Alcohol consumption and atherosclerotic burden in the proximal thoracic aorta.

BACKGROUND: The relationship between alcohol consumption and ischemic stroke or aortic atherosclerosis is unclear, but a protective effect of moderate consumption on stroke risk has been suggested. We conducted a cross-sectional analysis in a population-based sample to evaluate the possible association between alcohol consumption and aortic atherosclerotic plaque (AAP), which is associated with increased stroke risk.
METHODS: As part of the NINDS-funded Aortic Plaques and Risk of Ischemic Stroke (APRIS) study, 464 subjects over the age of 55 were studied (mean age 69.1 ± 9.0 with 251 males and 213 females), including 255 patients with first ischemic stroke and 209 stroke-free controls. Transesophageal echocardiogram was performed for the detection of AAP. Alcohol consumption was measured in number of drinks per week during the previous year using a standardized questionnaire, and categorized as: (1) none or minimal (<1 drink per month); (2) light to moderate (between 1 drink per month and 2 drinks daily); and (3) heavy (>2 daily). Multivariate conditional logistic regression analysis was used to calculate the odds ratios (ORs) and 95% confidence interval (CI) for alcohol consumption and AAP after adjustment for the potential confounding risk factors (age, sex, hypertension, diabetes, dyslipidemia, and cigarette smoking).
RESULTS: Overall, AAP was detected in 326 subjects (70.4%), and 174 subjects (37.6%) had AAP ≥ 4 mm, which carry higher stroke risk. No or minimal alcohol consumption was present in 241 subjects (53.2%), and 177 subjects (39.0%) had light to moderate consumption. Prevalence of light to moderate alcohol consumption was significantly lower in stroke patients than in controls (35.5% vs. 60.3%, p < 0.001) and in subjects who had AAP compared with those without it (41.6% vs. 58.8%, p = 0.008). After adjusting for significant predictors of atherosclerosis, alcohol consumption of any degree was inversely associated with AAP (OR 0.61; 95% CI 0.37-0.98, p = 0.042). The significance of the association was borderline for AAP ≥ 4 mm (OR 0.64, 95% CI 0.41-1.00, p = 0.054). In the dose-response analysis, only light to moderate alcohol consumption was significantly associated with a lower risk of having any AAP (adjusted OR 0.45; 95% CI 0.29-0.68, p < 0.001) or AAP ≥ 4 mm (adjusted OR 0.51; 95% CI 0.34-0.77, p = 0.001).
CONCLUSIONS: Our data indicate that light to moderate alcohol consumption is associated with lower atherosclerotic burden in the proximal aortic arch. This observation may explain at least in part the lower risk of ischemic stroke observed in moderate alcohol consumers.