The aim of this study was to determine whether endothelial function and inappropriate peripheral vasomotion have a significant role in the pathogenesis of neurally mediated syncope.

In 16 patients (mean age 28.2±5.8 years) with previous vaso-vagal syncope and in matched healthy subjects, endothelium-dependent flow-mediated dilation (FMD) and endothelium-independent response to glyceryl trinitrate (GTN), 25 μg, were measured in the brachial artery from high-resolution ultrasonography. Heart rate variability (HRV) analysis at rest and during tilt test was compared between two groups.

In the subjects with positive tilt test, all HRV parameters were significant higher respect to subjects with negative tilt test (P<0.001). The patients with positive tilt test, showed persistent, marked variability of heart rate (HR), due to increased vagal activity with withdrawal sympathetic tone and consequently reduction of blood pressure (BP) (−30.4±4.2 mmHg, P<0.001) accompanied by a decrease in HR (−24.3±4.5 beats/min, P<0.001) compared to negative tilt test subjects. These findings prove the real presence of vagal hypertone in patients with syncope. In our study, HR reached values lower than 40 beats/min. FMD in patients with neurally mediated syncope were significantly greater than those in controls (respectively, 9.2±2.8% vs. 4.6±1.4%, P<0.01) whereas no differences were shown in the response to GTN (18.4±4.4% vs. 16.1±4.2%, n.s.).

The augmented endothelial function and the abnormal vasodilation of peripheral arteries in association with bradycardia play an important role in the development of vaso-vagal syncope in young subjects.