Alcohol Consumption and Lower Extremity Arterial Disease Among Older Adults
Alcohol Consumption and Lower Extremity Arterial Disease Among Older Adults
Few studies of the relation of alcohol intake to lower-extremity arterial disease (LEAD) have included clinical events and objective measurements repeated longitudinally. As part of the Cardiovascular Health Study, a study of older adults from four US communities, 5,635 participants reported their use of beer, wine, and spirits yearly. Incident LEAD was identified by hospitalization surveillance. Technicians measured ankle-brachial index 6 years apart in 2,298 participants. A total of 172 cases of LEAD were documented during a mean of 7.5 years of follow-up between 1989 and 1999. Compared with abstention, the multivariable-adjusted hazard ratios were 1.10 (95% confidence interval (CI): 0.71, 1.71) for <1 alcoholic drink per week, 0.56 (95% CI: 0.33, 0.95) for 1-13 drinks per week, and 1.02 (95% CI: 0.53, 1.97) for ≥14 drinks per week (p for quadratic trend = 0.04). These relations were consistent within strata of sex, age, and apolipoprotein E genotype, and neither lipids nor inflammatory markers appeared to be important intermediates. Change in ankle-brachial index showed a similar relation (p for quadratic trend = 0.01). Alcohol consumption of 1-13 drinks per week in older adults may be associated with lower risk of LEAD, but heavier drinking is not associated with lower risk.
Considerable epidemiologic evidence suggests that moderate alcohol drinkers have lower risks of coronary heart disease than do abstainers or very light drinkers. However, the association of alcohol consumption with lower-extremity arterial disease (LEAD) is less clear, despite the fact that LEAD affects approximately 10 million adults in the United States alone. Two prospective cohort studies have assessed alcohol use and risk of symptomatic LEAD; neither of them included objective measurements of LEAD. Three other studies have assessed this relation cross-sectionally using ankle-brachial index (ABI) measurements, with inconsistent results. To our knowledge, no previous studies have assessed alcohol intake and changes in objectively measured LEAD in a longitudinal fashion.
Kennedy et al. recently identified predictors of 6-year decline in ABI among older adults participating in the Cardiovascular Health Study (CHS). In age-, sex-, and race-adjusted analyses, levels of high density lipoprotein (HDL) cholesterol tended to be inversely associated with risk, while fibrinogen levels were positively associated with risk. Given that alcohol use increases HDL cholesterol levels and lowers fibrinogen levels in clinical trials and is associated with higher HDL cholesterol levels and lower fibrinogen levels in the CHS, it seems reasonable to hypothesize that alcohol use could be inversely associated with deterioration in ABI through effects on these risk factors.
Given the paucity of information about alcohol use and LEAD, we examined the association of alcohol intake with several measures of LEAD in the CHS, a population-based cohort study of community-dwelling older adults.
Few studies of the relation of alcohol intake to lower-extremity arterial disease (LEAD) have included clinical events and objective measurements repeated longitudinally. As part of the Cardiovascular Health Study, a study of older adults from four US communities, 5,635 participants reported their use of beer, wine, and spirits yearly. Incident LEAD was identified by hospitalization surveillance. Technicians measured ankle-brachial index 6 years apart in 2,298 participants. A total of 172 cases of LEAD were documented during a mean of 7.5 years of follow-up between 1989 and 1999. Compared with abstention, the multivariable-adjusted hazard ratios were 1.10 (95% confidence interval (CI): 0.71, 1.71) for <1 alcoholic drink per week, 0.56 (95% CI: 0.33, 0.95) for 1-13 drinks per week, and 1.02 (95% CI: 0.53, 1.97) for ≥14 drinks per week (p for quadratic trend = 0.04). These relations were consistent within strata of sex, age, and apolipoprotein E genotype, and neither lipids nor inflammatory markers appeared to be important intermediates. Change in ankle-brachial index showed a similar relation (p for quadratic trend = 0.01). Alcohol consumption of 1-13 drinks per week in older adults may be associated with lower risk of LEAD, but heavier drinking is not associated with lower risk.
Considerable epidemiologic evidence suggests that moderate alcohol drinkers have lower risks of coronary heart disease than do abstainers or very light drinkers. However, the association of alcohol consumption with lower-extremity arterial disease (LEAD) is less clear, despite the fact that LEAD affects approximately 10 million adults in the United States alone. Two prospective cohort studies have assessed alcohol use and risk of symptomatic LEAD; neither of them included objective measurements of LEAD. Three other studies have assessed this relation cross-sectionally using ankle-brachial index (ABI) measurements, with inconsistent results. To our knowledge, no previous studies have assessed alcohol intake and changes in objectively measured LEAD in a longitudinal fashion.
Kennedy et al. recently identified predictors of 6-year decline in ABI among older adults participating in the Cardiovascular Health Study (CHS). In age-, sex-, and race-adjusted analyses, levels of high density lipoprotein (HDL) cholesterol tended to be inversely associated with risk, while fibrinogen levels were positively associated with risk. Given that alcohol use increases HDL cholesterol levels and lowers fibrinogen levels in clinical trials and is associated with higher HDL cholesterol levels and lower fibrinogen levels in the CHS, it seems reasonable to hypothesize that alcohol use could be inversely associated with deterioration in ABI through effects on these risk factors.
Given the paucity of information about alcohol use and LEAD, we examined the association of alcohol intake with several measures of LEAD in the CHS, a population-based cohort study of community-dwelling older adults.
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