Cardiac electrophysiologic and hemodynamic correlates of neurally mediated syncope.

This study assessed the temporal relation of RR interval, AH interval and systemic blood pressure changes during induced symptomatic bradycardia-hypotension episodes in 14 patients with recurrent syncope suspected of being neurally mediated. Upright tilt with isoproterenol reproduced symptoms in 9 of 14 patients (positive response) and was negative in 5 of 14 (negative response). Isoproterenol alone shortened supine RR intervals in all patients. With tilt, however, isoproterenol prolonged RR intervals in those with positive results (supine 519 +/- 124 ms vs tilt 845 +/- 212 ms, p less than 0.005) while further shortening RR intervals among negative responders (supine 436 +/- 90 ms vs tilt 377 +/- 82 ms, p less than 0.05). Similarly, tilt with isoproterenol prolonged AH intervals in patients with positive responses despite RR prolongation, while shortening AH in negative responders. Additionally, with combined tilt and isoproterenol, systemic arterial pressure decreased significantly in patients with positive responses (systolic 99 +/- 13 vs 57 +/- 13 mm Hg, p less than 0.001, diastolic 62 +/- 17 vs 28 +/- 9 mm Hg, p less than 0.001) but not in patients with negative responses. Further, onset of hypotension (42 +/- 14 seconds after tilt) preceded onset of RR interval prolongation (52 +/- 23 seconds after tilt). Syncope (142 +/- 72 seconds after tilt) coincided closely with nadir of systemic pressure (136 +/- 74 seconds) and both tended to precede maximum RR prolongation (152 +/- 87 seconds). Thus, the bradycardia and hypotension associated with neurally mediated syncope exhibit characteristic but distinctly different time courses, with arterial pressure changes developing earlier and coinciding more closely with symptom development.