Another Way to Prove the Presence and Participation of an Accessory Pathway in Supraventricular Tachycardia?

An electrophysiologic study was performed in a 33-year-old woman with a 25-year history of recurrent palpitations. Four multielectrode catheters were advanced to the high right atrium, His bundle region, mid-coronary sinus, and right ventricular apex. Baseline conduction intervals were normal, including an HV interval of 45 msec. During inducible regular long RP interval supraventricular tachycardia (SVT) with a cycle length (CL) of 400 msec, the atrioventricular (AV) relationship was 1:1, and earliest atrial activation was recorded along the mid-coronary sinus. The termination of two ventricular pacing trains initiated during tachycardia are shown in Figures 1 and 2 (CL = 380 and 370 msec, respectively). What is the diagnosis? Where is the pacing site located? Surface recordings from leads I, II, III, V1, V5, and bipolar intracardiac recordings from electrode pairs at the high right atrium (hRA), His bundle region (His), coronary sinus (CS, 1 = distal and 10 = proximal), and right ventricular apex (RVA). A recording from the proximal electrode pair on the ablation catheter is also shown (ABL p). A long RP interval tachycardia (CL = 400 msec) continues after the termination of ventricular pacing (CL = 380 msec) that was initiated during tachycardia. Note that the QRS duration during ventricular pacing is only 75 msec, and that an antegrade His potential occurs immediately preceding the pacing stimulus. SA = the interval from pacing stimulus to earliest atrial electrogram; PPI = post pacing interval; VA = the interval from the onset of ventricular activation to the earliest atrial electrogram. A long RP interval tachycardia (CL = 400 msec) continues after the termination of ventricular pacing (CL = 370 msec) that was initiated during tachycardia. Note that the QRS duration during ventricular pacing is only 90 msec. The antegrade His potential seen in Figure 1 is likely coincident with the pacing stimulus. The format is the same as in Figure 1. The differential diagnosis of this narrow QRS complex, long RP interval SVT includes left atrial tachycardia (AT), orthodromic atrioventricular reciprocating tachycardia (OAVRT) using a slowly conducting left sided accessory pathway (AP), and atypical atrioventricular node reentry tachycardia (AVNRT) with retrograde activation over a left atrionodal extension.1–3 The latter possibility is unusual but important to recognize, since it can be cured by catheter ablation at the posteroseptal tricuspid annulus where slow pathway ablation is commonly performed.4 In Figures 1 and 2, the atria are accelerated to the pacing rate, the atrial activation sequence during ventricular pacing is identical to the tachycardia, and the tachycardia continues after the cessation of ventricular pacing, implying that the tachycardia was transiently entrained. The duration of the QRS complexes during ventricular pacing is only 75 and 90 msec, respectively. These QRS complexes, though of a different morphology than the conducted beats that follow, are too narrow to be explained by pacing alone; they represent fusion of the paced antidromic wavefront with the orthodromic wavefront from the preceding beat. The last entrained atrial wavefront conducts to the ventricle via the AV conduction system without fusion, satisfying the first criterion for entrainment5 and proving that the tachycardia was transiently entrained. The slightly wider paced QRS complexes during entrainment at the shorter CL of 370 msec indicate progressive fusion, satisfying the second criterion for entrainment.5 Since the orthodromic wavefront from the preceding beat must be using the AV conduction system to reach the ventricles and fuse with the antidromic wavefront, the orthodromic wavefront must be using an AP to conduct to the atria and continuously reset (entrain) the tachycardia. Thus, transient entrainment with manifest QRS fusion by ventricular pacing proves that the SVT is reentrant, that an AP is participating, and that the ventricle is a required component of the circuit, excluding both atypical AVNRT and AT in the absence of a proximate AP. Theoretically, a simultaneous AT originating very close to an AP, or simultaneous atypical AVNRT with an atrial exit close to an AP, are not excluded by these findings, though such an exceptional circumstance would require a double tachycardia or a double loop tachycardia where one of the tachycardias is OAVRT. Ablation of the AP would ultimately be required both clinically and to unmask the second tachycardia mechanism. Two questions arise: (i) why is manifest QRS fusion during entrainment of SVT by ventricular pacing not more commonly appreciated and (ii) why was it so easily appreciated in this case? Manifest fusion during transient entrainment of AVNRT by ventricular pacing is impossible in the absence of an AP. The stimulated wavefront must conduct retrogradely through the His bundle to reach the AVN, so that there is no possibility for concomitant antegrade conduction from the AVN to the ventricle. The collision between the antidromic wavefront and the orthodromic wavefront from the preceding beat must occur in the AVN, where it is concealed, so that the QRS morphology is always that of a fully paced beat. This explains why manifest QRS fusion is not observed during entrainment by ventricular pacing in the most common SVT encountered in the electrophysiology laboratory. But why is it not more commonly appreciated during entrainment of OAVRT by ventricular pacing? In an early study of transient entrainment using OAVRT with left sided APs as a model, Okumura and colleagues concluded that when pacing the RV apex, a site that is both orthodromically distal to the slow conduction zone (the AVN) and far from the OAVRT circuit, fusion is not demonstrable because collision of wavefronts occurs in the AVN.5 Under these circumstances, the stimulus must be delivered early enough to be able to travel to the circuit in time to reset it, which is early enough that it depolarizes most, if not all, of the ventricular myocardium before the orthodromic wavefront from the preceding beat can exit the slow conduction zone. However, Ormaetxe and coworkers demonstrated manifest fusion when using RV apical pacing to entrain OAVRT using septal APs, where the circuit is much closer to the pacing site.6 In our case, the demonstration of fusion was facilitated by pacing the posterobasal left ventricle (note the R waves in V1, consistent with left ventricular rather than RV pacing) close to the OAVRT circuit, yielding a postpacing interval within 20 msec of the tachycardia CL. In addition, by pacing the base of the left ventricle, close to the ventricular insertion of the AP and far from the more apical distal arborization of the His Purkinje system, the orthodromic wavefront from the preceding beat was allowed to rapidly depolarize a large amount of ventricular myocardium, producing a very short QRS duration. Finally, the ventricular pacing site could be considered to be orthodromically proximal rather than distal to the zone of slow conduction, since the AP had a long conduction time, though this alone is an insufficient explanation, since RV apical pacing did not result in manifest fusion during entrainment. This AP was successfully ablated at a left lateral position where the local VA interval was 180 msec, confirming its long conduction time. No other tachycardias were inducible. This case demonstrates that manifest QRS fusion during transient entrainment of SVT by ventricular pacing is another way of proving that an AP is participating in OAVRT. The demonstration of QRS fusion can be facilitated by pacing close to the ventricular insertion of the AP.

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