Freitas J, Pereira S, Lago P, Costa O, Carvalho M J, Falcão de Freitas A
Centro de Estudos da Função Autonómica, Hospital de São João, Porto, Portugal.
Europace. 1999 Oct;1(4):258-65. doi: 10.1053/eupc.1999.0050.
Autonomic dysfunction seems to play a central role in the pathophysiology of neurocardiogenic syncope (NCS) but conflicting data have recently become available. We evaluated autonomic nervous system (ANS) function (heart rate variability (HRV), systolic blood pressure variability (SBPV) and baroreceptor gain (BRG)) and non-invasive haemodynamics (cardiac output and total peripheral resistance) in patients with neurocardiogenic syncope. Retrospectively, we evaluated 12 NCS patients (positive head-up tilt without pharmacological provocation) in the basal state and at initial tilt, 12 non-NCS patients with tilt-negative syncope and 12 aged-matched normal controls. Prospectively, we evaluated 16 NCS patients to analyse the haemodynamics and ANS activity throughout the tilt test (beginning of tilt and before syncope occurs). HRV and SBPV were accessed by fast Fourier transforms (FFT) and spontaneous BRG by temporal sequences, slope and a index. Modelflow was used to quantify the non-invasive haemodynamics. None of the autonomic and haemodynamic parameters at baseline or in the first 10 min of tilt was different among the respective NCS, non-NCS syncope and normal control groups, except for SBP, which was higher at baseline in controls. Throughout the tilt test in the prospective NCS group, the heart rate increased (88-95 beats x min(-1), P<0.05), systolic blood pressure decreased (123-109 mmHg, P<0.01), and arterial baroreceptor gain was reduced (7.6 to 5.5 ms mmHg(-1), P<0.01) and the absolute high frequency component of HRV (HF HRV) decreased (150-80 ms(-2), P<0.05), before syncope occurred. There was no change in the low frequency component of HRV (LF HRV), SBPV, cardiac output (CO) or total peripheral resistance (TPR). Tilt-induced syncope could not be predicted by non-invasive haemodynamic or autonomic parameters at rest or in the initial minutes of tilt. The decrease in arterial baroreceptor gain could be a precocious expression of the transient autonomic dysfunction that characterizes the occurrence of neurocardiogenic syncope.
自主神经功能障碍似乎在神经心源性晕厥（NCS）的病理生理学中起核心作用，但最近出现了相互矛盾的数据。我们评估了神经心源性晕厥患者的自主神经系统（ANS）功能（心率变异性（HRV）、收缩压变异性（SBPV）和压力感受器增益（BRG））以及无创血流动力学（心输出量和总外周阻力）。我们回顾性地评估了12例NCS患者（无药物激发的阳性直立倾斜试验）在基础状态和初始倾斜时的情况，12例倾斜试验阴性的非NCS晕厥患者以及12例年龄匹配的正常对照。前瞻性地，我们评估了16例NCS患者，以分析倾斜试验全过程（倾斜开始时和晕厥发生前）的血流动力学和ANS活动。HRV和SBPV通过快速傅里叶变换（FFT）获取，自发性BRG通过时间序列、斜率和一个指数获取。使用Modelflow对无创血流动力学进行量化。在各自的NCS、非NCS晕厥和正常对照组中，除了对照组基线时收缩压较高外，基线或倾斜开始后10分钟内的自主神经和血流动力学参数均无差异。在前瞻性NCS组的倾斜试验全过程中，在晕厥发生前，心率增加（88 - 95次/分钟，P<0.05），收缩压降低（123 - 109 mmHg，P<0.01），动脉压力感受器增益降低（7.6至5.5 ms/mmHg，P<0.01），HRV的绝对高频成分（HF HRV）降低（150 - 80 ms⁻²，P<0.05）。HRV的低频成分（LF HRV）、SBPV、心输出量（CO）或总外周阻力（TPR）无变化。倾斜诱发的晕厥无法通过静息时或倾斜开始几分钟内的无创血流动力学或自主神经参数进行预测。动脉压力感受器增益的降低可能是神经心源性晕厥发生时特征性短暂自主神经功能障碍的早熟表现。
