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Postgraduate Education Corner: CONTEMPORARY REVIEWS IN SLEEP MEDICINE |

Sleep and Hypertension

David A. Calhoun, MD; Susan M. Harding, MD, FCCP
Author and Funding Information

From the Vascular Biology and Hypertension Program (Dr Calhoun), Division of Cardiovascular Diseases, and Sleep/Wake Disorders Center (Dr Harding), Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL.

Correspondence to: David A. Calhoun, MD, Division of Cardiovascular Diseases, University of Alabama at Birmingham, 1530 3rd Ave S, Birmingham, AL 35294-1150; e-mail: dcalhoun@uab.edu


Funding/Support: This study was funded by the National Institutes of Health, National Heart, Lung, and Blood Institute [Grant 2R01–HL075614-5, “Etiology of Sleep Apnea-Related Hyperaldosteronism,” David A. Calhoun, Principal Investigator, and Susan M. Harding, Co-investigator].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;138(2):434-443. doi:10.1378/chest.09-2954
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Ambulatory BP studies indicate that even small increases in BP, particularly nighttime BP levels, are associated with significant increases in cardiovascular morbidity and mortality. Accordingly, sleep-related diseases that induce increases in BP would be anticipated to substantially affect cardiovascular risk. Both sleep deprivation and insomnia have been linked to increases in incidence and prevalence of hypertension. Likewise, sleep disruption attributable to restless legs syndrome increases the likelihood of having hypertension. Observational studies demonstrate a strong correlation between the severity of obstructive sleep apnea (OSA) and the risk and severity of hypertension, whereas prospective studies of patients with OSA demonstrate a positive relationship between OSA and risk of incident hypertension. Intervention trials with continuous positive airway pressure (CPAP) indicate a modest, but inconsistent effect on BP in patients with severe OSA and a greater likelihood of benefit in patients with most CPAP adherence. Additional prospective studies are needed to reconcile observational studies suggesting that OSA is a strong risk factor for hypertension with the modest antihypertensive effects of CPAP observed in intervention studies.

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