Sympatho-vagal responses in patients with sleep and typical vasovagal syncope

Sympatho-vagal responses in patients with sleep and typical vasovagal syncope
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DOI:
10.1042/cs20080497
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发表时间:
2009-11-01
期刊:
影响因子:
6
通讯作者:
Wieling, Wouter
Wieling, Wouter
中科院分区:
医学2区
文献类型:
--
作者:
Jardine, David L.;Krediet, C. T. Paul;Wieling, Wouter

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睡眠晕厥是最近被描述的一种干扰睡眠的血管迷走性晕厥。这种情况的病理生理机制尚不确定,但已经提出了一种“中枢”非压力感受性反射介导的触发机制。在本研究中,我们验证了一种假设,即睡眠晕厥患者对非压力反射有异常的交感迷走神经反应,但对压力反射刺激有正常反应。我们收集了SS患者(血管迷走性晕厥伴睡眠晕厥,n=16)和NSS患者(血管迷走性晕厥不伴睡眠晕厥,n=35)的历史数据,包括人口学、晕厥期间的触发因素和症状。比较SS患者与正常对照组(n=16)的平均血压(MBP)、心率(FIR)和肌交感神经活动(MSNA)在HG(握力)、CPTS(冷加压试验)、HUT(直立倾斜)和倾斜诱导的晕厥前的变化。患者和对照组的年龄和性别分布相似[SS患者,年龄46.0+/-4岁(69%女性);NSS患者,47.3+/-4岁(63%女性);对照组,43.7+/-5岁(69%女性)]。与NSS患者相比,SS患者报告了更多的晕厥发作:(I)由恐惧引发(75对37%;P=0.001);(Ii)水平卧位(44对6%;P=0.001);以及(ii!)合并腹部症状(69例,9%;P=0.001)。与对照组相比,SS患者对HG的血压反应减弱(P=0.016),两组晕厥患者对CPT的突发性频率和发生率反应均减弱(SS,P=0.011和0.003;NSS,P=0.021和0.049)。MSNA对HUT的回应也没有不同。对于非压力感受性反射和压力感受性反射反应,晕厥组之间的任何MSNA指数都没有差异。无论有无睡眠晕厥,血管迷走性晕厥患者对非压力感受性反射和压力感受性反射刺激的交感-迷走神经反应非常相似。这与睡眠晕厥是血管迷走性晕厥的一个亚型是一致的。对非压力感受性反射通路的交感反应减弱可能在血管迷走性晕厥的机制中起重要作用。
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), FIR (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 (ii!) 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.