Role of endogenous adenosine in vasovagal syncope.
Adenosine may be a potential mediator in the pathogenesis of vasovagal syncope. Intravenous adenosine increases sympathetic discharge and provokes vasovagal syncope in sensitive subjects. No data are available for endogenous adenosine. The authors compared the results of head-up tilt-table testing (HUT) (45 minutes at 60 degrees) of three arbitrary groups of subjects: sensitive (n = 25, age 34 y, vasovagal syncope, positive HUT), moderately sensitive (n = 28, age 34 y, vasovagal syncope, negative HUT), and nonsensitive (n = 19, age 30 y). A positive test result produced syncopal symptoms with hypotension and/or bradycardia. Single-lead electrocardiogram (ECG) was recorded, and arterial pressure was measured noninvasively. Fourier transform was used for power-spectral heart rate variability (HRV) analysis of 5-minute ECG data. In the nonsensitive and moderately sensitive groups, HUT was repeated with intravenous dipyridamole, an adenosine transport blocker. In the sensitive group, HUT was repeated with oral theophylline, an adenosine receptor blocker, or placebo. In the moderately sensitive group, a third HUT was performed with dipyridamole and oral theophylline. If adenosine plays a role in vasovagal syncope, then dipyridamole would induce more positive HUT responses, a positive HUT response would be prevented by theophylline, and hemodynamic and HRV data in positive HUT responses induced by dipyridamole should reproduce those observed during spontaneous positive HUT responses. Dipyridamole induced positive HUT responses in 57% of the moderately sensitive group and 21% of the nonsensitive group (p < 0.05). Theophylline treatment was not efficient in preventing HUT-induced syncope in sensitive subjects; however, it prevented dipyridamole-induced syncope in 75% of the moderately sensitive group. Dipyridamole immediately increased arterial pressure, heart rate, and total HRV in all (p <0.05). In sensitive subjects, these responses were different: small for arterial pressure and for total and low-frequency HRV, and large for heart rate. It is concluded that endogenous adenosine, like exogenous adenosine, may induce vasovagal syncope. However, the mechanism of adenosine-induced syncope is probably different from that of HUT-induced vasovagal syncope.
Sinkovec
M
M
Department of Cardiology, University Medical Center, Ljubljana, Slovenia. matjaz.sinkovec@kclj.si
Grad
A
A
Rakovec
P
P
D000241:Adenosine / Q000037:antagonists & inhibitors / Q000502:physiology*; D000328:Adult; D000368:Aged; D004176:Dipyridamole / Q000494:pharmacology; D004562:Electrocardiography; D005260:Female; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D011187:Posture / Q000502:physiology; D058915:Purinergic P1 Receptor Antagonists; D019462:Syncope, Vasovagal / Q000503:physiopathology*; D014665:Vasodilator Agents / Q000494:pharmacology
D058915:Purinergic P1 Receptor Antagonists; D014665:Vasodilator Agents; D004176:Dipyridamole; D000241:Adenosine