Arrhythmias & electrophysiology
Sleep-disordered breathing destabilizes ventricular repolarization: Cross-sectional, longitudinal, and experimental evidence
Authors' conclusion
The results show that both prevalent SDB and incident SDB are associated with ventricular repolarization instability and suggest intermittent hypoxemia as the underlying mechanism that may contribute to increased mortality in SDB.
Study context
- Population
- Sleep Heart Health Study participants with no known comorbidities, not taking drugs affecting cardiac repolarization; healthy adults (experimental cohort)3 cohorts: 122, 52, 19
- Exposure
- Severe sleep-disordered breathing (SDB) vs no SDB; incident SDB; acute intermittent hypoxia vs ambient air
- Outcome
- Beat-to-beat QT variability index (QTVI)
Methodological detailsmatched samples, Sleep Heart Health Study cohorts, ECG measures from 1-lead ECGs
- Matched samples
- Sleep Heart Health Study cohorts
- ECG measures from 1-lead ECGs
Main finding
As reported in the abstract
QTVI, severe SDB vs no SDB (cross-sectional)
- Severe SDB vs No SDB: P = 0.027
- Matched sample
Observational data: associations, not effects.
Further findings
Predictors of QT variability index (QTVI)
- Total sleep time with <90% oxygen saturation, but not arousal frequency, predicted QTVI
- QTVI during sleep predicted all-cause mortality
QTVI with incident SDB (longitudinal) · 5 years
- Mean QTVI increased from −1.23 to −0.86
- P = 0.017
- Matched sample
QTVI with acute intermittent hypoxia in healthy adults (experimental) · 4 hours
- QTVI progressively increased
- P = 0.016
Original publication
Sleep-disordered breathing destabilizes ventricular repolarization: Cross-sectional, longitudinal, and experimental evidence. Heart Rhythm. Published 28 August 2024. doi:10.
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