Jardine David L, Krediet C T Paul, Cortelli Pietro, Frampton Christopher M, Wieling Wouter
Department of General Medicine, Christchurch Hospital, Christchurch, New Zealand.
Clin Sci (Lond). 2009 Sep 7;117(10):345-53. doi: 10.1042/CS20080497.
Sleep syncope is a recently described form of vasovagal syncope that interrupts sleep. The pathophysiology of this condition is uncertain but a 'central' non-baroreflex-mediated trigger has been suggested. In the present study, we tested the hypothesis that patients with sleep syncope have abnormal sympatho-vagal responses to non-baroreflex, but normal responses to baroreflex stimuli. We collected historical data from SS patients (patients with vasovagal syncope with sleep syncope; n=16) and NSS patients (patients with vasovagal syncope without sleep syncope; n=35), including demography, and triggers and symptoms during syncope. MBP (mean blood pressure), HR (heart rate) and MSNA (muscle sympathetic nerve activity) in SS patients were compared with NSS patients and matched controls (n=16) during HG (handgrip), CPTs (cold pressor tests), HUT (head-up tilting) and tilt-induced pre-syncope. Patients and controls were of similar age and gender distribution [SS patients, age 46.0+/-4 years (69% female); NSS patients, 47.3+/-4 years (63% female); controls, 43.7+/-5 years (69% female)]. Compared with NSS patients, SS patients reported more fainting episodes: (i) triggered by phobias (75 compared with 37%; P=0.001); (ii) while in the horizontal position (44 compared with 6%; P=0.001); and (iii) associated with abdominal symptoms (69 compared with 9%; P=0.001). Compared with controls, the MBP response to HG was attenuated in SS patients (P=0.016), and MSNA (burst frequency and incidence) responses to CPT were attenuated in both syncope groups (SS, P=0.011 and 0.003 respectively; NSS, P=0.021 and 0.049 respectively). MSNA responses to HUT did not differ. For both non-baroreflex and baroreflex responses, there were no differences in any of the MSNA indices between the syncope groups. Patients with vasovagal syncope, with or without sleep syncope, have very similar sympatho-vagal responses to both non-baroreflex and baroreflex stimuli. This is consistent with sleep syncope being a subform of vasovagal syncope. Attenuation of sympathetic responses to non-baroreflex pathways may be important in the mechanism of vasovagal syncope.
睡眠性晕厥是一种最近才被描述的血管迷走性晕厥形式,它会中断睡眠。这种病症的病理生理学尚不确定,但有人提出存在一种“中枢性”非压力感受器介导的触发因素。在本研究中,我们检验了这样一个假设:睡眠性晕厥患者对非压力感受器刺激有异常的交感 - 迷走反应,但对压力感受器刺激有正常反应。我们收集了睡眠性晕厥患者(血管迷走性晕厥合并睡眠性晕厥患者;n = 16)和非睡眠性晕厥患者(血管迷走性晕厥但无睡眠性晕厥患者;n = 35)的历史数据,包括人口统计学信息以及晕厥期间的触发因素和症状。在进行握力试验(HG)、冷加压试验(CPTs)、头高位倾斜试验(HUT)以及倾斜诱发的接近晕厥状态时,我们比较了睡眠性晕厥患者与非睡眠性晕厥患者以及匹配的对照组(n = 16)的平均血压(MBP)、心率(HR)和肌肉交感神经活动(MSNA)。患者和对照组在年龄和性别分布上相似[睡眠性晕厥患者,年龄46.0±4岁(69%为女性);非睡眠性晕厥患者,47.3±4岁(63%为女性);对照组,43.7±5岁(69%为女性)]。与非睡眠性晕厥患者相比,睡眠性晕厥患者报告的晕厥发作更多:(i)由恐惧症触发(75%对37%;P = 0.001);(ii)处于水平位时(44%对6%;P = 0.001);以及(iii)伴有腹部症状(69%对9%;P = 0.001)。与对照组相比,睡眠性晕厥患者对握力试验的平均血压反应减弱(P = 0.016),并且在两个晕厥组中,对冷加压试验的肌肉交感神经活动(爆发频率和发生率)反应均减弱(睡眠性晕厥组,分别为P = 0.011和0.003;非睡眠性晕厥组,分别为P = 0.021和0.049)。对倾斜试验的肌肉交感神经活动反应没有差异。对于非压力感受器和压力感受器反应,晕厥组之间在任何肌肉交感神经活动指标上均无差异。有或无睡眠性晕厥的血管迷走性晕厥患者对非压力感受器和压力感受器刺激具有非常相似的交感 - 迷走反应。这与睡眠性晕厥是血管迷走性晕厥的一种亚型相一致。交感神经对非压力感受器通路反应的减弱可能在血管迷走性晕厥的机制中起重要作用。