Sleep-Disordered Breathing Destabilizes Ventricular Repolarization.

Sleep-Disordered Breathing Destabilizes Ventricular Repolarization.
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睡眠呼吸障碍会破坏心室复极的稳定性。

DOI:
10.1101/2023.02.10.23285789
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发表时间:
2024
期刊:
medRxiv : the preprint server for health sciences
影响因子:
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通讯作者:
Punjabi,NareshM
Punjabi,NareshM
中科院分区:
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文献类型:
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作者:
Solhjoo,Soroosh;Haigney,MarkC;Siddharthan,Trishul;Koch,Abigail;Punjabi,NareshM

文献摘要

相似文献

目的研究间歇性低氧血症与QT变异性指数(QTVI)之间的关系。QTVI是一种衡量心脏复极不稳定性的指标,与心律失常、心脏性猝死和死亡率相关。第一个队列用于横断面分析,是122名患有和不患有严重SDB的参与者的配对样本。第二个队列用于纵向分析,由52名有无SDB事件的配对样本组成。横断面和纵向队列选自睡眠心脏健康研究参与者。第三组包括19名健康成年人,分别在两天内暴露在急性间歇性低氧和环境空气中。结果与无SDB组比较,重度SDB组QTVI值(重度SDB组为-1.19vs.TST1.43,P=0.027)、心率(68.34vs.64.92次/分钟;P=0.028)和低氧血症负荷(−<90%)明显增加(TST9011.39%vs.1.32%,P&lt;0.001)。TST90,而不是唤醒频率,是QTVI的预测因子。睡眠中QTVI是全因死亡率的预测指标。随着SDB的发生,QTVI值从−的1.23增加到−的0.86(P=0.017)。健康成人暴露于急性间歇低氧4h后,QTVI逐渐增加(从基线的−1.85增加到−1.64,P=0.016)。结论室性复极不稳定性是室性心律失常和心源性猝死的易感因素。间歇性低氧血症破坏了心室复极的稳定性,并可能导致SDB死亡率的增加。
RationaleSleep-disordered breathing (SDB) increases the risk of cardiac arrhythmias and sudden cardiac death.ObjectivesTo characterize the associations between SDB, intermittent hypoxemia, and the beat-to-beat QT variability index (QTVI), a measure of ventricular repolarization lability associated with a higher risk for cardiac arrhythmias, sudden cardiac death, and mortality.MethodsThree distinct cohorts were used for the current study. The first cohort, used for cross-sectional analysis, was a matched sample of 122 participants with and without severe SDB. The second cohort, used for longitudinal analysis, consisted of a matched sample of 52 participants with and without incident SDB. The cross-sectional and longitudinal cohorts were selected from the Sleep Heart Health Study participants. The third cohort comprised 19 healthy adults exposed to acute intermittent hypoxia and ambient air on two separate days. Electrocardiographic measures were calculated from one-lead electrocardiograms.ResultsCompared to those without SDB, participants with severe SDB had greater QTVI (-1.19 in participants with severe SDB vs. −1.43 in participants without SDB, 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. QTVI during sleep was predictive of all-cause mortality. With incident SDB, mean QTVI increased from −1.23 to −0.86 over 5 years (P = 0.017). Finally, exposing healthy adults to acute intermittent hypoxia for four hours progressively increased QTVI (from −1.85 at baseline to −1.64 after four hours of intermittent hypoxia; P = 0.016).ConclusionsPrevalent and incident SDB are associated with ventricular repolarization instability, which predisposes to ventricular arrhythmias and sudden cardiac death. Intermittent hypoxemia destabilizes ventricular repolarization and may contribute to increased mortality in SDB.