What is the role of alcohol in dilated cardiomyopathy?

Dilated cardiomyopathy is considered alcohol-induced if associated with prolonged alcohol abuse (>5 years), defined by the World Health Organization as >40 g/day in women and >80 g/day in men, and if it remits, sometimes completely, on an alcohol-free high-thiamine diet. Alcohol accounts for up to 40% of cases of cardiomyopathy. Women are at particular risk.

Alcohol consumption can be difficult to estimate. The CAGE questionnaire (Table), which has a sensitivity of 80% to 90% and specificity of 77% to 89%, has a negative predictive value of 98% in discriminating alcoholics from social drinkers. Circulating y-glutamyl transferase (GGT) and mean corpuscular volume (MCV) have negative predictive values of 86% and 84%. Elevated carbohydrate deficient transferrin (CDT) may be the most sensitive and specific marker of alcohol abuse. Elevation is believed due to the decreased glycoprotein glycosyl-transferase activity involved in transferrin N-glycan synthesis and to increased sialidase activity. Combined CDT and GGT elevation has a sensitivity of 90%.

Have you ever felt you should cut down on your drinking?

Have people annoyed you by criticizing your drinking?

Have you ever felt bad or guilty about your drinking?

Have you ever had a drink first thing in the morning (an eye-opener) to steady your nerves or get rid of a hangover?

Table. The CAGE questionnaire (Cut down, Annoyed by criticism, Guilty about drinking, Eye-opener drinks [a test for alcoholism]).

Symptomatic heart failure is present in one third of long-standing alcoholics; the remaining two thirds with no symptoms of heart disease show echocardiographic

abnormalities and, in 10% of cases, dilated cardiomyopathy. Alcohol has negative inotropic and arrhythmo-genic properties, to which patients with established cardiac disease are particularly vulnerable. Dangerous tachyarrhythmias include atrial fibrillation. Acute hemodynamic decompensation may therefore result.

Even short-term use can cause changes in myocardial histology. Toxicity is dose-related, with the primary culprits being ethanol and its cellular metabolite, acetaldehyde. Alcohol inhibits protein synthesis by cardiomyocytes and calcium storage by sarcoplasmic reticulum. It impairs the mitochondrial oxidative burst and actin/myosin interaction. It may also alter magnesium and iron metabolism.

Clinical trials do not show a linear correlation between alcohol intake and cardiomyopathy. Cofactors are likely to be involved, eg, a familial factor (a genomic contribution has been documented, suggesting a hereditary predisposition). Differences in antimyosin antibody prevalence between patients with and without alcoholic cardiomyopathy suggest the contribution of immunologic factors. Thus, alcohol toxicity could induce car-diomyocyte necrosis, which in turn stimulates an immunologic response to cardiac antigens.

Alcoholic cardiomyopathy needs to be differentiated from thiamine-deficient cardiomyopathy (beri-beri) and idiopathic dilated cardiomyopathy with coincidental alcohol abuse. In neither case does alcohol abstinence lead to recovery. Alcoholics also tend to have other nutritional deficiencies, especially of vitamin B1 and magnesium; supplementation with these factors mitigates the histologic damage to the heart. Differential diagnosis from idiopathic dilated cardiomyopathy with coincidental alcohol abuse can be difficult. Histology is no help. The only criterion is clinical remission on an appropriate alcohol-free diet. Alcohol withdrawal is potentially dangerous, being associated with sympathetic activation and altered anion/cation balance in the body fluids, due to tachycardia, hypertension, alkalosis, hypocapnia, fever, diarrhea, vomiting, and sweating. Symptoms appear 7 or 8 hours after the last drink and are related to the duration and severity of abuse. The treatment of alcoholic heart failure is similar to that of regular heart failure, with due regard for altered drug catabolism in the presence of hepatic dysfunction. Catabolism is increased in the recovering alco- holic, while the opposite is true during acute intoxication (alcohol induces hepatic P450 cytochrome expression). Caution is required when using anticoagulants since their effects are potentiated by alcohol. Withdrawal can result in full recovery, with resolution of the cardiac lesions. The predictors of cardiac recovery, in particular the degree of histologic damage, are unknown. In a recent report, full cardiac remission after alcohol withdrawal in a patient diagnosed with alcoholic cardiomyopathy led to the discovery of underlying hypertrophic cardiomyopathy.


dilated cardiomyopathy; etiology; risk factor; alcohol; alcoholic cardiomyopathy; treatment; prognosis

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