Neurohormonal profile before and after beta-blockade in patients with neurocardiogenic syncope

Our objective was to evaluate the effects of beta-blockers on the neurohorm onal profile, particularly vasopressin (VP) release, in vasovagal syncope a nd to gain further insight on the pathophysiology of this syndrome. Patient s (less than or equal to 75 years) with no cardiovascular, neurological dis orders, or contraindications to the use of isoproterenol or beta-blockers a nd being explored for unexplained syncope were included. An 80 degrees HUT was performed under identical conditions. After a 25-min period of passive tilt, isoproterenol was infused at a rate of 1-5 mu g/mn if required. Two g roups matched for age and sex were considered: a HUT-positive and a HUT-neg ative group. The HUT-positive group was then given beta-blockers, subsequen tly reassessed, and divided into two subgroups: a beta-blocker nonresponder group and a beta-blocker responder group. Blood samples for assays of nore pinephrine (NE), epinephrine (E) and VP were taken at baseline and the end of the procedure. in all, 44 subjects entered the study, 22 in each group. The HUT-positive group exhibited an obvious lesser increase in plasma NE an d a clear-cut rise in plasma E and VP compared to the HUT-negative group (P < 0.05). Even though no patient in the HUT-positive group reported recurre nt symptoms under treatment, the second HUT could distinguish two subgroups : a beta-blocker nonresponder group (n = 12) whose HUT remained positive an d a beta-blocker responder group (n = 10) whose HUT was normalized. The tim e course of plasma E and VP during the second HUT was similar to that for t he HUT-positive and HUT-negative groups. In conclusion, the efficacy of bet a-blockers is associated not only with a reduction of the sympathoadrenal s timulation seen in vasovagal syncope but also with a lower release of VP su ggesting that low-pressure baroreceptors might be involved in VP release.