Literature DB >> 2433319

Proarrhythmic effects of antiarrhythmic drugs during programmed ventricular stimulation in patients without ventricular tachycardia.

P K Au, A K Bhandari, R Bream, D Schreck, R Siddiqi, S H Rahimtoola.   

Abstract

The proarrhythmic effects of class IA antiarrhythmic drugs were prospectively evaluated during programmed ventricular stimulation in 24 consecutive patients with frequent ventricular premature beats whose baseline study, performed while no antiarrhythmic drugs were being taken, showed no inducible sustained ventricular arrhythmias. No patient had nonsustained (greater than 5 beats) or sustained ventricular tachycardia by history or baseline 24 hour ambulatory electrocardiographic monitoring. Sequential stimulation studies using up to three extra-stimuli were performed after administration of procainamide, quinidine and disopyramide on different days. Proarrhythmic response was defined as induction of one or more of the following: sustained monomorphic ventricular tachycardia; sustained polymorphic ventricular tachycardia; ventricular fibrillation; reproducibly inducible nonsustained monomorphic ventricular tachycardia. During 55 antiarrhythmic drug trials (24 of procainamide, 21 of quinidine, 10 of disopyramide) in the 24 patients, 6 patients had a proarrhythmic response: sustained monomorphic ventricular tachycardia in 3, ventricular fibrillation in 2, nonsustained monomorphic ventricular tachycardia in 1. Thus, 11% of drug trials resulted in a proarrhythmic response and 25% of patients had a proarrhythmic response to one of the drugs tested. A proarrhythmic response to one drug did not predict a similar response to another drug of the same class. The 6 patients with a proarrhythmic response did not differ significantly from the other 18 patients with regard to underlying heart disease, electrocardiographic or baseline 24 hour ambulatory electrocardiographic characteristics; however, they did have a higher incidence of digoxin usage (p less than 0.02), a shorter baseline right ventricular effective refractory period (p less than 0.01) and a smaller increment in effective refractory period during antiarrhythmic drug testing (p = 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1987        PMID: 2433319     DOI: 10.1016/s0735-1097(87)80394-7

Source DB:  PubMed          Journal:  J Am Coll Cardiol        ISSN: 0735-1097            Impact factor:   24.094


  5 in total

1.  Electrophysiologic mechanisms of adverse effects of class I antiarrhythmic drugs (cibenzoline, pilsicainide, disopyramide, procainamide) in induction of atrioventricular re-entrant tachycardia.

Authors:  A Fujiki; M Tani; S Yoshida; H Inoue
Journal:  Cardiovasc Drugs Ther       Date:  1996-05       Impact factor: 3.727

Review 2.  Proarrhythmia, a serious complication of antiarrhythmic drugs.

Authors:  P J Podrid
Journal:  Curr Cardiol Rep       Date:  1999-11       Impact factor: 2.931

Review 3.  Poisoning due to class IA antiarrhythmic drugs. Quinidine, procainamide and disopyramide.

Authors:  S Y Kim; N L Benowitz
Journal:  Drug Saf       Date:  1990 Nov-Dec       Impact factor: 5.606

4.  H2-receptor antagonism is not pro-arrhythmic in a chronic canine model.

Authors:  A C Uprichard; D W Harron
Journal:  Basic Res Cardiol       Date:  1990 Sep-Oct       Impact factor: 17.165

Review 5.  Antiarrhythmic drug treatment: need for continuous vigilance.

Authors:  H J Wellens; J L Smeets; M Vos; A P Gorgels
Journal:  Br Heart J       Date:  1992-01
  5 in total

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