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.