SYMPATHETIC AND BARORECEPTOR REFLEX FUNCTION IN NEURALLY-MEDIATED SYNCOPE EVOKED BY TILT

The pathophysiology of neurally mediated syncope is poorly understood. It has been widely assumed that excessive sympathetic activation in a setting of left ventricular hypovolemia stimulates ventricular affere nts that trigger hypotension and bradycardia. We tested this hypothesi s by determining if excessive sympathetic activation precedes developm ent of neurally mediated syncope, and if this correlates with alterati ons in baroreflex function. We studied the changes in intraarterial bl ood pressure (BP), heart rate (KR), central venous pressure (CVP), mus cle sympathetic nerve activity (MSNA), and plasma catecholamines evoke d by upright tilt in recurrent neurally mediated syncope patients (SYN , 5 +/- 1 episodes/mo, n = 14), age- and sex-matched controls (CON, n = 23), and in healthy subjects who consistently experienced syncope du ring tilt (FS+, n = 20). Baroreflex responses were evaluated from chan ges in HR, BP, and MSNA that were obtained after infusions of phenylep hrine and sodium nitroprusside. Compared to CON, patients with SYN had blunted increases in MSNA at low tilt levels, followed by a progressi ve decrease and ultimately complete disappearance of MSNA with syncope . SYN patients also had attenuation of norepinephrine increases and lo wer baroreflex slope sensitivity, both during tilt and after pharmacol ogic testing. FS+ subjects had the largest decrease in CVP with tilt a nd had significant increases in MSNA and heart rate baroreflex slopes. These data challenge the view that excessive generalized sympathetic activation is the precursor of the hemodynamic abnormality underlying recurrent neurally mediated syncope.