Role of the serotonergic system in the genesis of vasovagal syncope

Aims The hypotensive reflex responsible for vasovagal syncope appears related to a reduction in sympathetic neural outflow. Several animal studies suggest that serotonin may play a role in the genesis of this reflex, through inhibition of sympathetic activity. However, the role of the serotonergic system is unknown in humans. The purpose of the study was to investigate the role of the serotonergic system in the genesis of vasovagal syncope by means of the level of platelet and plasma serotonin, as well as plasma catecholamines. during tilt-induced syncope. Methods and Results Fifteen patients (age 34 +/- 16 years) with vasovagal syncope underwent a head-up tilt test (HUT, 60 degrees, 45 min). If syncope did not develop, 300 mug nitroglycerin was administered sublingually and patients continued to be tilted for a further 20 min. Blood samples were obtained in the supine position, and then after 3, 10, 15, 30, 45, 48 and 65 min of HUT. If syncope developed, blood samples were obtained at the beginning of the prodrome, during syncope and after the recovery of consciousness. Platelet and plasma serotonin and plasma catecholamines were measured using high-pressure liquid chromatography with electrochemical detection. Ten patients developed syncope during the unmedicated HUT and four after nitroglycerin. In these patients plasma adrenaline significantly increased from the last programmed sample before the prodrome to its beginning and showed a further increase during loss of consciousness, whereas plasma noradrenaline did not increase, as an expression of inhibition of sympathetic neural outflow. In the patients experiencing syncope, both platelet and plasma serotonin showed no significant change after tilt-up, at the beginning of prodrome, during syncope and after recovery of consciousness. Conclusion These results do not suggest that the serotonergic system plays a role in the pathophysiology of vasovagal syncope. (Europace 2000: 2: 172-180) (C) 2000 The European Society of Cardiology.