Discussion
Iesaka and colleagues1 first reported adenosine-sensitive AT originating from the vicinity of the AV node and the responsible mechanism was considered to be reentry. Considering the sensitivity to adenosine, calcium channel-dependent tissue such as a retroaortic node or AV ring, which consists of AV node-like structures, is speculated to be involved in the SCZ of the AT circuit5. A conventional catheter electrode cannot record the potentials from tissues with Ca channel-dependent conduction, and hence this AT as well as AV nodal reentrant tachycardia (AVNRT) reveals a centrifugal activation on the 3D electroanatomical map. As an alternative strategy to ablation at the EAS representing the exit of the SCZ close to the AV node, previous reports safely eliminated ATs at the entrance of the SCZ that was considered to be located between the EAS and pacing site where manifest entrainment was demonstrated.2,3 In this strategy, manifest entrainment is defined by the orthodromic capture of the electrogram at the EAS with a long conduction time by the immediately previous pacing impulse (n-1), and the antidromic capture of the other sites by the immediate impulse (n) in one paced beat except for the last entrained beat, equivalent to constant fusion. The reported pacing sites demonstrating manifest entrainment were the RAA, high anterolateral RA, high posteroseptal RA, CTI, NCS6, and MA7; however, in our current case, manifest entrainment could not be observed from those sites and could be only from the anteroseptal LA. To our knowledge, the current case is the first report of a case that demonstrated manifest entrainment from the anteroseptal LA and in which successful ablation was achieved at remote site from the EAS, as indicated by a manifest entrainment-guided strategy in the LA. A previous report2 showed that the atrial electrograms at the successful ablation site appeared later than that of the EAS by 7~26 ms, and the distance between the successful ablation site and EAS was 7~19 mm. In our case, the local potential of the last ablation site (site B) had a delay of 8 ms compared to that of the EAS-LA (Figure 2B), and the distance from the site B to the EAS-LA was 13 mm. These findings suggested that the size of the tachycardia circuit and very long conduction time of the SCZ in this case were comparable to that of the previous report, and the successful ablation site was presumed to be located on the side of the entrance of the SCZ.
Inagaki and colleagues7 reported an adenosine-sensitive AT case that demonstrated manifest entrainment from 1 o’clock on the MA. As in their case, if the SCZ is located along the anterior MA, manifest entrainment may be observed from the distal CS electrode. However, if the SCZ is located along the LA septum as in our case, demonstration of manifest entrainment from the CS electrodes seems to be difficult, and entrainment mapping approaching the LA may be required. In their case, the target ablation site was the EAS on the anteroseptum of the LA (10 o’clock on the MA) and was considered to be the exit of the SCZ.
Lyan and colleagues8 reported a total of 16 of 68 cases of ATs originating from the para-Hisian region that had ablation in the LA, with only 4 of those, including those with a failed NCS ablation, resulting in the successful elimination of the AT, and ablation in the LA was effective only when the LA activation was earlier than the RA activation as in our case. They also showed the occurrence of transient AV block with 1 unsuccessful case that was ablated in the LA, and in our case as well, an RF application at the EAS-LA caused transient PR interval prolongation and failed to eliminate the AT. An RF application on the anteroseptum of the atrium near the AV annulus has the potential risk of causing inadvertent AV block even from the LA; therefore, a manifest entrainment guided ablation strategy can be a reasonable option in these cases.
After cessation of the entrainment pacing from site A, a premature atrial complex (PAC) with an early local electrogram recorded by the mapping catheter reset the AT (Figure 3A). The conduction interval between the distal electrode of the mapping catheter and CS distal electrode during entrainment pacing from site A and a PAC was the same (35ms), hence this PAC was presumed to be caused by the mapping catheter. Of note, the last entrained ventricular beat was the second one after the pacing stimulus, indicating a markedly long AV interval; however, a ventricular captured beat by a PAC was the first one after the PAC with a short AV interval despite a shorter coupling interval than the PCL. This finding may be explained by orthodromic capture of the EAS-LA with subsequent capture of the AV node during entrainment pacing (Figure 3B) and capture of the AV node by a PAC before the tachycardia wavefront exited from the SCZ (Figure 3C). During differential atrial overdrive pacing, the last entrained ventricular beat was also the first one with a short AV interval (Figure 1C) due to the antidromic wavefront directly capturing the AV node without propagating to the SCZ because neither the HRA or CS proximal electrode were located proximal to SCZ. This disproportionate AV interval in an adenosine-sensitive AT case was previously reported by Maruyama and colleagues9 as a “disproportionate delay”. This finding suggested that the SCZ and AV node were in close proximity but not connected, and would provide useful information regarding a challenging differential diagnosis of an adenosine-sensitive AT and AVNRT including a superior type slow pathway10.