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Quantifying Infra-slow Dynamics of Spectral Power and Heart Rate in Sleeping Mice
Published on: August 2, 2017
Sleep-disordered breathing destabilizes ventricular repolarization: Cross-sectional, longitudinal, and experimental
Soroosh Solhjoo1, Mark C Haigney2, Naresh M Punjabi3
1Johns Hopkins University School of Medicine, Baltimore, Maryland; F. Edward Hébert School of Medicine, Bethesda, Maryland.
Sleep-disordered breathing (SDB) is linked to unstable heart rhythms and increased mortality. Intermittent hypoxemia, a common SDB feature, appears to drive this instability, impacting QT variability index (QTVI).
Area of Science:
- Cardiology
- Sleep Medicine
- Physiology
Background:
- Sleep-disordered breathing (SDB) is a known risk factor for cardiac arrhythmias and sudden cardiac death.
- Ventricular repolarization lability, measured by the QT variability index (QTVI), is associated with increased cardiac event risk.
Purpose of the Study:
- To investigate the relationship between SDB, intermittent hypoxemia, and QTVI.
- To determine if SDB and hypoxemia predict adverse cardiac events and mortality.
Main Methods:
- Cross-sectional and longitudinal analyses of SDB cohorts (n=122 and n=52) from the Sleep Heart Health Study.
- Experimental study exposing healthy adults (n=19) to acute intermittent hypoxia.
- Electrocardiographic measures, including QTVI, were analyzed.
Main Results:
- Severe SDB was associated with significantly higher QTVI.
- Reduced oxygen saturation during sleep predicted QTVI, not arousal frequency.
- QTVI during sleep predicted all-cause mortality.
- Incident SDB led to a significant increase in QTVI over 5 years.
- Acute intermittent hypoxia progressively increased QTVI in healthy adults.
Conclusions:
- Both prevalent and incident SDB are associated with ventricular repolarization instability.
- Intermittent hypoxemia is implicated as the mechanism driving QTVI changes in SDB.
- These findings suggest a pathway linking SDB, repolarization instability, and increased mortality.
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