Type of alcoholic beverage and risk of myocardial infarction.

We examined the relation of alcoholic beverage type and risk of myocardial infarction (MI) in a case-control study among 340 cases of MI and an equal number of age-, sex-, and community-matched controls. Alcohol consumption was estimated using a food frequency questionnaire, with alcohol drinkers defined as those consuming > or = 1/2 drink/day on average of any alcoholic beverage. Beer, wine, and liquor drinkers had at least half of their consumption from 1 beverage type. Fasting venous blood samples were obtained and analyzed for lipid profiles. Compared with nondrinkers, after adjustment for age and sex, reductions in risk of MI were similar for regular drinkers of any type of alcoholic beverage (relative risk [RR] 0.54; 95% confidence interval [CI] 0.37 to 0.79; p = 0.001), beer (RR 0.55; 95% CI 0.31 to 0.97; p <0.05), wine (RR 0.48; 95% CI 0.27 to 0.87; p <0.05), and liquor (RR 0.59; 95% CI 0.38 to 0.91; p <0.05) drinkers. Comparable benefits remained apparent even after multivariate adjustment for a wide range of nonlipid coronary risk factors. High-density lipoprotein (HDL) levels were significantly higher in all 4 beverage categories when compared with levels in nondrinkers, and as expected, adjustment for total HDL, a major direct effect of alcohol, substantially attenuated the protective effect in all 4 beverage categories. Relative risks were 0.94 for any beverage, 1.09 for beer, 0.97 for wine, and 0.83 for liquor after further adjustment. This strongly suggests that the protective effect of each beverage type is, in large part, mediated by increased HDL. These data indicate that regular consumption of small to moderate amounts of alcoholic beverages, regardless of the type, reduces the risk of MI, and further suggest that there is benefit, in large part, from increases in HDL levels.

Antithrombotic and thrombolytic therapies for acute myocardial infarction.

Antithrombotic and thrombolytic therapies confer clear net benefits in the treatment of acute myocardial infarction. Antithrombotic therapy with aspirin yields conclusive reductions in vascular mortality as well as reinfarction and stroke, and should be administered to all patients with suspected acute myocardial infarction. There is presently no clear evidence of net benefits from adding either delayed subcutaneous or immediate intravenous heparin to an antithrombotic regimen of aspirin. Direct thrombin inhibitors have theoretical advantages over heparin as antithrombotic agents, but further data are needed from large-scale randomized trials to determine whether these agents confer net benefits when given in conjunction with aspirin. Thrombolytic therapy yields clear reductions in mortality and should be considered for all patients with suspected acute myocardial infarction presenting within 12 h of symptom onset. The differences in the efficacy, safety or ease of administration of the various thrombolytic agents are small compared with the substantial benefits that would result from the wider use and earlier administration of any of the available agents. More widespread use of antithrombotic and thrombolytic therapies for acute myocardial infarction could prevent tens of thousands of premature deaths annually in the USA alone, and hundreds of thousands worldwide.

Alcohol and coronary heart disease.

The consumption of alcohol and its impact on health have been of great interest to researchers for many years, but remains complex for several reasons. First, with the exception of violent deaths attributable to intoxication, risks and benefits of alcohol consumption are likely to accrue over years or even decades. Second, quantitative assessment of drinking is generally based on self-report, and this may lead to some degree of misclassification. Third, drinking habits change over time, and thus, it may be important to update drinking habits periodically during any prospective study. Fourth, consumption of alcoholic beverages tends to be imbedded in cultural practices and associated with a number of lifestyle factors. For example, age, sex, race, smoking, ethnic background, and education are related to alcohol intake and may confound relationships with disease. Fifth, alcohol is derived from a number of different beverages whose other components may increase or decrease risk of disease aside from, or in addition to, the specific effect of ethanol. In addition, most studies tend to take into account average daily intake, disregarding issues of how or when the alcoholic beverage was consumed. For example, southern Europeans tend to drink wine with meals, while northern Europeans tend to drink distilled spirits, often at times other than mealtime. The risks and benefits of alcohol consumption certainly seem to be quite different for an individual who consumes seven beers on a Saturday night compared with an individual who consumes a half of a glass of wine with lunch and dinner every day, despite the obvious similarities in average weekly consumption. Finally, the precise mechanisms by which alcohol raises or lowers risks of various disease are only now beginning to be understood. (Trends Cardiovasc Med 1996;6:175-178).

Potentiation of atherosclerotic lesions in rabbits by a high dietary level of vitamin E.

1. Two experiments were conducted to determine whether or not high dietary levels of vitamin E affect the development of atherosclerotic lesions in aortas of cholesterol-fed (5 g/kg diet) rabbits that were mechanically deendothelialized by balloon catheterization. 2. In the first experiment, the aortas of rabbits fed 2000 mg vitamin E/kg diet (i.e. 50-fold their nutritional requirement) for 8 weeks showed no gross morphological differences, either within or outside experimentally damaged areas, from those of rabbits fed the nutritionally adequate control level (40 mg/kg) of the vitamin. 3. In the second experiment, rabbits fed 10,000 mg vitamin E/kg diet (i.e. 250-fold requirement) for 14-15 weeks showed significantly greater endothelial loss and plaque formation at aortic sites outside of the mechanically damaged area than did controls. Plasma cholesterol levels were very high (9000-14,000 mg/l) and were not affected by dietary vitamin E level until 10-12 weeks when they were reduced moderately (18%). 4. It is concluded that very high levels of vitamin E can potentiate spontaneous atherosclerotic lesions, and it is suggested that this effect may depend on high cholesterol status.