This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Duff, H. J. Articles by Wyse, D. G. Search for Related Content PubMed PubMed Citation Articles by Duff, H. J. Articles by Wyse, D. G.

Circulation, Vol 79, 1257-1263, Copyright © 1989 by American Heart Association

ARTICLES

Amiloride. Antiarrhythmic and electrophysiologic actions in patients with inducible sustained ventricular tachycardia

HJ Duff, LB Mitchell, KM Kavanagh, DE Manyari, AM Gillis and DG Wyse
Department of Medicine, University of Calgary, Faculty of Medicine, Alberta, Canada.

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 less than 0.05). 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.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				K. Petrecca, R. Atanasiu, S. Grinstein, J. Orlowski, and A. Shrier Subcellular localization of the Na+/H+ exchanger NHE1 in rat myocardium Am J Physiol Heart Circ Physiol, February 1, 1999; 276(2): H709 - H717. [Abstract] [Full Text] [PDF]

				M. A. Ralston, M. R. Murnane, D. V. Unverferth, and C. V. Leier Serum and Tissue Magnesium Concentrations in Patients with Heart Failure and Serious Ventricular Arrhythmias Ann Intern Med, December 1, 1990; 113(11): 841 - 846. [Abstract] [PDF]