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(Circulation. 2003;107:1620.)
© 2003 American Heart Association, Inc.

Clinical Investigation and Reports

Dysfunctional Baroreflex Regulation of Sympathetic Nerve Activity in Patients With Vasovagal Syncope

Markus Béchir, MD; Christian Binggeli, MD; Roberto Corti, MD; Rémy Chenevard, MD; Lukas Spieker, MD; Frank Ruschitzka, MD; Thomas F. Lüscher, MD; Georg Noll, MD

From the Cardiovascular Center, Cardiology, University Hospital, Zürich, Switzerland.

Correspondence to Georg Noll, MD, FESC, Cardiology, University Hospital, Rämistrasse 100, 8091 Zürich, Switzerland. E-mail karnog{at}usz.unizh.ch

Background— The interplay of resting muscle sympathetic nerve activity (MSA) and the baroreceptor reflex in patients with vasovagal syncope remains elusive. Hence, the aim of the present study was to investigate MSA, baroreceptor sensitivity, heart rate, and blood pressure under resting conditions and during orthostatic stress in patients with a history of vasovagal syncope.

Methods and Results— MSA was measured using microneurography at rest and during lower body negative pressure (LBNP) to mimic orthostatic stress in patients with a history of vasovagal syncope (n=10) and in age-matched healthy controls (n=8). Heart rate and blood pressure were simultaneously recorded. Cardiac baroreceptor sensitivity was calculated with the spectral technique ( coefficient). Resting MSA in the patients with syncope was significantly increased as compared with controls (42.4±2.3 versus 26.5±3.6 bursts/min, P=0.001), whereas activation of MSA during orthostatic stress in the patient group was significantly blunted (5.1±1.6 versus 15.2±2.1 bursts/min at LBNP -50 mm Hg, P=0.002). In the patients with syncope, cardiac baroreceptor sensitivity was significantly reduced under supine resting conditions (8.5±0.7 versus 13.0±1.1 ms/mm Hg, P=0.001), as well as under orthostatic stress (7.3±0.7 versus 13.4±1.5 ms/mm Hg, P=0.003).

Conclusions— This study shows that in patients with vasovagal syncope, resting MSA is increased and baroreflex regulation during orthostatic stress is blunted, thus leading to impaired MSA adaptation. These results provide new insights into mechanisms of vasovagal syncope and suggest that pharmacological modulation of baroreceptor sensitivity may represent a promising treatment of neuromediated syncope.

Key Words: syncope • baroreceptors • nervous system, sympathetic

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