Journal of hypertension · 2021
The association of actigraphy-assessed sleep duration with sleep blood pressure, nocturnal hypertension, and nondipping blood pressure: the coronary artery risk development in young adults (CARDIA) study.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Abdalla Marwah, Sakhuja Swati, Akinyelure Oluwasegun P, Thomas S Justin, Schwartz Joseph E, Lewis Cora E, Shikany James M, Lloyd-Jones Donald, Booth John N, Shimbo Daichi, Hall Martica H, Muntner Paul
Аннотация
OBJECTIVE: Nocturnal hypertension and nondipping systolic blood pressure (SBP) are associated with increased cardiovascular disease (CVD) risk. Short and long sleep duration (SSD and LSD) are also associated with increased CVD risk and may be risk factors for nocturnal hypertension and nondipping SBP. We examined the association between SSD and LSD with sleep BP, nocturnal hypertension, and nondipping SBP among 647 white and African American Coronary Artery Risk Development in Young Adults (CARDIA) study participants who completed 24-h ambulatory BP monitoring, wrist actigraphy, and sleep diaries in 2015-2016.
METHODS: The times when participants were asleep and awake were determined from actigraphy complemented by sleep diaries. Nocturnal hypertension was defined as sleep BP ≥120/70 mmHg and nondipping SBP as mean sleep-to-awake SBP ratio >0.90. Sleep duration was categorized as SSD (<6 h), normal sleep duration (NSD: 6-8.9 h), and LSD (≥9 h).
RESULTS: The prevalence of SSD and LSD were 13.9 and 21.1%, respectively. Compared to participants with NSD, participants with LSD had higher mean sleep SBP (2.1 mmHg, 95% confidence interval [CI] 0.2, 4.1 mmHg) and diastolic BP (1.7 mmHg, 95% CI 0.5, 3.0 mmHg). Participants with LSD had a higher prevalence of nocturnal hypertension (prevalence ratio [PR]: 1.26, 95% CI 1.03-1.54) and nondipping SBP (PR 1.33, 95% CI 1.03-1.72) compared to participants with NSD. There was no evidence of an association between SSD and sleep SBP or DBP, nocturnal hypertension, or nondipping SBP.
CONCLUSIONS: These findings suggest that LSD may be associated with nocturnal hypertension and nondipping SBP.
METHODS: The times when participants were asleep and awake were determined from actigraphy complemented by sleep diaries. Nocturnal hypertension was defined as sleep BP ≥120/70 mmHg and nondipping SBP as mean sleep-to-awake SBP ratio >0.90. Sleep duration was categorized as SSD (<6 h), normal sleep duration (NSD: 6-8.9 h), and LSD (≥9 h).
RESULTS: The prevalence of SSD and LSD were 13.9 and 21.1%, respectively. Compared to participants with NSD, participants with LSD had higher mean sleep SBP (2.1 mmHg, 95% confidence interval [CI] 0.2, 4.1 mmHg) and diastolic BP (1.7 mmHg, 95% CI 0.5, 3.0 mmHg). Participants with LSD had a higher prevalence of nocturnal hypertension (prevalence ratio [PR]: 1.26, 95% CI 1.03-1.54) and nondipping SBP (PR 1.33, 95% CI 1.03-1.72) compared to participants with NSD. There was no evidence of an association between SSD and sleep SBP or DBP, nocturnal hypertension, or nondipping SBP.
CONCLUSIONS: These findings suggest that LSD may be associated with nocturnal hypertension and nondipping SBP.