Unusual resetting of superior‐type fast–slow atrioventricular nodal reentrant tachycardia with cycle length alternans by early spontaneous premature ventricular contraction

The pacing maneuvers for supraventricular tachycardia with cycle length alternans are sometimes difficult, especially when diagnostic ventricular pacing does not conduct to the atrium. Even in such a situation, critical diagnostic findings can be obtained by spontaneous premature ventricular contraction. A 75-year-old woman underwent catheter ablation for paroxysmal supraventricular tachycardia. An electrophysiological study was performed under conscious sedation. The baseline study showed a short A-H interval without ventricular preexcitation, accompanied by a smooth conduction curve. Retrograde conduction also showed a smooth conduction curve with a concentric activation pattern, which was compatible with retrograde fast pathway conduction. During right ventricular double extrastimuli, a narrow complex tachycardia was induced with a double atrial response (Figure 1A). The atrial activation pattern of the second beat of the double atrial response and the tachycardia was also concentric but different from the retrograde fast pathway. In addition, the tachycardia exhibited regular cycle length alternans with no change in the atrial sequence. Right ventricular overdrive pacing failed to capture the tachycardia (Figure 1B), and differential atrial overdrive pacing also failed to demonstrate V-A linking1 because of frequent termination during the pacing and lack of reproducibility. At this point, the differential diagnoses were superior-type fast–slow atrioventricular nodal reentrant tachycardia (sup-F/S AVNRT) and para-His atrial tachycardia, but these were difficult to distinguish from the findings of the pacing maneuvers. However, an unusual response was observed during an early spontaneous premature ventricular conduction (PVC); the early PVC reset the tachycardia with a delay of the second next atrial beat after the PVC, without critically affecting the atrial and His electrograms immediately after the PVC (Figure 2 and Supplementary Figure). As the resetting occurred without changing the atrial activation pattern, we diagnosed sup-F/S AVNRT. Radiofrequency ablation from the noncoronary cusp terminated the tachycardia and rendered it noninducible. This case showed an unusual resetting of sup-F/S AVNRT caused by a spontaneous PVC. Sup-F/S AVNRT is a rare type of F/S AVNRT with the earliest retrograde atrial activation at the anteroseptum near the fast pathway region.2 The even more unusual findings of this case are as follows: (1) While the spontaneous PVC reset the sup-F/S AVNRT, the RVOD could not; (2) the resetting of the sup-F/S AVNRT was observed as a delay of the second next atrial beat after the PVC; and (3) a regular cycle length alternans was observed without changing the atrial sequence. A possible explanation for why the spontaneous PVC reset the tachycardia but the RVOD could not is the difference in the proximity to the AVNRT circuit. The spontaneous PVC was accompanied by a presystolic potential in the His region, suggesting that the PVC may have originated near the His bundle and was less susceptible to the infra-His conduction delay than the RVOD. However, the resetting of the second next atrial beat and cycle length alternans cannot be explained by the proximity of the PVC origin to the AVNRT circuit alone. We propose a mechanism assuming longitudinal dissociation in the lower-turn-around site of the sup-F/S AVNRT circuit, which may be able to explain these phenomena integrally (Figure 3A). In this model, the longitudinally dissociated lower-turn-around site is assumed to be the cause of cycle length alternans. While the early spontaneous PVC could not conduct to the atrium via the retrograde superior slow pathway for the “short” A-A interval, it could cause concealed conduction to the superior slow pathway for the “long” A-A interval. The concealed conduction could delay the second next atrial beat by affecting the relative refractory period of the superior slow pathway used during the “long” A-A interval. A second possible mechanism is resetting via the concealed bystander nodo-ventricular/nodo-fascicular (NV/NF) pathway (Figure 3B).3, 4 Ota et al. reported a similar phenomenon in which the termination of the common F/S AVNRT occurred with the block of the second next atrial beat after the His-refractory PVC.5 The NV/NF pathway was probably connected to the superior slow pathway if it existed because the delay of the atrial beat preceded that of His.5 In this case, the NF pathway was more likely rather than the NV pathway, as RVOD could not show the resetting. A third possible mechanism is a complete compensation of the PVC prematurity by the conduction delay within the retrograde superior slow pathway. This mechanism could mask the resetting of the atrial beat immediately after the PVC. However, if this mechanism were in place, the second next atrial beat would have shown an advancement rather than delay because of the conduction recovery of the superior slow pathway. In conclusion, we have presented an unusual resetting response of sup-F/S AVNRT with cycle length alternans caused by an early spontaneous premature ventricular contraction. Although we could not finally discriminate the two hypotheses, including the longitudinal dissociation of the superior slow pathway and the concealed bystander NF pathway, this case illustrates the usefulness of the findings related to the spontaneous PVC when diagnostic pacing maneuvers fail to differentiate sup-F/S AVNRT from para-His atrial tachycardia. Takayuki Sekihara was involved in investigation, concepturalization, and original draft writing. Tomoaki Nakano was involved in investigation, review, and editing. Akira Yoshida, Takafumi Oka, and Yasushi Sakata were involved in review and editing. We greatly appreciate our hospital's clinical engineers. Authors declare no conflict of interests for this article. Available upon reasonable request. Figure S1. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.