Smith Janet H, Baumert Mathias, Nalivaiko Eugene, McEvoy Ronald Douglas, Catcheside Peter G
Discipline of Physiology, School of Molecular and Biomedical Science, University of Adelaide, Adelaide, Australia.
J Sleep Res. 2009 Jun;18(2):188-95. doi: 10.1111/j.1365-2869.2008.00720.x.
Sudden cardiac death appears to be more prevalent during the normal sleeping hours in obstructive sleep apnoea (OSA) patients compared with the general population as well as to cardiovascular disease patients. The reasons for this remain unclear, but there are three likely main contributors to nocturnal death in OSA patients; cardiac arrhythmias, stroke/ruptured cerebral aneurism and myocardial infarction. Particularly marked cardiovascular system activation with arousal may play a role in initiating sudden adverse cardiovascular events in OSA. The purpose of this study was to investigate cardiac RR, QT and PR interval changes in the electrocardiogram (ECG) associated with spontaneous and respiratory-related arousals in OSA patients. A detailed observational study of ECG records obtained during conventional diagnostic sleep study with no further interventions was carried out in 20 patients (12 males, age 42.8 +/- 2.1 years, body mass index 35.1 +/- 1.9 kg m(-2), and respiratory disturbance index 51.8 +/- 6.4 events/hour). RR and QT intervals showed significant shortening during arousals. RR interval shortening was found to be greater during respiratory arousals when compared to spontaneous arousals. PR interval showed a trend toward a greater prolongation during respiratory arousal. QT interval shortening was weakly correlated with arterial oxygen saturation levels preceding arousal. In conclusion, these data suggest that despite greater cardiac acceleration following respiratory versus spontaneous arousals from sleep, QT shortening and PR prolongation responses are similar independent of arousal type. These data support that arousals produce quite marked and differential cardiac conduction system activation in OSA and that the degree and pattern of activation may be partly influenced by the presence and severity of preceding respiratory events.
与普通人群以及心血管疾病患者相比,阻塞性睡眠呼吸暂停(OSA)患者在正常睡眠时间发生心源性猝死的情况似乎更为普遍。其原因尚不清楚,但OSA患者夜间死亡可能主要有三个因素:心律失常、中风/脑动脉瘤破裂和心肌梗死。睡眠中觉醒时特别明显的心血管系统激活可能在引发OSA患者突发不良心血管事件中起作用。本研究的目的是调查OSA患者心电图(ECG)中与自发觉醒和呼吸相关觉醒相关的RR、QT和PR间期变化。对20例患者(12例男性,年龄42.8±2.1岁,体重指数35.1±1.9 kg/m²,呼吸紊乱指数51.8±6.4次/小时)在常规诊断性睡眠研究期间获得的ECG记录进行了详细的观察性研究,未进行进一步干预。觉醒期间RR和QT间期显著缩短。与自发觉醒相比,呼吸觉醒期间RR间期缩短更明显。PR间期在呼吸觉醒期间有延长更明显的趋势。QT间期缩短与觉醒前的动脉血氧饱和度水平呈弱相关。总之,这些数据表明,尽管呼吸觉醒比睡眠自发觉醒后心脏加速更明显,但QT缩短和PR延长反应与觉醒类型无关,是相似的。这些数据支持觉醒在OSA中会引起相当明显且不同的心脏传导系统激活,并且激活的程度和模式可能部分受到先前呼吸事件的存在和严重程度的影响。