A Short HV Interval Tachycardia Terminated by His‐Refractory Premature Atrial Extra‐Stimulation: What Is the Mechanism?

A 70-year-old man with a history of frequent episodes of paroxysmal palpitations spanning over 10 years was admitted to our hospital for radiofrequency catheter ablation (RFCA). He had no prior history of antiarrhythmic treatment or RFCA. An electrocardiogram (ECG) taken during sinus rhythm (SR) revealed a left anterior fascicular block and a PR interval of 140 ms without evidence of pre-excitation. During the baseline electrophysiology study, ventricular pacing demonstrated ventriculoatrial dissociation, and no tachycardia was induced, even with isoproterenol infusion. Pre-excitation was absent during atrial pacing or extra-stimulation. Figure 1A presents intracardiac tracings of a programmed atrial extra-stimulation (400/300 ms), showing an AH interval of 147 ms and a HV interval of 49 ms during both SR and atrial pacing. In contrast, Figure 1B demonstrates a regular narrow complex tachycardia with a cycle length (CL) of 338 ms and a shortened HV interval of 19 ms, induced by programmed atrial extra-stimulation (400/290 ms) with an AH jump of 118 ms. The tachycardia was terminated by His-refractory premature atrial extra-stimulation (Figure 2A). Notably, the tachycardia, characterized by a short HV interval, was reproducibly induced by programmed atrial extra-stimulation with an AH jump and consistently terminated by His-refractory premature atrial extra-stimulation. Based on the tracings in Figures 1 and 2A, what is the most likely mechanism of this narrow QRS complex tachycardia with a short HV interval? The differential diagnosis for this regular narrow complex tachycardia with a short HV interval includes the following possibilities: (1) Atrial tachycardia (AT) with a concomitant antegrade accessory pathway; (2) atrioventricular nodal reentrant tachycardia (AVNRT) with a concomitant antegrade accessory pathway; (3) antidromic atrioventricular reciprocating tachycardia (AVRT) utilizing an accessory pathway as the antegrade limb; (4) junctional tachycardia (JT) with 1:1 ventriculoatrial (VA) conduction; (5) ventricular tachycardia (VT) with 1:1 VA conduction. The tachycardia could be reproducibly induced and terminated by atrial extra-stimulation, suggesting reentry as the most likely mechanism. Notably, the QRS morphology during tachycardia (Figure 1B) differs from that observed during atrial pacing or SR, although it is only slightly widened to 102 ms. This finding, combined with the narrow QRS duration and the short HV interval during tachycardia, suggests an origin near the His region, either from a supraventricular or ventricular mechanism. Figure 2A illustrates a tachycardia episode with a CL of 355 ms, where a single His-refractory premature atrial extra-stimulation terminated the tachycardia without affecting the immediate His-ventricle CL. In Figure 2B, during another tachycardia episode with a CL of 357 ms, the same maneuver advanced the following His-ventricular CL by 17 ms, rather than the immediate next beat. These observations strongly favor the diagnosis of slow-fast AVNRT as the fundamental mechanism, with a concomitant bystander antegrade accessory pathway—specifically, a nodoventricular bypass tract (NVT)—present. This conclusion effectively excludes alternative diagnoses, such as: AT with a concomitant accessory pathway, Antidromic AVRT using an accessory pathway as the antegrade limb, JT, and VT. The first beat after tachycardia termination in Figure 2A shows a shortened HV interval of 38 ms, which remains shorter than the baseline HV interval during SR. The QRS morphology demonstrates fusion between the tachycardia and SR, particularly in the V5 and V6 leads (red arrow). This phenomenon can be explained by the partially recovered antegrade conduction of the fast pathway (FP) and the partially retained antegrade conduction of the slow pathway (SP), leading to a fused HV interval and QRS complex beat resulting from simultaneous conduction through both pathways. Another possible explanation is that tachycardia termination following atrial single extra-stimulation was coincidental. However, the consistent and reproducible termination of tachycardia with His-refractory programmed atrial single extra-stimulation makes a random occurrence unlikely and supports a reentrant mechanism involving the atrioventricular node (AVN) and concomitant bystander accessory pathway. The main challenge in this case lies in explaining why the accessory pathway conducts only during tachycardia episodes but not during SR. The proposed explanation is that the accessory pathway originates from the SP and connects to the ventricular myocardium near the His bunlde, forming a NVT. This explains why it is involved only during tachycardia episode. During SR, the atrial impulse travels through both the FP and SP. When it reaches the lower part of the AVN via the SP, it encounters refractory conduction because the impulse has already passed through the FP (Figure 3A). During tachycardia initiation, the impulse blocks in the FP and shifts to the SP, causing an AH jump and initiating the tachycardia (Figure 3B). However, both the His bundle and NVT are out the tachycardia circuit; the NVT acts solely as a bystander antegrade pathway, facilitating antegrade conduction only during tachycardia episodes [1]. The HV interval of 19 ms observed during tachycardia is essentially a pseudo-shortened interval due to the entrainment effect of the NVT, which advances the onset of the QRS complex by approximately 30 ms (from 49 to 19 ms) compared to AVNRT without the NVT. Furthermore, the ventriculoatrial dissociation observed during the baseline electrophysiology study suggests that the FP is retrogradely activated by the SP, not by the NVT during tachycardia. Finally, SP RFCA was performed, and junctional rhythm was observed with QRS morphology and HV interval similar to those seen during tachycardia, rendered the disappearance of the SP and the tachycardia non-inducible. At the 1-year follow-up, the patient remained free of tachycardia. In conclusion, we report a case of slow-fast AVNRT with a manifest, bystander NVT originating from the SP and connecting to the ventricular myocardium near the His bundle, which mimics VT during tachycardia episodes. This work was funded by the Tianjin Key Medical Discipline Construction Project (No. TJYXZDXK-020A). The authors have nothing to report. The authors declare no conflicts of interest. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.