Background: We examined associations of three markers of subclinical cardiovascular disease (intimal-medial thickening, coronary artery calcification, and ankle-brachial index) with changes in self-reported walking over time. Methods: Data were from 6,490 Multi-Ethnic Study of Atherosclerosis participants (aged 45–84 years), free of clinical cardiovascular disease at baseline. Outcomes, assessed four times over 11 years, included self-reported walking pace (none to striding pace; score, 0–4) and total walking time (minutes/week). Linear generalized estimating equation models estimated associations of baseline intimal-medial thickening (zscored), coronary artery calcification (Agatston units), and ankle-brachial index (ratio of ankle-to-arm systolic blood pressure) with walking pace and walking time modeled continuously in separate analyses. Results: Median follow-up was 9.2 years (maximum, 11.4). Walking pace (estimate, −0.042 points [95% CI; −0.048, −0.036], p < 0.0001) and walking time (estimate, −4.71 minutes [95% CI: −8.54, −0.88], p = 0.016) decreased yearly. Greater baseline intimal-medial thickening related to faster decline in walking pace in multivariable analyses: walking pace score decreased 0.004 points (95% CI: −0.008, −0.001) more per year for each 1-SD higher intimal-medial thickening z-score, equivalent to an additional 10% slower yearly walking. Greater coronary artery calcification was associated with slower walking but inconsistently related to decline in walking pace. Higher ankle-brachial index was associated with faster baseline walking pace (estimate, 0.043 points [95% CI: 0.027, 0.059] per 1-SD) but unrelated to changes in walking pace. Cardiovascular disease measures were unrelated to total walking time. Conclusions: Greater subclinical cardiovascular disease is associated with prevalent slower self-reported walking pace in middle-aged and older adults but has limited impact on changes in walking over time.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journals of Gerontology - Series A Biological Sciences and Medical Sciences|
|State||Published - Mar 1 2018|
Bibliographical noteFunding Information:
This work was supported by contracts N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, and N01-HC-95169 from the National Heart, Lung, and Blood Institute (NHLBI) and by grants UL1-TR-000040 and UL1-TR-001079 from the National Center for Advancing Translational Science (NCATS). S.A.E.R. also received support from the Applied Clinical Research Program and Program in Health Disparities Research at the University of Minnesota. A.A. additionally was supported by grant U01-HL096902.
© The Author(s) 2017.
- Physical function