Influence of the site of stimulation on the resetting phenomenon in ventricular tachycardia.

Uniform, sustained ventricular tachycardia (VT) in the setting of prior myocardial infarction is believed to be due to reentry. The ability to reset VT with programmed extrastimuli requires that the premature impulse reach and enter the reentrant circuit. To evaluate the importance of the site of pacing on the ability to reset VT, single ventricular extrastimuli were delivered during 32 morphologically distinct, uniform VTs from both the right ventricular (RV) apex and RV outflow tract. Single ventricular extrastimuli resulted in resetting of VT from the RV apex only in 6 VTs, from the RV outflow tract only in 2, from both sites in 11 VTs and neither site in 13. When VT reset at both RV sites, 1 RV site or neither RV site was compared, a left bundle branch block VT QRS morphologic pattern was found to be more common in VT reset at both sites than at neither site (8 of 11 vs 4 of 13, p less than 0.05). No other differences in VT characteristics analyzed were found between these groups. Multiple ventricular extrastimuli were delivered in 16 VTs; in 6 of these, resetting was shown from at least 1 additional site, as compared to the response with single ventricular extrastimuli. In summary, site of stimulation can influence the ability of premature extrastimuli to reset uniform VT, and site dependence of VT resetting diminishes when multiple extrastimuli are used. This suggests that refractoriness or conduction delay in tissue between the pacing site and tachycardia circuit are important determinants of ability to reset VT from a particular site.