Sneddon J F, Counihan P J, Bashir Y, Haywood G A, Ward D E, Camm A J
Department of Cardiological Sciences, St. George's Hospital Medical School, London, England.
J Am Coll Cardiol. 1993 Apr;21(5):1193-8. doi: 10.1016/0735-1097(93)90245-v.
The purpose of this study was to assess vagal tone and cardiopulmonary baroreceptor activity in patients with tilt-induced neurally mediated syncope.
The causes of individual susceptibility to orthostatic stress leading to recurrent neurally mediated syncope remain obscure. The trigger for sympathetic withdrawal and increased vagal activity is believed to be stimulation of ventricular mechanoreceptors.
Seventeen patients (mean age 50.6 years) with recurrent syncope and a positive response on a 45-min 60 degrees head-up tilt test were compared with a control group of 17 patients (mean age 47.5 years) with unexplained syncope and negative tilt test findings. Vagal activity was assessed by high pressure baroreceptor testing and by temporal and spectral analysis of heart rate variability during Holter ambulatory electrocardiographic monitoring. Cardiopulmonary baroreceptor sensitivity was assessed by measurement of forearm vascular responses to lower body negative pressure.
Mean high pressure baroreceptor sensitivity was 16.4 +/- 12.2 ms/mm Hg in the group with a positive tilt test response compared with 15.1 +/- 13.0 ms/mm Hg in the control group (p = NS). There were no significant differences between the groups in any of the temporal or spectral measures of heart rate variability. The increase in forearm vascular resistance in response to lower body negative pressure was 11.5 +/- 14.2 U in patients with tilt-induced syncope and 3.5 +/- 3.2 U in the control group at -5 mm Hg, 16.8 +/- 18.6 U and 4.8 +/- 5.3 U, respectively, at -10 mm Hg and 26.4 +/- 24.3 U and 10.2 +/- 7.8 U, respectively, at -20 mm Hg (p < 0.001).
Patients with tilt-induced neurally mediated syncope have augmented cardiopulmonary baroreceptor responses to orthostatic stress. This finding sheds new light on the etiology of neurally mediated syncope.
本研究旨在评估倾斜诱发的神经介导性晕厥患者的迷走神经张力和心肺压力感受器活性。
导致复发性神经介导性晕厥的个体对直立位应激易感性的原因仍不清楚。交感神经撤退和迷走神经活动增加的触发因素被认为是心室机械感受器的刺激。
将17例复发性晕厥且45分钟60度头高位倾斜试验呈阳性反应的患者（平均年龄50.6岁）与17例不明原因晕厥且倾斜试验结果为阴性的对照组患者（平均年龄47.5岁）进行比较。通过高压压力感受器测试以及动态心电图监测期间心率变异性的时域和频域分析来评估迷走神经活动。通过测量前臂血管对下体负压的反应来评估心肺压力感受器敏感性。
倾斜试验反应阳性组的平均高压压力感受器敏感性为16.4±12.2毫秒/毫米汞柱，而对照组为15.1±13.0毫秒/毫米汞柱（p=无显著性差异）。两组在心率变异性的任何时域或频域指标上均无显著差异。在下体负压为-5毫米汞柱时，倾斜诱发晕厥患者前臂血管阻力增加为11.5±14.2单位，对照组为3.5±3.2单位；在-10毫米汞柱时，分别为16.8±18.6单位和4.8±5.3单位；在-20毫米汞柱时，分别为26.4±24.3单位和10.2±7.8单位（p<0.001）。
倾斜诱发的神经介导性晕厥患者对直立位应激的心肺压力感受器反应增强。这一发现为神经介导性晕厥的病因学提供了新的线索。
