br Commentary The concept of entrainment mapping for ablatio

Commentary The concept of entrainment mapping for ablation of VT is that targeting the site will interrupt the reentrant VT circuit. This site must be located, not only within the circuit, but also in a protected and relatively narrow isthmus. During entrainment mapping, the QRS morphology, S-QRS interval, and PPI should be checked. If the site is within the VT circuit, and within a relatively protected zone of slow conduction, the following characteristics should be observed. Ablation at sites that demonstrated combinations of these favored characteristics resulted in VT termination in approximately 37% of applications [1]. In the present case, the successful ablation site exhibited manifest entrainment, a PPI longer than the VT–CL by 120ms, and an S-QRS interval longer than the Eg-QRS by 100ms. Why did ablation at this site successfully suppress the VT? If you check the electrogram at the ablation site carefully you can detect a small fragmented electrogram before the PP (Fig. 1A). This diastolic potential (DP) preceded the onset of the QRS complex by 220ms and the last stimulus to the DP was 560ms, which was equal to the VT–CL. During the entrainment pacing with a 9.9V output both the DP and PP might be simultaneously captured. To confirm that the DP was within the VT circuit, selective entrainment pacing of the DP was performed prior to the RF glucokinase inhibitor application. When the output was reduced to 8.0V, the PP appeared after the stimulus and the DP was selectively captured (Fig. 2A). The surface ECG suddenly became identical to VT1, and the S-QRS interval increased to 220ms. After stable entrainment pacing of the DP, the PPI was measured again (Fig. 2B). At that time the PPI was 600ms and just 20ms longer than the VT–CL. The Eg (DP)-QRS interval during the VT was 220ms, was equal to the S-QRS interval during the entrainment pacing of the DP. Furthermore, the S-QRS interval was 38% of the VT–CL, suggesting it was located within the central isthmus of the circuit [1]. Therefore, we delivered RF energy at this site and successfully suppressed VT1. Why did both VT1 and VT2 become non-inducible after the RF energy applications in this area? A possible explanation is that those circuits had a common pathway. Before the ablation we performed pace mapping from this area (Fig. 3). Pacing was started at a high output and then the output was reduced until capture was lost. Initially the paced QRS configuration was similar to VT1, and then changed to a QRS configuration similar to VT2, and finally became a similar configuration to VT3. In fact, VT3 also became non-inducible following the additional RF energy applications to an opposite site of the low voltage area. During a 2-year follow-up, when the patient received low-dose amiodarone, no episodes of VT recurrence were detected.
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