Neurally mediated hypotension and bradycardia: which nerves? How mediated?

The present study. In this issue of the Journal (1) investigators from the University of Minnesota report the third in a series of studies focusing on the phenomenon of “neurally mediated snycope.” In the present study, six patients (Group I) who presented with “cardiovascular collapse apparently associated with cardiac asystole” underwent head-up tilt testing before and during infusion of isoproterenol, as reported previously (2) after a negative electrophysiologic study. The responses of these patients were compared with those of two groups of ageand gender-matched control patients. Group II comprised patients with a history of syncope (but without a history of asystole) and a negative electrophysiologic study. Group III comprised patients with recurrent syncope and findings at electrophysiologic study sufficient to explain their clinical presentations. All patients in Groups I and II developed hypotension and bradycardia with head-up tilt alone or with head-up tilt during isoproterenol infusion. Such a response was not seen in Group III patients. These investigators (2,3) have shown previously that hypotension and bradycardia can be provoked in a substantial proportion of patients with unexplained syncope and nondiagnostic findings at electrophysiologic study. The patients described in the present study differ from those reported previously primarily in the severity of their presenting symptoms as well as in their responses to the tiltlisoproterenol test. Therefore, the present study extends the spectrum of the clinical and laboratory manifestations of “neurally mediated syncope” described previously by these investigators (2.3) and Waxman and colleagues (4). Mechanisms that mediate the spontaneous or provoked episodes of hypotension and hradycardia. These mechanisms are unclear. It has been hypothesized that exaggerated