Effect of high-current stimulation in patients with sustained ventricular tachycardia rendered noninducible by antiarrhythmic drugs

Abstract

Successful antiarrhythmic drug therapy for sustained ventricular tachycardia (VT) is presumed to be related to effects on myocardium within the reentrant circuit. To test the hypothesis that prevention of VT induction may be related to effects on myocardium other than that directly involved in the tachycardia circuit, high-current stimulation was used to achieve shorter coupling intervals in 22 patients with sustained uniform VT that was rendered noninducible by antiarrhythmic agents during stimulation at twice threshold. Sustained uniform VT was induced in 10 patients in response to high-current stimulation (group 1), including 4 tachycardias with the same morphology observed in the baseline study. There were no inducible arrhythmias in 12 patients (group 2). Patients were receiving several different antiarrhythmic regimens, but there was no particular drug associated with the induction of VT using high-current stimulation. There was no statistically significant difference between groups 1 and 2 in baseline VT cycle length (247 ± 41 vs 253 ± 44 ms), drug-induced increase in effective refractory period (20 ± 15 vs 16 ± 7%), QRS duration (25 ± 10 vs 20 ± 17%) or maximal current strength delivered (10.9 ± 5.3 vs 9.3 ± 4.0 mA). There was no significant difference in local activation with high-current stimulation between groups 1 and 2. In conclusion, sustained uniform VT was induced in 45% (10 of 22) of patients whose arrhythmias were rendered noninducible by antiarrhythmic agents during programmed stimulation at twice threshold. This suggests that prolongation of refractoriness at the site of stimulation or slowing in conduction time of extrastimuli to the presumed reentrant circuit, or both, may be one mechanism by which antiarrhythmic drugs prevent induction of VT during programmed stimulation.