Background: The goal was to investigate the relation of alcohol consumption to the presence of calcified atherosclerotic plaque in the coronary arteries(CAC) and aorta. Previous results have been conflicting, showing ...Background: The goal was to investigate the relation of alcohol consumption to the presence of calcified atherosclerotic plaque in the coronary arteries(CAC) and aorta. Previous results have been conflicting, showing increases, decreases, or no effect of alcohol on risk of calcified plaque. Methods: We evaluated the relation of alcohol intake to presence of CAC and calcified plaque in the aorta among 3166 white and African American subjects from the NHLBI Family Heart Study who underwent cardiac computed tomography scans. Results: With adjustments for age, race, study center, body mass index, hyperglycemia/diabetes, hypertension, and smoking, odds ratios(and 95%CI) for CAC scores >100 in nondrinkers and consumers of 1 to 3, 4 to 7, 8 to 14, and >14 drinks per week were 1.0, 0.8(0.4, 1.3), 1.1(0.6, 1.9), 0.9(0.5, 1.5), and 1.5(0.9, 2.5), respectively, for men and 1.0, 0.9(0.5, 1.6), 1.3(0.8, 2.3), 1.3(0.7, 2.2), and 2.1(0.8, 5.9) for women. Sensitivity analyses with other cut-points for calcification gave similar results. Analyses of alcohol and aortic calcification showed similar, nonsignificant associations. Conclusions: Despite its frequently demonstrated beneficial effects on coronary artery disease risk, alcohol consumption in this study was not associated with calcified atherosclerotic plaque in the coronary arteries or in the aorta. This suggests that its effects on cardiovascular risk may occur through mechanisms other than those associated with the development of calcified plaque.展开更多
文摘Background: The goal was to investigate the relation of alcohol consumption to the presence of calcified atherosclerotic plaque in the coronary arteries(CAC) and aorta. Previous results have been conflicting, showing increases, decreases, or no effect of alcohol on risk of calcified plaque. Methods: We evaluated the relation of alcohol intake to presence of CAC and calcified plaque in the aorta among 3166 white and African American subjects from the NHLBI Family Heart Study who underwent cardiac computed tomography scans. Results: With adjustments for age, race, study center, body mass index, hyperglycemia/diabetes, hypertension, and smoking, odds ratios(and 95%CI) for CAC scores >100 in nondrinkers and consumers of 1 to 3, 4 to 7, 8 to 14, and >14 drinks per week were 1.0, 0.8(0.4, 1.3), 1.1(0.6, 1.9), 0.9(0.5, 1.5), and 1.5(0.9, 2.5), respectively, for men and 1.0, 0.9(0.5, 1.6), 1.3(0.8, 2.3), 1.3(0.7, 2.2), and 2.1(0.8, 5.9) for women. Sensitivity analyses with other cut-points for calcification gave similar results. Analyses of alcohol and aortic calcification showed similar, nonsignificant associations. Conclusions: Despite its frequently demonstrated beneficial effects on coronary artery disease risk, alcohol consumption in this study was not associated with calcified atherosclerotic plaque in the coronary arteries or in the aorta. This suggests that its effects on cardiovascular risk may occur through mechanisms other than those associated with the development of calcified plaque.
