Electrophysiologic effects and clinical efficacy of mexiletine used alone or in combination with class IA agents for refractory recurrent ventricular tachycardias or ventricular fibrillation

Abstract

The electrophysiologic effects and clinical efficacy of mexiletine used alone or in combination with class IA agents were studied in 35 patients with recurrent sustained ventricular tachycardia (VT) or ventricular fibrillation refractory to nonexperimental antiarrhythmic agents. At baseline before therapy, all patients had inducible VT by programmed stimulation (1 to 3 extrastimuli) and frequent (at least 30/hour) ventricular premature complexes (VPCs) during Holter monitoring. Mexiletine therapy was effective by programmed stimulation (VT no longer inducible or 15 or less beats) in 8 and ineffective in 27 patients. Twenty patients were discharged with mexiletine (14 of whom took an additional class IA agent). The discharge regimen was effective by programmed stimulation in 6 of these 20 patients. In 14 patients the discharge regimen was ineffective by programmed stimulation, but all patients had a marked reduction of ventricular ectopic activity (at least 83% reduction of VPCs and abolition of non sustained VT). During the follow-up period of 18 ± 13 months (mean ± standard deviation), 4 patients had recurrences (3 with an ineffective regimen by programmed stimulation and 1 with an effective regimen by programmed stimulation). Arrhythmia-free survival rates at 12 and 24 months were 86% and 77%, as determined by the Kaplan-Meier method, in patients with an ineffective regimen by programmed stimulation, and 80% and 80% in patients with an effective regimen by programmed stimulation (p = 0.979 by log rank test). This nonrandomized study suggests that in selected patients with inducible VT and frequent VPCs at baseline, persistent induction of VT by programmed stimulation during mexiletine therapy (alone or in combination with class IA agents) may not preclude good clinical outcome when it is accompanied by a marked reduction of spontaneous ventricular ectopic activity.