Abstract
Abstract Introduction Sleep duration is associated with stroke risk and is one of eight essential components of cardiovascular health according to the American Heart Association. As stroke disproportionately burdens Black and Hispanic populations in the United States, we hypothesized that long and short sleep duration would be associated with greater subclinical carotid atherosclerosis, a precursor of stroke, in the racially and ethnically diverse Northern Manhattan Study (NOMAS). Methods NOMAS is a study of community-dwelling adults that recorded self-reported nightly sleep duration and daytime sleepiness. Carotid plaque presence, total plaque area, and intima media thickness were measured by ultrasound. Linear and logistic regression models examined the cross-sectional associations of sleep duration groups (primary exposure) or daytime sleepiness (secondary exposure) with measures of carotid atherosclerosis. Models adjusted for age, sex, race/ethnicity, education, health insurance, smoking, alcohol use, physical activity, body mass index, hypertension, diabetes, hypercholesterolemia, and cardiac disease. Results The sample (n=1,553) had a mean age of 64.7±8.5 years and was 61.9% female, 64.8% Hispanic and 18.2% non-Hispanic Black. Of the sample, 55.6% had carotid plaque, 22.3% reported nightly short sleep (< 6 hours), 66.6% intermediate sleep (≥6 and < 9 hours), and 11.1% long sleep (≥9 hours). Compared to intermediate sleep, long sleep was associated with greater odds of carotid plaque presence (OR 1.5, 95% CI 1.1-2.2) and greater odds of plaque within the tertile of largest plaque area (OR 1.7, 95% CI 1.0-2.7), each relative to plaque absence after full covariate adjustment. Short sleep was associated with lower odds of plaque within the tertile of largest carotid plaque area but was not associated with plaque presence. Daytime sleepiness was not associated with carotid measures. Conclusion Subclinical carotid atherosclerosis may mediate previously observed relationships between long sleep and increased stroke risk. Support (if any) This work was supported by the National Institutes of Health through grants from the National Institute of Neurological Disorders and Stroke (R37 NS029993, PI: Sacco/Elkind) and the National Institute on Aging (R01 AG067568, PI: Ramos), and by The Evelyn F. McKnight Brain Institute.