patients with cirrhosis. Experimental and observational studies have found that cirrhosis is associated with myocardial dysfunction independent of alcohol exposure. The definition, causes, and manifestations of cirrhotic cardiomyopathy are not well established. The condition has been defined as an otherwise unexplained chronic cardiac dysfunction in patients with cirrhosis with impaired contractile responsiveness to stress and/or diastolic dysfunction. The clinical and hemodynamic findings may be similar to those of alcohol-induced cardiomyopathy, and some patients with alcohol-induced cardiomyopathy may develop further cardiac dysfunction when due to alcohol-induced cirrhotic liver failure. Unlike alcohol-induced cardiomyopathy, which can improve with alcohol abstinence, the cardiomyopathy of cirrhosis is only improved by restitution of adequate liver function, either because of liver recovery or transplantation [70-73]. Electrical abnormalities include QT interval prolongation, electrical and mechanical dyssynchrony, and chronotropic incompetence [72]. Most patients with this condition are diagnosed during clinical decompensation of cirrhosis with HF with preserved ejection fraction and/or high-output HF. (See "Cirrhosis in adults: Overview of complications, general management, and prognosis", section on 'Cirrhotic cardiomyopathy' and "Definition and classification of the cardiomyopathies", section on 'Cirrhotic cardiomyopathy'.)

A careful history and echocardiography (or other noninvasive cardiac imaging) may be helpful in distinguishing cirrhotic cardiomyopathy from alcohol-induced cardiomyopathy and other types of dilated cardiomyopathy. In cirrhotic cardiomyopathy, findings similar to alcohol-induced cardiomyopathy may include a dilated left atrium, thickened LV walls, and systolic and/or diastolic dysfunction [73]. Alcohol-induced cardiomyopathy is generally associated with LV dilation, which may or may not be present in patients with cirrhotic cardiomyopathy.

Other causes of atrial fibrillation — While AF is common in patients with alcohol-induced cardiomyopathy, AF also commonly occurs in individuals who consume alcohol who do not have evidence of structural heart disease. AF occurs in up to 60 percent of binge drinkers with or without evidence of underlying myocardial disease, and an increased risk of AF has been reported among males with chronic heavy alcohol consumption [49,51,74]. Most of the cases related to binge drinking occur over weekends or holidays, producing what has been termed "the holiday heart syndrome." (See "Epidemiology, risk factors, and prevention of atrial fibrillation", section on 'Alcohol'.)

Beriberi — Beriberi is a cause of high-output HF caused by severe thiamine (vitamin B1) deficiency. In contrast to alcohol-induced cardiomyopathy, beriberi heart disease manifests predominantly as right-sided HF, is associated with increased cardiac output (high output failure), and is rapidly reversible after thiamine therapy. (See "Causes and pathophysiology of high-output heart failure", section on 'Beriberi' and "Clinical manifestations, diagnosis, and management of high-output heart failure".)

TREATMENT

General measures — Patients should receive a balanced diet and any nutritional deficiencies should be corrected. Supplementation with vitamin B12, vitamin B6, and folate are important adjuncts, particularly for individuals with sustained heavy alcohol use. Electrolyte disturbances, including hypokalemia and hypomagnesemia, should be monitored and corrected. (See "Nutritional status in patients with sustained heavy alcohol use" and "Nutritional issues in adult patients with cirrhosis".)

Patients with alcohol-induced cardiomyopathy often have comorbidities such as depression, liver disease, drug abuse, smoking, and pulmonary disease [4], which need to be addressed concurrently through a multidisciplinary approach. Management of alcohol use disorder is discussed separately. (See "Alcohol use disorder: Treatment overview" and "Alcohol use disorder: Psychosocial management".)

Abstinence from alcohol — Patients with alcohol-induced cardiomyopathy require total and perpetual abstinence from alcohol consumption. (See "Alcohol use disorder: Treatment overview" and "Alcohol use disorder: Psychosocial management".)

Small observational studies have suggested that LV function improves in some patients with abstinence [48,75-82]. Short duration of HF symptoms prior to abstinence may favor recovery [77] (see "Alcohol use disorder: Psychosocial management"). No marker for reversibility has been identified. Though some studies have cited lack of myocardial interstitial fibrosis as a potential indicator of reversibility, limited data on morphometry have yielded mixed results [34,83].

