Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease (Aug 2019)

Subclinical Longitudinal Change in Ankle‐Brachial Index With Aging in a Community‐Dwelling Population Is Associated With Central Arterial Stiffening

  • Matt T. Oberdier,
  • Christopher H. Morrell,
  • Edward G. Lakatta,
  • Luigi Ferrucci,
  • Majd AlGhatrif

DOI
https://doi.org/10.1161/JAHA.118.011650
Journal volume & issue
Vol. 8, no. 15

Abstract

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Background Aging is associated with a modest decline in ankle‐brachial index (ABI); however, the underpinnings of this decline are not fully understood. The greater systolic ankle than brachial blood pressure, a normal ABI implies, is partially attributed to lower central than peripheral arterial stiffness. Hence, we examined the hypothesis that the age‐associated decline in ABI is associated with central arterial stiffening with aging, assessed by pulse wave velocity. Methods and Results We analyzed longitudinal data from 974 participants aged 27 to 95 years from the Baltimore Longitudinal Study of Aging who were free of clinically significant cardiovascular disease. Participants had an average of 4 visits with a 6.8‐year average follow‐up time. Linear mixed‐effects models showed that the average ABI decline beyond the age of 70 years was 0.03 per decade. In multiple regression analysis, the ABI rate of change was inversely associated with initial age (standardized β=−0.0711, P=0.0282), independent of peripheral disease factors and baseline ABI. After adjustment, the pulse wave velocity rate of change was inversely associated with ABI rate of change (standardized β=−0.0993, P=0.0040), rendering the association of the latter with initial age nonsignificant (standardized β=−0.0265, P=0.5418). Conclusions A modest longitudinal decline in ABI beyond the age of 70 years was shown to be independent of traditional risk factors for peripheral arterial disease but was accounted for by an increase in pulse wave velocity. A modest decline in ABI with aging might be a manifestation of changes in central hemodynamics and not necessarily attributable to peripheral flow–limiting factors.

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