Action of antiarrhythmic agents on the area of slow conduction in ventricular tachycardia.

The most common mechanism of monomorphic sustained ventricular tachycardia (VT) is reentry with an excitable gap, but the electrophysiological properties and response to antiarrhythmic agents in the area of slow conduction are not yet fully known. The conduction time through the area of slow conduction may show a frequency-dependent delay in some VT but in others, constant conduction time was observed as the paced cycle length was decreased while VT was entrained. VT with a so-called decremental property could be terminated more often with rapid pacing with less risk of acceleration of the VT rate. When the excitable gap was estimated by the width of the zone of entrainment: defined as the difference between the cycle length of VT and the longest VT-interrupting paced cycle length during transient entrainment, there was no difference in the width of the zone of entrainment between the responders (VT induction was prevented with drugs) and the non-responders (VT remained inducible). The cycle length of VT was not a predictor of drug-efficacy. However, when the drug-effect was assessed at the intermediate doses, VT of those with a significantly narrowed width of the zone of entrainment were subsequently suppressed when the same drug was added. In conclusion, the electrophysiological properties of the area is diverse and it might affect pacing-induced terminability. Whether an antiarrhythmic agent is able to prevent VT-induction or not can not be predicted from the basal electrophysiologic parameters, but a significant narrowing of the width of the zone of entrainment, and hence the excitable gap, can be a hallmark for drug-efficacy.