The potential efficacy of abstinence is illustrated by the following studies:

●In a series of 101 patients with alcohol-induced cardiomyopathy who were followed for a median period of 82 months, 42 percent of patients recovered (defined by an increase in LVEF of ≥10 percent to a final value of ≥40 percent). None of the patients who continued to drink heavily recovered. There was no difference in the recovery rate between abstainers (44 percent) and those who reduced drinking to moderate (45 percent). The independent predictors for LVEF recovery were the use of beta blocker therapy, narrow QRS complex (<120 ms), and the absence of diuretics use [82].

●In another series of 14 patients with alcohol-induced cardiomyopathy and severe HF, nine patients were followed for 36 months [81]. LVEF in the nine 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 alcohol-induced cardiomyopathy, five demonstrated normalization of LVEF to 55 percent or more and reduction of LV end-diastolic dimension to 5.7 cm or less after total abstinence for six months [80].

If abstinence cannot be achieved, we counsel the patient to reduce their alcohol consumption as much as possible. Studies have shown that improvement in LVEF can occur with "controlled" alcohol consumption (ie, 20 to 60 g per day).

●In a prospective study of 55 males with a cardiomyopathy who consumed ≥100 g alcohol per day for at least 10 years (figure 3) [84], the improvement in LVEF at one year was similar in abstainers and those who controlled their intake (20 to 60 g per day). By contrast, patients who continued to drink >80 g per day had a further deterioration in LVEF.

●Similarly, a study of 94 patients with alcohol-induced cardiomyopathy found that those who reduced their alcohol intake to moderate levels (<80 g per day; most <20 to 30 g per day) exhibited similar survival and improvement in LVEF as those who abstained from alcohol [52].

Pharmacologic therapy — Treatment of HF with reduced ejection fraction generally includes a combination of a diuretic, beta blocker, angiotensin-converting enzyme (ACE) inhibitor, angiotensin receptor-neprilysin inhibitor or angiotensin II receptor blocker, a mineralocorticoid receptor antagonist, and an sodium-glucose co-transporter 2 inhibitor as indicated. (See "Overview of the management of heart failure with reduced ejection fraction in adults".)

In patients with asymptomatic LV systolic dysfunction with LVEF ≤40 percent, pharmacotherapy coupled with abstinence may halt or reverse the negative remodeling of the myocardium (see "Management and prognosis of asymptomatic left ventricular systolic dysfunction"). With abstinence and/or pharmacologic therapy, an increase in LVEF to >40 percent has a good prognosis with very low mortality [82].

In a case control study of patients with alcohol-induced cardiomyopathy (n = 60), the use of either carvedilol (6.25 to 12.5 mg twice daily) or trimetazidine (20 mg three times daily) with conventional HF drugs for 12 weeks was associated with higher LVEF and lower C-reactive protein, as well as longer walking distance in six minutes [85]. The conventional drugs used included ACE inhibitors, digoxin, diuretics, and spironolactone. The heart rate, blood pressure, cardiothoracic ratio, and LV internal diameter were lower with either carvedilol or trimetazidine than the control group. While these benefits were expected with carvedilol, the use of trimetazidine was novel.

Management of arrhythmias — Arrhythmias are treated according to standard recommendations. (See "Ventricular arrhythmias: Overview in patients with heart failure and cardiomyopathy" and "The management of atrial fibrillation in patients with heart failure".)

PROGNOSIS — Patients who abstain from alcohol or moderate alcohol use have a prognosis better than or similar to that seen with idiopathic dilated cardiomyopathy, while continued heavy alcohol is associated with a worse prognosis.

Some studies have found similar mortality rates in patients with alcohol-induced cardiomyopathy who stop drinking as in patients with idiopathic cardiomyopathy and worse outcomes in patients with alcohol-induced cardiomyopathy who continue to drink. As an example, a study of 50 patients with alcohol-induced cardiomyopathy found that the cardiac death rate at four-year follow-up 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 alcohol-induced cardiomyopathy who continued to drink (figure 4) [14]. In another study of 338 males with a dilated cardiomyopathy, 23 percent had an alcohol-induced cardiomyopathy; those who continued to drink had a lower seven-year transplant-free survival compared with those who stopped drinking or those with an idiopathic cardiomyopathy (27 versus 45 and 53 percent) [86]. One review estimated the four-year mortality of alcohol-induced cardiomyopathy patients who continued to drink as 50 percent [87].

