Discussion
This case series illustrates the potential importance of the site of
stimulation when attempting to induce VT. In some patients,
non-inducibility may be due to the inability of paced wavefronts from
remote sites to engage potential reentry circuits, despite the use of
multiple extrastimuli and adrenergic agents. The concept of enhanced VT
induction probability by the addition of more stimulation sites,
including the LV has been described
previously.5,6,14,15 PES from the RV endocardium and
LV epicardium has previously been compared in patients following
surgical treatment of VT.16 The authors concluded that
stimulation from either site yielded comparable results. The study was
done post operatively, however, and was geared towards evaluating
whether post-operative residual VT was predictive of future VT
recurrence.
All six patients we describe in our case series had clinical VTs that
were not induced with PES from the common RV sites (Table 1). All
subjects had scar related re-entrant VT that was successfully induced
from different alternate sites which markedly affected their subsequent
clinical management. In five of the six patients (cases 1-5), the
clinical VT was induced when PES was performed at a site anatomically
closer to the expected critical VT isthmus. This observation supports
that the proximity of the pacing site to the reentry circuit as an
important factor beyond the probabilistic nature of PES yield in some
patients. The pacing site is likely an important determinant of whether
an extrastimulus wavefront will both reach the VT exit site sufficiently
early to block due to refractoriness, and then propagate into the
entrance and through the critical isthmus with sufficient delay to allow
recovery at the exit site to allow VT initiation. This is likely related
to both the anatomic and electrophysiologic properties of the scar and
surrounding tissue as well as the distance from the stimulation site to
various points in the circuit. At a stimulation site remote to the scar,
or one where propagation velocity of the intervening tissue between the
site and the circuit is slow, the paced wavefront may not reach the
isthmus within the critical time window required to initiate VT.
Conversely, by moving the stimulation site closer to the circuit, the
paced wavefront is more likely to reach the critical isthmus and exit
site with the appropriate relative timing to initiate reentry (figures 5
and video 1). Although our series suggests that close proximity to the
reentry circuit is an important factor, perhaps by allowing premature
stimuli to reach the circuit with less delay propagating through
surrounding tissue, the direction from which the stimulated wave front
arrives at the circuit is also likely important and a remote site may be
more effective than a close site in some cases.
The sixth case illustrates the importance of the electrophysiologic
properties of the intervening tissue between the stimulation site and
the circuit in contrast to simple anatomic proximity. This patient had
VT from the basal RV septum induced with atrial stimulation but not with
aggressive stimulation from the RV apex and RVOT. In this case, right
bundle branch block was present so atrial pacing activated the ventricle
over the left bundle during atrial pacing, and perhaps resembled LV
stimulation. The importance of atrial stimulation in the induction of
idiopathic fascicular VT, which utilizes parts of the conduction system,
has been described previously.17 Here, we posit that
the conduction system was not formally involved in the circuit but did
allow the paced wavefront to quickly engage the ventricular tissue
proximate to the circuit despite its origin in the atrium.
The potential value of PES from different sites, including the RV
epicardium in patients with suspected Arrhythmogenic Right Ventricular
Cardiomyopathy (ARVC) is well demonstrated in the first case. The
separation of the epicardial and endocardial layers in ARVC with long
conduction delays from epicardium to endocardium have been previously
described,18 but, to our knowledge, this is the first
reported case of epicardial-specific VT inducibility in a patient with
suspected ARVC.
This case series illustrates that alternate sites for PES, perhaps that
are in close anatomic or electrophysiologic proximity to potential
reentry circuits, are a reasonable consideration when trying to induce a
clinical arrhythmia in patients with previously documented VT or in
assessing arrhythmia risk in some patients with concern for VT (as
illustrated by case 5). Alternative sites might also be considered when
it is desirable to induce a specific clinical VT morphology, when only
others are inducible with initial PES; as in patients who have repeated
recurrence of a clinical VT after substrate guided ablation. Further
studies are needed to evaluate the optimal pacing sites for assessing
the value of inducibility during/following ablation procedures.