Abstract 19013: Longitudinal Changes in Ankle and Brachial Pressures in a Community Dwelling Population: Results From the Baltimore Longitudinal Study of Aging

Abstract

Reduction in ankle-brachial index (ABI) is a marker of peripheral arterial disease (PAD) and is attributed to flow limiting lesions. It is unclear whether the major changes in blood pressure with aging affect ankle and brachial pressures differently and result in changes in ABI with advancing age. We studies 719 participants (2176 observations) from the Baltimore Longitudinal Study of Aging who were free of clinical cardiovascular (CV) disease at baseline. Ankle and brachial systolic blood pressures (SBP) and their index (ABI) were measured in both sides using oscillometric device (Colin VP2000) and averages of both sides were calculated. Linear mixed effects models were used with age expressed as Entry-Age and Follow up Time (Time) to test for non-linear longitudinal changes in these parameters. About 15% of the sample had diabetes at baseline, 3.5% were current and 38% were former smokers. Adjusting for diabetes, smoking status and anti-hypertensive medications, men had greater ABI than women (B= 0.02, P=<0.001) with no statistically significant differences in trajectories. ABI changed with aging with statistically significant Entry-age X Time terms (P<0.01). Model predicted values (Figure 1) shows a longitudinal decline in ABI after the age of 65. In men, this decline was a result of a longitudinal decline in ankle SBP vs plateauing brachial SBP. In women, the decline in ABI was a result of a greater increase in brachial SBP compared to ankle SBP. In conclusion, aging is independently associated with a decline in ABI in a healthy population free of clinical C disease. There were gender different in the pressure profiles yielding this reduction in ABI. A pathological reduction in ABI could represent an exaggerated age-associated hemodynamic alterations and not exclusively due to flow limiting lesions. Further studies are needed to understand the underlying alterations in arterial properties and the clinical significance of this subclinical reduction in ABI.