Dataset Information

Subclinical Cardiovascular Disease and Changes in Self-Reported Mobility: Multi-Ethnic Study of Atherosclerosis.

ABSTRACT:

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 (z-scored), 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.

SUBMITTER: Everson-Rose SA

PROVIDER: S-EPMC5861943 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Background Sleep irregularity has been linked to incident cardiovascular disease. Less is known about associations of sleep regularity with atherosclerosis. We examined cross-sectional associations of actigraphy-assessed sleep duration and sleep timing regularity with subclinical atherosclerosis in the community-based MESA (Multi-Ethnic Study of Atherosclerosis). Methods and Results MESA Sleep Ancillary Study participants (N=2032; mean age, 68.6±9.2 years; 37.9% White) completed 7-day wrist actigraphy. Participants underwent assessments of coronary artery calcium, carotid plaque presence, carotid intima-media thickness, and the ankle-brachial index. Sleep regularity was quantified by the 7-day with-in person SD of sleep duration and sleep onset timing. Relative risk regression models were used to calculate prevalence ratios and 95% CIs. Models are adjusted for demographics, cardiovascular disease risk factors, and other objectively assessed sleep characteristics including obstructive sleep apnea, sleep duration, and sleep fragmentation. After adjustment, compared with participants with more regular sleep durations (SD ≤60 minutes), participants with greater sleep duration irregularity (SD >120 minutes) were more likely to have high coronary artery calcium burden (>300; prevalence ratio, 1.33 [95% CI, 1.03-1.71]) and abnormal ankle-brachial index (<0.9; prevalence ratio, 1.75 [95% CI, 1.03-2.95]). Compared with participants with more regular sleep timing (SD ≤30 minutes), participants with irregular sleep timing (SD >90 minutes) were more likely to have high coronary artery calcium burden (prevalence ratio, 1.39 [95% CI, 1.07-1.82]). Associations persisted after adjustment for cardiovascular disease risk factors and average sleep duration, obstructive sleep apnea, and sleep fragmentation. Conclusions Sleep irregularity, particularly sleep duration irregularity, was associated with several measures of subclinical atherosclerosis. Sleep regularity may be a modifiable target for reducing atherosclerosis risk. Future investigation into cardiovascular risk reduction interventions targeting sleep irregularity may be warranted.