Sympatho-vagal responses in patients with sleep and typical vasovagal syncope.
Sleep syncope is a recently described form of vasovagal syncope that interrupts sleep. The pathophysiology of this condition is uncertain but a 'central' non-baroreflex-mediated trigger has been suggested. In the present study, we tested the hypothesis that patients with sleep syncope have abnormal sympatho-vagal responses to non-baroreflex, but normal responses to baroreflex stimuli. We collected historical data from SS patients (patients with vasovagal syncope with sleep syncope; n=16) and NSS patients (patients with vasovagal syncope without sleep syncope; n=35), including demography, and triggers and symptoms during syncope. MBP (mean blood pressure), HR (heart rate) and MSNA (muscle sympathetic nerve activity) in SS patients were compared with NSS patients and matched controls (n=16) during HG (handgrip), CPTs (cold pressor tests), HUT (head-up tilting) and tilt-induced pre-syncope. Patients and controls were of similar age and gender distribution [SS patients, age 46.0+/-4 years (69% female); NSS patients, 47.3+/-4 years (63% female); controls, 43.7+/-5 years (69% female)]. Compared with NSS patients, SS patients reported more fainting episodes: (i) triggered by phobias (75 compared with 37%; P=0.001); (ii) while in the horizontal position (44 compared with 6%; P=0.001); and (iii) associated with abdominal symptoms (69 compared with 9%; P=0.001). Compared with controls, the MBP response to HG was attenuated in SS patients (P=0.016), and MSNA (burst frequency and incidence) responses to CPT were attenuated in both syncope groups (SS, P=0.011 and 0.003 respectively; NSS, P=0.021 and 0.049 respectively). MSNA responses to HUT did not differ. For both non-baroreflex and baroreflex responses, there were no differences in any of the MSNA indices between the syncope groups. Patients with vasovagal syncope, with or without sleep syncope, have very similar sympatho-vagal responses to both non-baroreflex and baroreflex stimuli. This is consistent with sleep syncope being a subform of vasovagal syncope. Attenuation of sympathetic responses to non-baroreflex pathways may be important in the mechanism of vasovagal syncope.
Jardine
David L
DL
Department of General Medicine, Christchurch Hospital, Christchurch, New Zealand. david.jardine@cdhb.govt.nz
Krediet
C T Paul
CT
Cortelli
Pietro
P
Frampton
Christopher M
CM
Wieling
Wouter
W
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017704:Baroreflex / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D016022:Case-Control Studies; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000294:innervation; D011187:Posture / Q000502:physiology; D012893:Sleep Wake Disorders / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D019462:Syncope, Vasovagal / Q000503:physiopathology*; D018667:Tilt-Table Test; D014630:Vagus Nerve / Q000503:physiopathology*; D055815:Young Adult