Alcohol intake is not associated with subclinical coronary atherosclerosis

Tofferi, Jeanne K.; Taylor, Allen J.; Feuerstein, Irwin M.; O'Malley, Patrick G.

doi:10.1016/j.ahj.2004.05.023

« Previous Next »American Heart Journal
Volume 148, Issue 5 , Pages 803-809, November 2004

Alcohol intake is not associated with subclinical coronary atherosclerosis☆

Jeanne K. Tofferi, MD, MPH
- Department of Medicine, Walter Reed Army Medical Center, Washington, DC, USA
- Uniformed Services University of the Health Sciences, Bethesda, Md, USA
Allen J. Taylor, MD
- Department of Medicine, Walter Reed Army Medical Center, Washington, DC, USA
- Uniformed Services University of the Health Sciences, Bethesda, Md, USA
Irwin M. Feuerstein, MD
- Department of Radiology, Walter Reed Army Medical Center, Washington, DC, USA
- Uniformed Services University of the Health Sciences, Bethesda, Md, USA
Patrick G. O'Malley, MD, MPH
- Department of Medicine, Walter Reed Army Medical Center, Washington, DC, USA
- Uniformed Services University of the Health Sciences, Bethesda, Md, USA
- Reprint requests: Patrick G. O'Malley, MD, MPH, Division of General Internal Medicine, Walter Reed Army Medical Center, 6900 Georgia Ave, Washington, DC, 20307–5001, USA.

Received 10 October 2003; accepted 9 May 2004.

Abstract

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.