Susceptibility to transient
hypotension-
bradycardia of neurally mediated origin has been attributed in part to accentuated afferent neural traffic arising from cardiopulmonary mechanoreceptors, and consequently, may be diminished by agents with
anticholinergic and negative inotropic effects, such as
disopyramide phosphate. This study assessed electrocardiographic and hemodynamic responses to upright tilt testing (alone or during
isoproterenol infusion) before and after
disopyramide therapy in 10 patients (age range 16 to 74 years) with recurrent
syncopal episodes of neurally mediated origin. Untreated,
syncope occurred at less than or equal to 7 minutes of tilt alone (6 patients) or tilt plus
isoproterenol at less than or equal to 3 micrograms/min (4 patients) and was associated with
hypotension (mean arterial pressure, 40 +/- 16 mm Hg vs baseline 76 +/- 10 mm Hg, p less than 0.001) and inappropriate heart rate slowing (mean heart rate, 59 +/- 39 beats/min vs baseline 88 +/- 18 beats/min, p less than 0.005). After oral
disopyramide 150 mg 3 times daily (mean plasma level, 3.0 +/- 0.64 micrograms/ml), all patients tolerated 10 minutes of both tilt and tilt plus
isoproterenol (maximum dose, 3 micrograms/min) without symptoms,
hypotension (mean arterial pressure; tilt 1 min, 79 +/- 7 mm Hg vs tilt 10 min, 77 +/- 8 mm Hg, difference not significant) or
bradycardia (mean heart rate; tilt 1 min, 81 +/- 12 beats/min vs tilt 10 min, 83 +/- 11 beats/min, difference not significant). Furthermore, during subsequent 20 +/- 5 months of
disopyramide therapy, all but 1 patient remain asymptomatic. Thus, oral
disopyramide may be effective for preventing inducible and spontaneous neurally mediated
syncope.