title: Vagal and sympathetic mechanisms in patients with orthostatic vasovagal syncope.
abstract: BACKGROUND
  Autonomic and particularly sympathetic mechanisms play a central role in the pathophysiology of vasovagal syncope. We report direct measurements of muscle sympathetic nerve activity in patients with orthostatic vasovagal syncope.
  
  
  RESULTS
  We studied 53 otherwise healthy patients with orthostatic syncope. We measured RR intervals and finger arterial pressures and in 15 patients, peroneal nerve muscle sympathetic activity before and during passive 60 degree head-up tilt, with low-dose intravenous isoproterenol if presyncope did not develop by 15 minutes. We measured baroreflex gain before tilt with regression of RR intervals or sympathetic bursts on systolic or diastolic pressures after sequential injections of nitroprusside and phenylephrine. Orthostatic vasovagal reactions occurred in 21 patients, including 7 microneurography patients. Presyncopal and nonsyncopal patients had similar baseline RR intervals, arterial pressure, and muscle sympathetic nerve activity. Vagal baroreflex responses were significantly impaired at arterial pressures below (but not above) baseline levels in presyncopal patients. Initial responses to tilt were comparable; however, during the final 200 seconds of tilt, presyncopal patients had lower RR intervals and diastolic pressures than nonsyncopal patients and gradual reduction of arterial pressure and sympathetic activity. Frank presyncope began abruptly with precipitous reduction of arterial pressure, disappearance of muscle sympathetic nerve activity, and RR interval lengthening.
  
  
  CONCLUSIONS
  Patients with orthostatic vasovagal reactions have impaired vagal baroreflex responses to arterial pressure changes below resting levels but normal initial responses to upright tilt. Subtle vasovagal physiology begins before overt presyncope. The final trigger of human orthostatic vasovagal reactions appears to be the abrupt disappearance of muscle sympathetic nerve activity.
authors.affiliation: Medical College of Virginia, Virginia Commonwealth University, and Hunter Holmes McGuire Department of Veterans Affairs Medical Center, Richmond 23249, USA.
authors.forename: C A
authors.initials: CA
authors.lastname: Morillo
authors.forename: D L
authors.initials: DL
authors.lastname: Eckberg
authors.forename: K A
authors.initials: KA
authors.lastname: Ellenbogen
authors.forename: L A
authors.initials: LA
authors.lastname: Beightol
authors.forename: J B
authors.initials: JB
authors.lastname: Hoag
authors.forename: K U
authors.initials: KU
authors.lastname: Tahvanainen
authors.forename: T A
authors.initials: TA
authors.lastname: Kuusela
authors.forename: A M
authors.initials: AM
authors.lastname: Diedrich
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017704:Baroreflex; D001794:Blood Pressure; D002648:Child; D004562:Electrocardiography; D005260:Female; D006801:Humans; D007024:Hypotension, Orthostatic / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009132:Muscles / Q000294:innervation; D010991:Plethysmography; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D019462:Syncope, Vasovagal / Q000503:physiopathology*; D014630:Vagus Nerve / Q000503:physiopathology*