Pecha Simon, Hakmi Samer, Wilke Iris, Yildirim Yalin, Hoffmann Boris, Reichenspurner Hermann, Willems Stephan, von Kodolitsch Yskert, Aydin Ali
Department of Cardiovascular Surgery, University Heart Center, University Hospital Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.
Department of Cardiology/Electrophysiology, University Heart Center, University Hospital Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.
Heart Vessels. 2016 Jan;31(1):74-9. doi: 10.1007/s00380-014-0576-6. Epub 2014 Aug 28.
Vascular reflex mechanisms contribute to vasovagal syncope. However, the alterations in central haemodynamics in patients with vasovagal syncope are unknown. 30 consecutive patients (36.5 ± 15 years, 14 females) with recurrent vasovagal syncope (VVS) and a positive tilt table test were compared to 39 age- and sex-matched controls (36.9 ± 16 years, 15 females) with a negative tilt table result and no history of syncope. Central aortic pressure parameters including augmentation index and central pulse pressure as markers of aortic stiffness were generated non-invasively by applanation tonometry of the radial artery and use of a validated mathematical transfer function. No difference in aortic augmentation index was observed between groups. (VVS 9 ± 2.6 vs. Control 11 ± 2.4, p = 0.8). However, in patients with vasovagal syncope the aortic pressure waveform significantly differed from healthy controls. A prolonged time to the peak of aortic pressure wave (aortic T2) was observed in patients with vasovagal syncope (226 ± 24 vs. 208 ± 21 ms, p = 0.001). Furthermore time to the first shoulder of the aortic pressure wave (aortic T1) was slightly shorter compared to healthy controls, but did not reach statistical significance (106 ± 22 vs. 110 ± 12 ms, p = 0.33). Patients with vasovagal syncope have an altered aortic pressure waveform at rest, but no signs of elevated aortic stiffness. The underlying mechanisms for these findings may potentially result from a complex imbalance of the autonomic nervous system with a continuous deregulation of the sympathetic and parasympathetic reflex arcs.
血管反射机制与血管迷走性晕厥有关。然而，血管迷走性晕厥患者的中心血流动力学改变尚不清楚。将30例连续的复发性血管迷走性晕厥（VVS）且倾斜试验阳性的患者（年龄36.5±15岁，女性14例）与39例年龄和性别匹配的倾斜试验结果阴性且无晕厥病史的对照者（年龄36.9±16岁，女性15例）进行比较。通过桡动脉压平式眼压测量法和使用经过验证的数学传递函数，无创生成包括增强指数和中心脉压等中心主动脉压力参数作为主动脉僵硬度的指标。两组之间未观察到主动脉增强指数的差异。（VVS组为9±2.6，对照组为11±2.4，p = 0.8）。然而，血管迷走性晕厥患者的主动脉压力波形与健康对照者有显著差异。血管迷走性晕厥患者观察到主动脉压力波峰值时间延长（主动脉T2）（226±24 vs. 208±21毫秒，p = 0.001）。此外，与健康对照者相比，主动脉压力波第一个切迹的时间（主动脉T1）略短，但未达到统计学意义（106±22 vs. 110±12毫秒，p = 0.33）。血管迷走性晕厥患者在静息时主动脉压力波形改变，但无主动脉僵硬度升高的迹象。这些发现的潜在机制可能源于自主神经系统复杂的失衡，交感和副交感反射弧持续失调。
