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Obstructive sleep apnoea during REM sleep and incident non-dipping of nocturnal blood pressure: a longitudinal analysis of the Wisconsin Sleep Cohort
  1. Babak Mokhlesi1,
  2. Erika W Hagen2,
  3. Laurel A Finn2,
  4. Khin Mae Hla3,
  5. Jason R Carter4,
  6. Paul E Peppard2
  1. 1Department of Medicine, Section of Pulmonary and Critical Care, Sleep Disorders Center, University of Chicago, Chicago, Illinois, USA
  2. 2Department of Population Health Sciences, School of Medicine and Public Health, University of Wisconsin—Madison, Madison, Wisconsin, USA
  3. 3Department of Medicine, School of Medicine and Public Health, University of Wisconsin—Madison, Madison, Wisconsin, USA
  4. 4Department of Kinesiology and Integrative Physiology, Michigan Technological University, Houghton, Michigan, USA
  1. Correspondence to Dr Babak Mokhlesi, Section of Pulmonary and Critical Care Medicine, Sleep Disorders Center, University of Chicago, 5841 S. Maryland Ave, MC6076/Room M630, Chicago, IL 60637, USA; bmokhles{at}medicine.bsd.uchicago.edu

Abstract

Background Non-dipping of nocturnal blood pressure (BP) is associated with target organ damage and cardiovascular disease. Obstructive sleep apnoea (OSA) is associated with incident non-dipping. However, the relationship between disordered breathing during rapid eye movement (REM) sleep and the risk of developing non-dipping has not been examined. This study investigates whether OSA during REM sleep is associated with incident non-dipping.

Methods Our sample included 269 adults enrolled in the Wisconsin Sleep Cohort Study who completed two or more 24 h ambulatory BP studies over an average of 6.6 years of follow-up. After excluding participants with prevalent non-dipping BP or antihypertensive use at baseline, there were 199 and 215 participants available for longitudinal analysis of systolic and diastolic non-dipping, respectively. OSA in REM and non-REM sleep were defined by apnoea hypopnoea index (AHI) from baseline in-laboratory polysomnograms. Systolic and diastolic non-dipping were defined by systolic and diastolic sleep/wake BP ratios >0.9. Modified Poisson regression models estimated the relative risks for the relationship between REM AHI and incident non-dipping, adjusting for non-REM AHI and other covariates.

Results There was a dose–response greater risk of developing systolic and diastolic non-dipping BP with greater severity of OSA in REM sleep (p-trend=0.021 for systolic and 0.024 for diastolic non-dipping). Relative to those with REM AHI<1 event/h, those with REM AHI≥15 had higher relative risk of incident systolic non-dipping (2.84, 95% CI 1.10 to 7.29) and incident diastolic non-dipping (4.27, 95% CI 1.20 to 15.13).

Conclusions Our findings indicate that in a population-based sample, REM OSA is independently associated with incident non-dipping of BP.

  • Sleep apnoea

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