Antidysrhythmic drug therapy for the termination of stable, monomorphic ventricular tachycardia: a systematic review

Ian S deSouza1, Jennifer L Martindale1, Richard Sinert1

  • 1SUNY Downstate/Kings County Hospital, New York, USA.

Abstract

Insights

Procainamide, ajmaline, and sotalol effectively terminate stable ventricular tachycardia (VT), outperforming lidocaine. Amiodarone showed no superior efficacy compared to procainamide in VT treatment.

Area of Science:

  • Cardiology
  • Pharmacology
  • Clinical Medicine

Background:

  • Monomorphic ventricular tachycardia (VT) is a significant arrhythmia requiring effective drug therapy.
  • Current treatment guidelines often recommend lidocaine as a first-line agent for stable VT.

Purpose of the Study:

  • To systematically review and compare the efficacy of various intravenous antidysrhythmic drugs for terminating stable, monomorphic VT.
  • To evaluate the relative effectiveness of procainamide, ajmaline, sotalol, and amiodarone against lidocaine and each other.

Main Methods:

  • Systematic literature review of EMBASE, MEDLINE, and Cochrane databases (1965-July 2013).
  • Inclusion of 3 prospective and 2 retrospective studies involving adult patients with stable monomorphic VT.
  • Calculation of relative risks (RR) and number needed to treat (NNT) for VT termination, alongside methodological quality assessment.

Main Results:

  • Procainamide demonstrated superior VT termination rates compared to lidocaine (RR 3.7 prospective, 2.2 retrospective).
  • Ajmaline (RR 5.3) and sotalol (RR 3.9) also showed significantly higher efficacy than lidocaine in prospective studies.
  • Procainamide was more effective than amiodarone (RR 4.3) in retrospective analysis; however, all included studies had quality limitations.

Conclusions:

  • Procainamide, ajmaline, and sotalol are more effective than lidocaine for stable monomorphic VT termination.
  • Amiodarone's efficacy is comparable to procainamide, but evidence is limited.
  • Further high-quality research is needed to definitively establish optimal drug therapy for stable monomorphic VT.

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