Sleep-Disordered Breathing Destabilizes Ventricular Repolarization

Abstract

ABSTRACTRationaleSleep-disordered breathing (SDB) increases the risk of cardiac arrhythmias, sudden death, and all-cause mortality.ObjectivesTo characterize the associations between SDB, intermittent hypoxemia, and the QT variability index (QTVI), a measure of ventricular repolarization lability associated with a higher risk for cardiac arrhythmias, sudden death, and cardiovascular mortality.MethodsPolysomnograms from three cohorts were used: a matched sample of 122 participants with and without severe SDB, a matched sample of 52 participants with and without incident SDB, and a cohort of 19 healthy adults exposed to intermittent hypoxia and ambient air on two separate days. Electrocardiographic measures were calculated from one-lead electrocardiograms.Measurements and Main ResultsCompared to those without SDB, participants with severe SDB had larger QTVI (−1.19 vs. -1.43,P=0.027), heart rate (68.34 vs. 64.92 beats/minute;P=0.028), and hypoxemia burden during sleep as assessed by the total sleep time with oxygen saturation less than 90% (TST90; 11.39% vs. 1.32%,P<0.001). TST90, but not the frequency of arousals, was a predictor of QTVI. Heart rate and QTVI during sleep were predictive of all-cause mortality. In the cohort with incident SDB, the mean QTVI increased from -1.23 to -0.86 over 5 years (P=0.017). Finally, in the cohort of healthy adults, exposure to intermittent hypoxia for four hours increased QTVI (−1.85 vs. -1.64;P=0.016).ConclusionsPrevalent and incident SDB are associated with ventricular repolarization instability, which predisposes to ventricular arrhythmias and sudden cardiac death. Intermittent hypoxemia can destabilize ventricular repolarization and may mediate the increased mortality in SDB.