Key result
Actigraphy-derived sleep efficiency was positively associated with brachial artery flow-mediated dilation in adults with untreated hypertension (β = 0.28, P = 0.012).
Why the study?
Impaired endothelial function may be one mechanism linking poor sleep quality to CVD risk, motivating an evaluation of objective sleep quality and endothelial function in untreated hypertensive adults.
Is actigraphy-derived sleep efficiency associated with endothelial function in adults with untreated hypertension?
Cross-Sectional (n=127)
Is actigraphy-derived sleep efficiency associated with endothelial function in adults with untreated hypertension?
Effect estimate: β = 0.28
p-value: p=0.012
Poor sleep efficiency, measured objectively by actigraphy, is associated with impaired endothelial function in untreated hypertensive adults, highlighting sleep as a potential modifiable cardiovascular risk factor.
Hypothesis-generating in untreated hypertension; prospective trials needed before considering sleep interventions for endothelial function.
BACKGROUND: Poor sleep quality is increasingly recognized as an important and potentially modifiable risk factor for cardiovascular disease (CVD). Impaired endothelial function may be 1 mechanism underlying the association between poor sleep and CVD risk. The present study examined the relationship between objective measures of sleep quality and endothelial function in a sample of untreated hypertensive adults. METHODS: Participants were 127 men (N = 74) and women (N = 53), including 55 African Americans and 72 White Americans, aged 40-60 years (mean age, 45.3 ± 8.5 years), with untreated hypertension (systolic blood pressure 130-159 mm Hg and/or diastolic blood pressure 85-99 mm Hg). Noninvasive brachial artery flow-mediated dilation (FMD) was assessed by ultrasound. Sleep parameters, including sleep efficiency (SE), total sleep time (TST), and subjective sleep quality, were assessed over 7 consecutive days by wrist actigraphy. RESULTS: Participants averaged 7.76 ± 1 hours in bed, with an average SE of 78 ± 9%, and TST of 6 ± 1 hours. Brachial FMD averaged 3.5 ± 3.1%. In multivariate analyses controlling for sex, race, body mass index, clinic blood pressure, income, smoking, alcohol use, and baseline arterial diameter, SE was positively associated with FMD (β = 0.28, P = 0.012). Subjective sleep quality (β = -0.04, P = 0.63) and TST (β = -0.11, P = 0.25) were unrelated to FMD. CONCLUSIONS: Poor sleep as indicated by low SE was associated with impaired FMD. These findings for SE are consistent with previous observations of other measures implicating poor sleep as a CVD risk factor. Interventions that improve sleep may also help lower CVD risk.
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Hill et al. (2020) conducted a cross-sectional in Untreated hypertension (n=127). Actigraphy-derived sleep efficiency was evaluated on Brachial artery flow-mediated dilation (FMD) (β = 0.28, p=0.012). Actigraphy-derived sleep efficiency was positively associated with brachial artery flow-mediated dilation in adults with untreated hypertension (β = 0.28, P = 0.012).
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