2016
DOI: 10.1016/s0735-1097(16)30771-9
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Obstructive Sleep Apnea and Circulating Potassium Channel Levels

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Cited by 2 publications
(3 citation statements)
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“…A recent study showed that CPAP treatment improved gene expression of circulating potassium channels in patients with moderate OSA but not in those with severe OSA. 71 Downregulation of potassium channels in patients with OSA may explain prolonged QT interval and increased risk of ventricular arrhythmia and sudden cardiac death. 71 Hence, CPAP treatment may not reverse long-term structural remodeling which triggers arrhythmia; however, it may decrease further progression of such events.…”
Section: General Discussion and Future Directionsmentioning
confidence: 99%
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“…A recent study showed that CPAP treatment improved gene expression of circulating potassium channels in patients with moderate OSA but not in those with severe OSA. 71 Downregulation of potassium channels in patients with OSA may explain prolonged QT interval and increased risk of ventricular arrhythmia and sudden cardiac death. 71 Hence, CPAP treatment may not reverse long-term structural remodeling which triggers arrhythmia; however, it may decrease further progression of such events.…”
Section: General Discussion and Future Directionsmentioning
confidence: 99%
“…71 Downregulation of potassium channels in patients with OSA may explain prolonged QT interval and increased risk of ventricular arrhythmia and sudden cardiac death. 71 Hence, CPAP treatment may not reverse long-term structural remodeling which triggers arrhythmia; however, it may decrease further progression of such events. Therefore, treatment of OSA with CPAP therapy should be considered as an adjunct to the medical therapy for arrhythmia and/or other related conditions and not as a sole treatment.…”
Section: General Discussion and Future Directionsmentioning
confidence: 99%
“…The activity of hERG1 potassium channels, which contributes to the outward K + currents and underlies the long QT syndrome when mutated, was found to be significantly inhibited during mild oxidative stress [35] , as is the transient outward potassium current [36] . The high sensitivity and complex interplay of different ion channels under increased oxidative stress explains the electrocardiographic QT c and T peak -T end interval prolongation under intermittent hypoxia, reflecting prolonged repolarization and increased dispersion of repolarization, leading to increased reentry risk [37] , [38] , [39] , [40] .…”
Section: The Hypothesismentioning
confidence: 99%