Neural monitoring of vasovagal syncope.
Head-up tilt testing has become a valuable and widely accepted diagnostic tool for evaluation of patients with vasovagal syncope. This test has afforded clinical researchers the opportunity to focus on the hemodynamic, humoral, and neural changes that accompany syncope. We review the animal and clinical studies that provide insight into the possible pathophysiological mechanisms involved in vasovagal syncope. Hemodynamic measurements in patients with vasovagal syncope suggest that a relative decrease in ventricular size and increase in cardiac contractility may be seen in many patients with vasovagal syncope. Patients with vasovagal syncope have also demonstrated numerous "exaggerated" neurohumoral responses to syncope. Differential changes in plasma levels of epinephrine, renin, endothelin, vasopressin, cortisol, prolactin, beta endorphins, and substance P have been reported by some investigators either prior to or during a syncopal episode in patients with vasovagal syncope. The precise pathophysiological significance of these measurements is unknown at the present time. Measurements of autonomic tone may be accomplished indirectly with analysis of heart rate variability or baroreflex slope, or directly by sympathetic neural recordings of the peroneal nerve. We have demonstrated decreased baroreflex slopes in patients with vasovagal syncope. Using microneurography, we and others have demonstrated decreased sympathetic nerve activity occurring 11 +/- 3 seconds prior to syncope during head-up tilt table testing. A variety of other abnormal reflexes, including blunted forearm blood flow responses during exercise, have been demonstrated by others. These observations suggest that pacing instituted after the event may not be as helpful as the use of a hemodynamic sensor that will result in the initiation of pacing prior to sympathetic withdrawal or modify the decrease in sympathetic tone that occurs prior to syncope.
Ellenbogen
K A
KA
Department of Medicine, Medical College of Virginia, Richmond 23298-0053, USA. Kellenbogen@mem.po.com
Morillo
C A
CA
Wood
M A
MA
Gilligan
D M
DM
Eckberg
D L
DL
Smith
M L
ML
D000322:Adrenergic Agonists / Q000097:blood; D000818:Animals; D001341:Autonomic Nervous System / Q000503:physiopathology; D017704:Baroreflex / Q000502:physiology; D004723:Endorphins / Q000097:blood; D016232:Endothelins / Q000097:blood; D004837:Epinephrine / Q000097:blood; D005542:Forearm / Q000098:blood supply; D006339:Heart Rate / Q000502:physiology; D006352:Heart Ventricles / Q000473:pathology; D006439:Hemodynamics; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D009200:Myocardial Contraction; D018377:Neurotransmitter Agents / Q000502:physiology; D010543:Peroneal Nerve / Q000503:physiopathology; D005082:Physical Exertion / Q000502:physiology; D011388:Prolactin / Q000097:blood; D012039:Regional Blood Flow / Q000502:physiology; D012083:Renin / Q000097:blood; D013373:Substance P / Q000097:blood; D013564:Sympathetic Nervous System / Q000503:physiopathology; D019462:Syncope, Vasovagal / Q000175:diagnosis / Q000503:physiopathology*; D018667:Tilt-Table Test; D014667:Vasopressins / Q000097:blood
D000322:Adrenergic Agonists; D004723:Endorphins; D016232:Endothelins; D018377:Neurotransmitter Agents; D014667:Vasopressins; D013373:Substance P; D011388:Prolactin; D012083:Renin; D006854:Hydrocortisone; D004837:Epinephrine