Basics
Description
- There is a "U-shaped"¯ relationship between quantity of alcohol intake and risk for heart disease. Moderate alcohol consumption-2 drinks per day for males and 1 drink per day for females-is associated with a 30-40% reduction in coronary heart disease.
- Heavy alcohol intake and binge drinking have a toxic effect on the myocardium, causing impaired myocardial contractility, LV dilation, diastolic and systolic dysfunction, arrhythmias, and in some cases sudden cardiac death.
Epidemiology
- Alcohol is the leading cause of nonischemic dilated cardiomyopathy, accounting for 21-36% of cases in the Western world.
- Patients with alcoholic cardiomyopathy are predominantly male, with females comprising only ~14% of cases.
Risk Factors
- It has been estimated that alcohol intake >80-90 g/d (standard drink is 10-15 g of alcohol) for 5-15 yr may cause dilated cardiomyopathy. Larger daily intake may lead to more rapid development of cardiomyopathy. Amounts considered toxic vary per individual.
- Binge drinking (≥3 alcoholic drinks within 1-2 hr) has adverse cardiovascular effects, in contrast to consumption of moderate quantities of alcohol spread out over ≥3-4 days per week, which has beneficial effects.
- Malnutrition, which often coexists with alcoholism, may increase risk of heart failure.
Genetics
- Genetic variation likely accounts for the finding that only a fraction of heavy alcohol users develop alcoholic cardiomyopathy.
- Among Spanish alcoholic men, allelic variation in the ACE gene-specifically, homozygous DD genotype-correlated with reduced LV ejection fraction.
- Moderate alcohol drinkers homozygous for the Ī³2 alcohol dehydrogenase 1C (ADH1C) allele-the genotype associated with slow oxidization of alcohol-have higher HDL and significantly lower risk of MI.
General Prevention
- Based on observational data among The Framingham Heart Study, The Physicians' Health Study, and The Cardiovascular Health Study, light-to-moderate alcohol intake is correlated with a reduced risk of incident heart failure compared to no alcohol intake, 34-59% lower risk. Among individual studies, this association is seen in men and women, in persons <65 and ≥65 yr old, and in those with and without antecedent MI.
- Excessive daily alcohol intake and binge drinking should be avoided. Heavy alcohol consumption increases risk of heart failure; 1.7-fold higher risk of heart failure compared to nondrinkers in one study.
Pathophysiology
- Early stages in the natural history of alcoholic cardiomyopathy, which may not be symptomatic, include LV dilation, increased LV mass, and diastolic dysfunction (due in part to myocardial interstitial fibrosis).
- Late stages: LV dilation progresses, systolic dysfunction occurs, and patient develops signs and symptoms of heart failure. LV wall thickness is reduced or normal.
Etiology
- The underlying etiology of alcoholic cardiomyopathy is poorly understood. There are several potential mechanisms by which alcohol impairs myocardial function.
- Direct toxic effects of ethanol and its metabolites (acetaldehyde and acetate) on:
- Mitochondria: Ethanol esterifies fatty acids in the heart to produce fatty acid ethyl esters that accumulate in mitochondria and impair energy utilization.
- Sarcoplasmic reticulum: Ethanol interferes with lipid metabolism, altering the fatty acid composition of the sarcolemma membrane, and the functional properties of the sarcoplasmic reticulum.
- Contractile proteins: Acute ethanol ingestion may lead to depressed myocardial contractility via reduction of maximal muscle fiber shortening. Chronic ethanol exposure impairs myofibrillar protein synthesis.
- Calcium homeostasis: Calcium cycling may be impaired, disrupting cardiac excitation-contractile coupling.
- Myocytes: Ethanol induces myocyte apoptosis.
- Additives such as cobalt (formerly found in some beers), and lead (in moonshine alcohol) are also toxic to the heart.
- Neurohormonal effects:
- Ethanol induces activation of the sympathetic nervous system (norepinephrine), the renin angiotensin system (RAS), and the natriuretic peptide system. Sustained high level of norepinephrine induces myocyte hypertrophy, toxicity, apoptosis, and LV remodeling.
- Oxidative stress: Acute and chronic ethanol exposure reduces mitochondrial glutathione, resulting in damage to cellular structures from accumulation of reactive oxygen species.
- Nutritional deficiencies related to chronic alcohol abuse: Severe thiamine deficiency can cause capillary breakdown, peripheral vasodilation and edema, high-output cardiac failure, LV dilation, and eventually reduced LV systolic function (wet beriberi). Deficiencies of selenium, magnesium, phosphorus, and potassium may also cause myocardial dysfunction.
Associated Conditions
Atrial fibrillation, either due to cardiomyopathy, acute alcohol ingestion, or withdrawal.
Diagnosis
History
- Proper diagnosis of alcoholic cardiomyopathy requires accurate quantification of current and past alcohol use.
- Denial and minimization of alcohol intake are common among both alcohol abusers and "social drinkers."¯ Specific inquiry about intake of beer, wine, and liquor can result in eliciting 20% higher quantities.
Physical Exam
- Since accurate history of quantity of alcohol intake is difficult to elicit, look for signs of chronic heavy alcohol use to support the diagnosis of alcoholic cardiomyopathy:
- Telangiectasia; spider angiomata; palmar erythema; tremulousness; hepatomegaly (either from alcoholism or right-sided heart failure); splenomegaly; peripheral neuropathy; HTN; tachycardia; rhinophyma; obstructive lung disease; muscle weakness
- As with other etiologies of cardiomyopathy, look for evidence of left- and right-sided heart failure:
- Fatigue; weakness; exertional dyspnea; orthopnea; paroxysmal nocturnal dyspnea; elevated jugular venous pressure; peripheral edema; ascites; HTN; narrow pulse pressure; S3 (3rd heart sound); S4 (4th heart sound)
Tests
Lab
- ECG may show atrial arrhythmia; ectopy; bundle branch block; QT interval prolongation; poor R-wave progression; LV hypertrophy.
