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.