In one study, alcohol-induced cardiomyopathy was the underlying cause of sudden cardiac death in five percent of cases [88]. Of the patients with autopsy-proven alcohol-induced cardiomyopathy, only 22 percent had a cardiac diagnosis made prior to death, which suggests that the true prevalence of alcohol-induced cardiomyopathy was underestimated.

By contrast, other studies have found that the rate of progression and mortality in patients with alcohol-induced cardiomyopathy was significantly lower than seen in idiopathic cardiomyopathy [86,89]. The largest series of patients with alcohol-induced cardiomyopathy, and the earliest to include significant numbers of patients receiving beta blocker therapy as well as angiotensin-converting enzyme inhibitor (or angiotensin II receptor blocker) therapy, reported a better prognosis with alcohol-induced cardiomyopathy than with idiopathic dilated cardiomyopathy [52]. Transplant-free survival at median 59 months follow-up was significantly higher among the 94 patients with alcohol-induced cardiomyopathy compared with the 188 patients with dilated cardiomyopathy (67 versus 52 percent). During follow-up of patients with alcohol-induced cardiomyopathy, 63 percent reported abstinence, 32 percent had reduced intake to <80 g per day, and 5 percent consumed >80 g per day of alcohol.

Among patients with alcohol-induced cardiomyopathy, independent predictors of death or heart transplantation included AF, QRS duration >120 ms, and lack of beta blocker therapy. Of note, transplant-free survival was similar among abstainers and those who reduced alcohol intake to <80 g per day (most <20 to 30 g per day).

In-hospital mortality of alcohol-induced cardiomyopathy patients is around 4.5 percent; half of admissions are due to cardiac etiology, with a quarter due to acute HF [4]. Patients with alcohol-induced cardiomyopathy frequently have comorbidities that adversely influence prognosis such as depression, liver disease, drug abuse, hypertension, diabetes, smoking, and pulmonary disease.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Heart failure in adults".)

SUMMARY AND RECOMMENDATIONS

●Alcohol-induced cardiomyopathy is diagnosed in patients with all three of the following criteria: long-term heavy alcohol consumption (commonly defined as >80 g per day over a period of at least five years), features of dilated cardiomyopathy (left ventricular [LV] dilation and reduced LV ejection fraction [LVEF]), and absence of other causes of dilated cardiomyopathy. (See 'Diagnostic criteria' above.)

●The relationship between alcohol consumption and heart failure (HF) appears to be J-shaped, with reduced risk at low to moderate levels of alcohol consumption (ie, up to one drink per day for females and up to two drinks per day for males) but increased risk at higher levels of alcohol intake. (See 'Relation to alcohol consumption' above.)

●The pathogenesis of alcohol-induced cardiomyopathy is not well understood, but experimental data have suggested that ethanol consumption may directly or indirectly (via metabolites) cause oxidative stress, apoptosis, impaired mitochondrial bioenergetics, altered fatty acid metabolism, and increase myocardial protein catabolism. (See 'Pathogenesis' above.)

●The patient with alcohol-induced cardiomyopathy presents with symptoms and signs like those in patients with HF, asymptomatic LV systolic dysfunction, or dilated cardiomyopathy of any etiology. In addition, symptoms and signs of unhealthy alcohol use may be observed. (See 'Clinical manifestations' above.)

●The differential diagnosis of alcohol-induced cardiomyopathy includes other causes of HF, such as hypertensive, valvular, and ischemic heart disease and other inherited and systemic causes of dilated cardiomyopathy. CAD should be excluded. (See 'Differential diagnosis' above and 'Evaluation for CAD' above.)

●Patients with alcohol-induced cardiomyopathy require total and perpetual abstinence from alcohol consumption. If abstinence cannot be achieved, we counsel the patient to reduce their alcohol consumption as much as possible. (See 'Treatment' above.)

●Patients who abstain from alcohol or moderate alcohol use have a prognosis better than or similar to that seen with idiopathic dilated cardiomyopathy, while continued heavy alcohol use is associated with a worse prognosis. (See 'Prognosis' above.)