- Phlebotomy: Macrocytosis with or without anemia; elevated transaminases (2:1 or 3:1 ratio of AST to ALT); elevated GGT; thrombocytopenia; electrolyte abnormalities (hypokalemia; hypomagnesemia; hypophosphatemia).
- Endomyocardial biopsy: Is not routinely performed if history suggests chronic alcohol abuse as the etiology for cardiomyopathy.
Imaging
- CXR may show cardiomegaly and pulmonary congestion.
- Echo may show: Biatrial and/or biventricular dilatation; systolic and/or diastolic dysfunction; mitral and/or tricuspid regurgitation. Up to 30% of chronic alcoholics without symptoms of heart failure have reduced LV systolic function.
Pathological Findings
- Gross and histological findings are similar to that of idiopathic dilated cardiomyopathy: Interstitial fibrosis; myocyte dropout; myocyte hypertrophy; small-vessel coronary disease.
- Electron microscopy reveals enlarged, disorganized mitochondria and glycogen-containing vacuoles.
Differential Diagnosis
Other etiologies of dilated cardiomyopathy: Cocaine; HIV and other infections; inflammatory and autoimmune conditions; cancer chemotherapy (eg, doxorubicin; Herceptin; imatinib); stress (Takotsubo); peripartum; tachycardia; genetic and familial factors; idiopathic
Treatment
Medication
- Outpatient and inpatient management of heart failure is similar to that of other etiologies of heart failure.
- However, a simplified outpatient medication regimen may be required to improve compliance in patients who continue to abuse alcohol or have other psychosocial issues.
- Caution must be used with anticoagulation, if indicated, due to increased risk of bleeding from nutritional deficiencies, hepatic dysfunction, and trauma. Compliance with medication and INR checks may also be an issue.
- Supplemental multivitamin, thiamine, and folate may be required in active alcohol abusers who are prone to malnutrition. Potassium, magnesium, and phosphate may also need repletion.
- Benzodiazepines for alcohol withdrawal may be necessary for active drinkers admitted to the hospital.
Additional Treatment
General Measures
Alcohol cessation or significant reduction of intake is necessary.
Issues for Referral
A collaborative effort with primary care, psychiatry, and social services is essential to achieve abstinence from alcohol-the only way to reverse or halt progression of alcoholic cardiomyopathy.
Additional Therapies
Alcoholics Anonymous or other support group may be helpful in preventing ongoing alcohol abuse.
In-Patient Considerations
Admission Criteria
- As for acute decompensated heart failure of any etiology.
- Hospitalization for alcohol detoxification may be necessary.
Nursing
Routine checks for signs and symptoms of alcohol withdrawal (tachycardia; HTN; diaphoresis; tremors; hallucinations; hyperactive delirium), which most commonly occur in the 1st 24-48 hr after drinking cessation, and may persist for up to 7 days.
Discharge Criteria
- Stable weight and fluid balance for 24-48 hr without use of IV diuretics.
- Lack of signs or symptoms of alcohol withdrawal.
- Social plan for avoidance of alcohol abuse.
Ongoing Care
Follow-Up Recommendations
Patient Monitoring
- Routine weight checks
- Frequent primary care visits
- Routine social work visits may be helpful
Diet
- Sodium-restricted
- Potential need for supplemental multivitamin, thiamine.
Patient Education
Caution must be used in recommending light-to-moderate alcohol consumption for the prevention of coronary heart disease because individual genetic and environmental factors make it difficult to predict what quantity will have protective vs. harmful effects on the heart, other organs, and psychosocial factors.
Prognosis
- 50% mortality at 4 yr for alcoholic cardiomyopathy in the absence of abstinence. Abstainers' mortality at 4 yr is 1/6 that of patients who continue to drink.
- With complete abstinence or reduction to moderate levels of alcohol use, the cardiomyopathy may partially, or even completely, resolve. A 13% improvement in LV ejection fraction at 1 yr has been demonstrated in patients with alcoholic cardiomyopathy who abstained or reduced alcohol intake to 20-60 g/d. In general, the majority of improvement occurs in the 1st 6 mo of abstinence, but often continues to improve over 2 yr.
- Continued, sometimes covert, drinking makes it difficult to gauge the true effect of abstinence.
- There is an increased risk of sudden cardiac death, even in the absence of overt cardiac dysfunction.
Additional Reading
1
Skotzko CE, Vrinceanu A, Krueger L
Alcohol use and congestive heart failure: incidence, importance, and approaches to improved history taking. Heart Failure Rev. 2009;14(1):51-55. [View Abstract] 2
Walsh CR, MG Larson. Alcohol consumption and risk for congestive heart failure in the Framingham Heart Study. Ann Intern Med. 2002;136(3):181-191. [View Abstract]
Codes
ICD9
425.5 Alcoholic cardiomyopathy
SNOMED
83521008 dilated cardiomyopathy secondary to alcohol (disorder)
Clinical Pearls
- A "U-shaped"¯ relationship exists between quantity of alcohol intake and risk for heart disease.
- Alcohol is the leading cause of nonischemic dilated cardiomyopathy, accounting for 21-36% of cases in the Western World.
- It has been estimated that alcohol intake >80-90 g/d (a standard drink has 10-15 g of alcohol) for 5-15 yr may cause dilated cardiomyopathy.
- The toxic effect of alcohol on the myocardium is poorly understood, but evidence suggests that ethanol and its metabolites disrupt multiple aspects of cardiomyocyte function.
- With cessation of alcohol abuse, myocardial function may recover.