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 repolarisation lability that may predispose people to long-term cardiovascular mortality?
STUDY DESIGN AND METHODS: We analyzed 407,541 arousals in the overnight polysomnograms of 2558 older men in the Osteoporotic Fractures in Men Sleep Study. QT and RR intervals were measured beat-to-beat starting 15 seconds before arousal onset until 15 seconds past onset. Ventricular repolarisation lability was quantified by the QT variability index (QTVi).
RESULTS: During 10.1±2.5 years of follow-up, 1000 men died from 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 hazard analysis adjusted for age, BMI, cardiovascular and respiratory risk factors, sleep disordered breathing and arousal, diabetes and Parkinson's disease indicated that excessive QTVi during arousal was independently associated with all-cause and CV mortality (all-cause: HR=1.20 [1.04-1.38], p=0.012; CV: 1.29 [1.01 -1.65], p=0.043).
INTERPRETATION: Arousals affect ventricular repolarisation. A disproportionate increase in QT variability during arousal is associated with an increased all-cause and CV mortality and may reflect ventricular repolarisation 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 repolarisation lability and reduces subsequent mortality.
CLINICAL TRIAL REGISTRATION NUMBER: ClinicalTrials.gov Identifier: NCT00070681.
|Number of pages||14|
|Early online date||13 Oct 2022|
|Publication status||Published - Feb 2023|