Alcohol Intake is Not Associated With Subclinical Coronary
Background: The inverse relation between alcohol intake and clinical coronary artery disease (CAD) is well established, although the mechanisms remain speculative. We studied the relation between alcohol intake and subclinical CAD to assess the possible role of alcohol in atherogenesis.
Methods: We conducted a prospective study of 731 consecutive, consenting, active-duty US Army personnel (39 to 45 years of age) without known CAD who were undergoing a routine physical examination. Each participant was surveyed with the validated Block dietary questionnaire, which included detailed information on alcohol intake as wine, beer, or liquor. Subclinical CAD was determined by means of electron beam computed tomography to quantify coronary artery calcification (CAC).
Results: The mean age was 42 (±2); 83% were male, 71% were white, and 82% were college graduates. The prevalence of CAC was 18.6% (mean CAC score = 12 ± 69). Twenty-two percent drank alcohol daily, with an average of 2.4 drinks per day. Systolic blood pressure was correlated with number of drinks per day (r = 0.10, P = .025). Among drinkers, HDL was weakly correlated with daily alcohol consumption (r = 0.10, P = .025). There was no relation between the CAC score and the alcohol intake as measured by drinks per day (OR, 1.02; 95% CI, 0.64 to 1.63; 1.13, 0.59 to 2.15; 1.26, 0.69 to 2.59, for less than 1, 1 to 2, and more than 2 drinks per day, respectively). Stratified analyses based on type of alcohol and multivariate analyses indicated no independent relation between any type or quantity of alcohol intake and the presence or extent of coronary calcification.
Conclusions: Alcohol intake does not appear to be inversely related to subclinical CAC, implying that previous observations of a protective effect of alcohol on clinical CAD may involve factors related to plaque stability rather than atherogenesis.

The association between alcohol consumption and clinical coronary artery disease (CAD) is complex. More than 60 observational studies have documented that moderate alcohol use is protective against heart disease. The mechanism by which alcohol exerts its effects remains speculative. Postulated mechanisms include an associated increase in HDL, anticoagulant effects by either direct platelet inhibition and/or inhibition of the fibrinolytic system.

Whether alcohol affects risk for clinical CAD through an effect on atherogenesis or through interaction with underlying atherosclerotic plaque has significant implications in understanding the biology of atherosclerosis, as well as any potential therapeutic uses for alcohol in reducing CAD risk. Only one published study has investigated the relation between subclinical CAD and alcohol consumption, and it reported a lack of correlation between alcohol consumption and coronary artery calcification (CAC). However, this study involved a cohort in their mid-60s who were at moderately high risk for CAD, with only a crude assessment of alcohol consumption.

The objective of this study was to explore the independent relation between alcohol use and subclinical coronary atherosclerotic plaque burden, as measured by electron beam computed tomography (EBCT), in a consecutive sample of an asymptomatic, relatively young screening population with relatively early stages of subclinical atherosclerosis.