Laboratory of Molecular Cardiology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.
Scand J Clin Lab Invest. 2012 Jul;72(4):265-73. doi: 10.3109/00365513.2012.659282. Epub 2012 Feb 14.
To improve the pathophysiological understanding of cardioinhibitory and vasodepressor reflex syncope, by evaluating orthostatic effects on electrical and hemodynamic variables. To unravel the pathogeneses further, we studied these effects during both the passive head-up tilt test and the active standing test.
The current knowledge of the compromised autonomic balance in patients with reflex syncope is limited. The orthostatic responses to head-up tilt test in cardioinhibitory and vasodepressor patients differ, suggesting different pathogeneses; however, the more physiological active standing test represents daily life situations better.
We included 74 patients; 36 cardioinhibitory and 38 vasodepressor. Patients were compared with respect to vascular hemodynamics and heart rate variability during the change from supine to upright position. Resting electrolytes, brain natriuretic peptide (BNP), pro-atrial natriuretic peptide (pro-ANP), and the C-terminal of pro-vasopressin, copeptin were measured.
Resting systolic blood pressure was higher in cardioinhibitory (117.8 ± 15.7 mmHg) than in vasodepressor patients (109.1 ± 15.3 mmHg, p < 0.001). Changes in heart rate tended to be smaller in cardioinhibitory patients (6.7 ± 9.8 vs. 10.7 ± 8.9 bpm, p = 0.056). Heart rate variability was lower and changed less in cardioinhibitory patients (p < 0.05). Cardioinhibitory patients had higher pro-ANP levels (63.5 ± 18.8 pM) compared to vasodepressor patients (54.2 ± 31.4 pM, p = 0.018). Responses during active standing were attenuated compared to head-up tilt in both groups.
This study demonstrated that cardioinhibitory patients had higher blood pressure, attenuated hemodynamic responses, and reduced autonomic regulation compared to vasodepressor patients. Furthermore, cardioinhibitory patients showed a sympathetic predominance in their modulation of autonomic responses. Orthostatic responses induced by active standing were modest and did not sufficiently explain potential pathophysiological differences between cardioinhibitory and vasodepressor patients.
通过评估直立位对电生理和血液动力学变量的影响，提高对心脏抑制型和血管迷走性反射性晕厥的病理生理学认识。为了进一步揭示其发病机制，我们在被动头高位倾斜试验和主动站立试验中研究了这些效应。
目前对于反射性晕厥患者自主神经平衡受损的认识有限。心脏抑制型和血管迷走性患者在头高位倾斜试验中的直立反应不同，提示发病机制不同；然而，更符合生理状态的主动站立试验更能代表日常生活情况。
我们纳入了 74 名患者；36 名心脏抑制型和 38 名血管迷走性。比较患者从仰卧位变为直立位时血管血液动力学和心率变异性的变化。测量静息电解质、脑钠肽（BNP）、前心房利钠肽（pro-ANP）和加压素 C 端肽，即 copeptin。
心脏抑制型患者的静息收缩压（117.8 ± 15.7 mmHg）高于血管迷走性患者（109.1 ± 15.3 mmHg，p < 0.001）。心脏抑制型患者的心率变化趋势较小（6.7 ± 9.8 比 10.7 ± 8.9 bpm，p = 0.056）。心率变异性较低，且心脏抑制型患者变化较小（p < 0.05）。与血管迷走性患者相比，心脏抑制型患者的 pro-ANP 水平更高（63.5 ± 18.8 pM 比 54.2 ± 31.4 pM，p = 0.018）。与头高位倾斜相比，两组患者在主动站立时的反应均减弱。
本研究表明，与血管迷走性患者相比，心脏抑制型患者的血压更高，血液动力学反应减弱，自主神经调节减少。此外，心脏抑制型患者在自主神经反应调节中表现出交感神经优势。主动站立引起的直立反应适度，不足以充分解释心脏抑制型和血管迷走性患者之间潜在的病理生理差异。
