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Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Objective short sleep duration modifies the relationship between hypertension and all-cause mortality.
Journal of Hypertension 2017 April
OBJECTIVE: Short sleep duration has been associated with cardiovascular morbidity and mortality. However, previous studies were limited by using subjective sleep measures and treating sleep duration as a sole, independent predictor. Therefore, the role of sleep duration in predicting mortality is still not well understood. We posit that objective sleep duration is an effect modifier of the relationship between hypertension and all-cause mortality.
METHODS: We addressed this question in the Penn State Adult Cohort, a random, general population sample of 1741 men and women (48.7 ± 13.5 years) who were studied in the sleep laboratory and followed up for 15.5 ± 4.1 years. Hypertension was defined on the basis of SBP and DBP (≥140/≥90 mmHg) or use of antihypertensive medication. Polysomnographic sleep duration was classified into three clinically meaningful categories.
RESULTS: We tested the interaction between hypertension and polysomnographic sleep duration on all-cause mortality using multiple logistic regression while controlling for several potential confounders (P value = 0.03). The odds (95% confidence interval) of all-cause mortality associated with hypertension were 1.77 (1.07-2.92), 2.78 (1.47-5.24), and 3.93 (2.22-6.95) for individuals who slept at least 6, 5-6, and 5 h or less, respectively.
CONCLUSION: The risk of mortality associated with hypertension increases in a dose-response manner as a function of shorter sleep duration. Short sleep in hypertensive individuals may be a marker of the degree of central autonomic dysfunction. Future epidemiological studies should examine this effect modification using cause-specific mortality, whereas future clinical trials should examine whether lengthening sleep improves the prognosis of individuals with hypertension.
METHODS: We addressed this question in the Penn State Adult Cohort, a random, general population sample of 1741 men and women (48.7 ± 13.5 years) who were studied in the sleep laboratory and followed up for 15.5 ± 4.1 years. Hypertension was defined on the basis of SBP and DBP (≥140/≥90 mmHg) or use of antihypertensive medication. Polysomnographic sleep duration was classified into three clinically meaningful categories.
RESULTS: We tested the interaction between hypertension and polysomnographic sleep duration on all-cause mortality using multiple logistic regression while controlling for several potential confounders (P value = 0.03). The odds (95% confidence interval) of all-cause mortality associated with hypertension were 1.77 (1.07-2.92), 2.78 (1.47-5.24), and 3.93 (2.22-6.95) for individuals who slept at least 6, 5-6, and 5 h or less, respectively.
CONCLUSION: The risk of mortality associated with hypertension increases in a dose-response manner as a function of shorter sleep duration. Short sleep in hypertensive individuals may be a marker of the degree of central autonomic dysfunction. Future epidemiological studies should examine this effect modification using cause-specific mortality, whereas future clinical trials should examine whether lengthening sleep improves the prognosis of individuals with hypertension.
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