Garrigue Stéphane, Pépin Jean-Louis, Defaye Pascal, Murgatroyd Francis, Poezevara Yann, Clémenty Jacques, Lévy Patrick
Department of Cardiac Electrophysiology and Clinical Pacing Hôpital, University of Bordeaux and Grenoble, Grenoble, France.
Circulation. 2007 Apr 3;115(13):1703-9. doi: 10.1161/CIRCULATIONAHA.106.659706. Epub 2007 Mar 12.
Cardiovascular diseases leading to pacemaker implantations are suspected of being associated with a high rate of undiagnosed sleep apnea syndrome (SAS). We sought to determine the prevalence and consequences of SAS in pacemaker patients according to pacing indications: heart failure, symptomatic diurnal bradycardia, and atrioventricular block.
Ninety-eight consecutive patients (mean age, 64+/-8 years) not known to have sleep apnea were included; 29 patients were paced for dilated cardiomyopathy (29%), 33 for high-degree atrioventricular block (34%), and 36 for sinus node disease (37%). All underwent Epworth Sleepiness Scale assessment and polysomnography with the pacemaker programmed to right ventricular DDI pacing mode (lower pacing rate, 50 pulses per minute). SAS was defined as an apnea-hypopnea index > or = 10/h. Mean Epworth Sleepiness Scale was in the normal range (7+/-4), although 13 patients (25%) had an abnormal score > 11/h. Fifty-seven patients (59%) had SAS; of these, 21 (21.4%) had a severe SAS (apnea-hypopnea index > 30/h). In patients with heart failure, 50% presented with SAS (mean apnea-hypopnea index, 11+/-7) compared with 68% of patients with atrioventricular block (mean apnea-hypopnea index, 24+/-29) and 58% with sinus node disease (mean apnea-hypopnea index, 19+/-23).
In paced patients, there is an excessively high prevalence of undiagnosed SAS (59%). Whether treating SAS would have changed the need for pacing is unknown. Treatment effects should be further evaluated particularly because these patients are less symptomatic than typical SAS patients. In any case, SAS should be systematically searched for in paced patients owing to potential detrimental effects on their cardiovascular evolution.
导致起搏器植入的心血管疾病被怀疑与未诊断出的睡眠呼吸暂停综合征（SAS）的高发生率相关。我们试图根据起搏指征确定起搏器患者中SAS的患病率及后果：心力衰竭、症状性日间心动过缓和房室传导阻滞。
纳入98例此前不知患有睡眠呼吸暂停的连续患者（平均年龄64±8岁）；29例患者因扩张型心肌病接受起搏治疗（29%），33例因高度房室传导阻滞（34%），36例因窦房结疾病（37%）。所有患者均接受爱泼华嗜睡量表评估及多导睡眠监测，起搏器程控为右心室DDI起搏模式（较低起搏频率为每分钟50次脉冲）。SAS定义为呼吸暂停低通气指数≥10次/小时。尽管有13例患者（25%）的爱泼华嗜睡量表评分异常＞11分/小时，但平均爱泼华嗜睡量表评分仍在正常范围内（7±4）。57例患者（59%）患有SAS；其中21例（21.4%）患有严重SAS（呼吸暂停低通气指数＞30次/小时）。心力衰竭患者中，50%存在SAS（平均呼吸暂停低通气指数为11±7），相比之下，房室传导阻滞患者中有68%存在SAS（平均呼吸暂停低通气指数为24±29），窦房结疾病患者中有58%存在SAS（平均呼吸暂停低通气指数为19±23）。
在接受起搏治疗的患者中，未诊断出的SAS患病率过高（59%）。治疗SAS是否会改变起搏需求尚不清楚。尤其鉴于这些患者的症状比典型SAS患者轻，应进一步评估治疗效果。无论如何，由于对心血管进展可能存在有害影响，对于接受起搏治疗的患者应系统筛查SAS。
