It is well established that alcoholic heart muscle disease is a complication of long-term alcoholism and not malnutrition or other possible causes of dilated cardiomyopathy. In a dose-dependent fashion, left ventricular systolic function declines, implicating alcohol in at least 30% of all dilated cardiomyopathies (Lee & Regan, 2002). The contractility of heart muscle is decreased through alcohol's effect of increased calcium flow into muscle cells, decreased protein synthesis (possibly secondary to increased acetaldehyde), and mitochondrial disruption (e.g., depressed adenosine triphosphate (ATP) level, leakage of enzymes, and accumulation of glycogen) (Davidson, 1989).
Alcoholic cardiomyopathy should not be confused with heart disease occasionally resulting from congeners, as occurred in the 1960s when cobalt was added to beer to stabilize the foam. The symptoms are similar to other forms of congestive heart failure, and begin with shortness of breath and fatigue. Abstinence is necessary for recovery: A 54% morality rate from this disease is reported in those who continue to drink compared to 9% who abstain (Regan, 1990).
Transient hypertension is noted in nearly 50% of alcoholics undergoing detoxification and is related to quantity of drinking and severity of other withdrawal symptoms. Epidemiological studies have demonstrated that alcohol elevates blood pressure independently of age, body weight, or cigarette smoking (Klatsky, Friedman, & Armstrong, 1986). A 10-year follow-up study found even moderate intake of alcohol (<23 grams/day) significantly increased the risk for hypertension in men, independent of age and body mass index. The risk of hypertension was increased for women, but not significantly, when age and body mass index were controlled (Ohmori et al., 2002).
Heavy alcohol intake (>60 grams/day) is associated with increased risk of ischemic and hemorrhagic stroke. Mechanisms involved include alcohol-induced hypertension, coagulation disorders, atrial fibrillation, and reduction in cerebral blood flow (Reynolds, Lewis, Nolen, Kinney, & Sathya, 2003). Alcohol has been shown directly to cause vasoconstriction of cerebral blood vessels, and this effect can be reversed or prevented by calcium-channel blocking drugs and by magnesium (Altura & Altura, 1989).
Thus far, the effects of alcohol on the cardiovascular system are distinctly negative—cardiomyopathy, hypertension, and strokes. Yet beneficial effect has been observed, in that people who drink low to moderate amounts of alcohol are at lower risk for coronary artery disease. Light drinkers (two drinks per day) have a 20% reduction in risk for coronary artery disease (Klatsky, Friedman, & Armstrong, 1986). The protective effect of alcohol seems to follow a U-shaped curve, with nondrinkers and heavy drinkers showing greater risk for coronary artery disease (Criqui, 1990).
The mechanism by which alcohol provides some protective effect against coronary artery disease is in the elevation of high-density lipoproteins, decreased platelet aggregation, and fibrinolytic activity (Zakari, 1997).
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