Usefulness of disopyramide for prevention of upright tilt-induced hypotension-bradycardia

Simón Milstein, Jeffrey Buetikofer, Ann Dunnigan, David G. Benditt, Charles Gornick, Walter J. Reyes

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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 electrocardlographic and hemodynamie 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 ≤7 minutes of tilt alone (6 patients) or tilt plus isoproterenol at ≤3 μg/min (4 patients) and was associated with hypotension (mean arterial pressure, 40 ± 16 mm Hg vs baseline 76 ± 10 mm Hg, p <0.001) and inappropriate heart rate slowing (mean heart rate, 59 ± 39 beats/min vs baseline 88 ± 18 beats/min, p <0.005). After oral disopyramide 150 mg 3 times daily (mean plasma level, 3.0 ± 0.64 μg/ml), all patients tolerated 10 minutes of both tilt and tilt plus isoproterenol (maximum dose, 3 μg/min) without symptoms, hypotension (mean arterial pressure; tilt 1 min, 79 ± 7 min 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.

Original languageEnglish (US)
Pages (from-to)1339-1344
Number of pages6
JournalThe American Journal of Cardiology
Issue number20
StatePublished - Jun 1 1990

Bibliographical note

Funding Information:
From the Departments of Medicine and Pediatrics, University of Minnesota Medical School, Minneapolis, Minnesota. Dr. Milstein was sup ported in part by a grant from the Minnesota Affiliate of the American Heart Association. This work was completed during Dr. Benditt’s tenure as an Established Investigator of the American Heart Association, Dallas, Texas. Manuscript received November 20,1989; revised manuscript received and accepted January 25, 1990.


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