Sleep Arousal-Related Ventricular Repolarization Lability Is Associated With Cardiovascular Mortality in Older Community-Dwelling Men

Sobhan Salari Shahrbabaki, Dominik Linz, Susan Redline, Katie Stone, Kristine Ensrud, Mathias Baumert

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

Background: Sleep is fragmented by brief arousals, and excessive arousal burden has been linked to increased cardiovascular (CV) risk, but mechanisms are poorly understood. Research Question: Do arousals trigger cardiac ventricular repolarization lability that may predispose people to long-term cardiovascular mortality? Study Design and Methods: This study analyzed 407,541 arousals in the overnight polysomnograms of 2,558 older men in the Osteoporotic Fractures in Men sleep study. QT and RR intervals were measured beat-to-beat starting 15 s prior to arousal onset until 15 s past onset. Ventricular repolarization lability was quantified by using the QT variability index (QTVi). Results: During 10.1 ± 2.5 years of follow-up, 1,000 men died of any cause, including 348 CV deaths. During arousals, QT and RR variability increased on average by 5 and 55 ms, respectively, resulting in a paradoxical transient decrease in QTVi from 0.07 ± 1.68 to –1.00 ± 1.68. Multivariable Cox proportional hazards analysis adjusted for age, BMI, cardiovascular and respiratory risk factors, sleep-disordered breathing and arousal, diabetes, and Parkinson disease indicated that excessive QTVi during arousal was independently associated with all-cause and CV mortality (all-cause hazard ratio, 1.20 [95% CI, 1.04-1.38; P = .012]; CV hazard ratio, 1.29 [95% CI, 1.01 -1.65; P = .043]). Interpretation: Arousals affect ventricular repolarization. A disproportionate increase in QT variability during arousal is associated with an increased all-cause and CV mortality and may reflect ventricular repolarization maladaptation to the arousal stimulus. Whether arousal-related QTVi can be used for more tailored risk stratification warrants further study, including evaluating whether arousal suppression attenuates ventricular repolarization lability and reduces subsequent mortality. Clinical Trial Registration: ClinicalTrials.gov; No.: NCT00070681; URL: www.clinicaltrials.gov

Original languageEnglish (US)
Pages (from-to)419-432
Number of pages14
JournalCHEST
Volume163
Issue number2
DOIs
StatePublished - Feb 2023

Bibliographical note

Funding Information:
This study was supported by a grant from the Australian Research Council [DP0663345]. The MrOS study and the Study of Osteoporotic Fractures (SOF) are supported by National Institutes of Health (NIH) funding. The following institutes provided support: The National Institute on Aging, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the National Center for Advancing Translational Sciences, and NIH Roadmap for Medical Research [U01 AG027810, U01 AG042124, U01 AG042139, U01 AG042140, U01 AG042143, U01 AG042145, U01 AG042168, U01 AR066160, and UL1 TR000128]. The National Heart, Lung, and Blood Institute provided funding for the MrOS sleep ancillary study [R01 HL071194, R01 HL070848, R01 HL070847, R01 HL070842, R01 HL070841, R01 HL070837, R01 HL070838, and R01 HL070839] and the National Sleep Research Resource [R24-HL-114473]. The SOF sleep study was supported by grants AG021918, AG026720, AG05394, AG05407, AG08415, AR35582, AR35583, AR35584, R01 AG005407, R01 AG027576-22, 2 R01 AG005394-22A1, 2 R01 AG027574-22A1, HL40489, and T32 AG000212-14. S. R. was supported in part by the NIH [R35HL135818].

Publisher Copyright:
© 2022 The Author(s)

Keywords

  • QT variability index
  • all-cause mortality
  • cardiovascular mortality
  • sleep apnea
  • sleep arousal
  • ventricular repolarization

PubMed: MeSH publication types

  • Clinical Trial
  • Journal Article
  • Research Support, N.I.H., Extramural

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