Antiarrhythmic and Electrophysiologic Actions in Patients With Inducible Sustained Ventricular Tachycardia
نویسندگان
چکیده
This study assessed the antiarrhythmic activity of amiloride in 35 patients with inducible sustained ventricular tachycardia. Patients had failed to respond to 3.6±1.0 antiarrhythmic drugs. Ventricular tachycardia was reproducibly induced by programmed electrical stimulation in all patients at the baseline study. Amiloride was given at 10 and 20 mg/day p.o. on a twice-daily schedule that achieved serum concentrations of 21+± 17 and 36±18 ng/ml, respectively. The mean left ventricular ejection fraction was unchanged from 36±14% at baseline to 37±17% during amiloride treatment. Amiloride significantly increased serum potassium from 4.6± 0.4 to 5.1+ 0.4 mM. Four patients failed amiloride therapy with spontaneous nonsustained ventricular tachycardia. The remaining 31 patients were assessed by repeat programmed stimulation. Six patients had complete antiarrhythmic response, and an additional six patients had less than 15 beats of ventricular tachycardia induced. Therefore, amiloride was an efficacious antiarrhythmic treatment in 12 of 35 (34%) patients. Amiloride concentrations were significantly higher (52+±20 ng/ml) in patients that responded than in patients that did not respond (30±15 ng/ml). The only electrophysiologic measurement that changed significantly was the ventricular functional refractory period (from 269±24 to 283+±25 msec, p<O.05). Amiloride also suppressed frequent, spontaneous ventricular premature beats in eight of 15 patients (53%). No somatic side effects occurred. Two of the five patients discharged on amiloride therapy developed asymptomatic nonsustained ventricular tachycardia, and this prompted a change in antiarrhythmic therapy. Both died suddenly of arrhythmia during substitute empiric antiarrhythmic drug therapy. The other three patients have been followed for a mean of 18±7 months and have not had a recurrence of ventricular tachycardia. In conclusion, amiloride has antiarrhythmic activity in humans and has a low incidence of adverse effects. (Circulation 1989;79:1257-1263)
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