A spontaneous or pacing‐induced transition from slow‐fast atrioventricular nodal reentrant tachycardia to fast‐slow type using a superior slow pathway

A 55-year-old woman with no structural heart disease underwent evaluation and catheter ablation for recurrent short RP’ supraventricular tachycardia (SVT). Electrode catheters were positioned in the high right atrium (HRA), His bundle (HB), right ventricular apex (RVA), and coronary sinus (CS) (Figure 1A). At baseline, the patient exhibited normal atrial–His (AH) (80 ms) and His–ventricle (HV) (54 ms) intervals with a sinus cycle length (CL) of 664 ms (Figure 1B, Figure S1A). During ventricular single extrastimulation (VES) at an S1–S2 interval of 200–420 ms, a smooth ventriculoatrial (VA) conduction curve with decremental properties was observed. The earliest atrial activation site (EAAS) was reproducibly detected in the HB region, followed by anterograde conduction over a fast pathway (FP), thus suggesting the presence of a retrograde superior slow pathway (sup-SP) (Figure 1C).¹ Following isoproterenol infusion, atrial programmed stimulation revealed dual atrioventricular (AV) nodal physiology. Clinical tachycardia (SVT1) (Figure S1B) was reproducibly induced with a jump in the AH interval and terminated by HRA pacing. The tachycardia CL (TCL) was 312 ms with a septal VA interval of 54 ms (Figure 1D), suggesting that SVT1 appeared to be a slow-fast (S/F) AVNRT.² His synchronous premature ventricular contractions did not affect the next His potentials, excluding orthodromic reciprocating tachycardia with the nodoventricular/fascicular fiber as the retrograde limb. SVT1 spontaneously transitioned to SVT2 with a shorter TCL with the atrial activation sequence remaining unchanged (Figure 2, Figure S1C). The TCL of SVT2 was 288 ms with a septal VA interval of 154 ms, and the EAAS was observed in the HB region. In the third, fourth, and fifth cycle, apparent Wenckebach-periodic VA prolongation was exhibited. In the fifth cycle, a shortening of the His-His (HH) interval to 270 ms compared to the preceding measurement of 284 ms was observed. The sixth and seventh cycles showed a long RP’ appearance with a stable AH/HA interval and an atrial activation sequence similar to that during a retrograde conduction via the sup-SP. The above observations illustrate a spontaneous transition from S/F AVNRT with a bystander sup-SP to superior-type F/S AVNRT, triggered by a retrograde block at the upper common pathway (UCP) that manifested a retrograde atrial activation via the sup-SP. A shortening of the HH interval in the fifth cycle suggests that retrograde atrial activation antegradely returned to the His bundle via the FP.³ A similar tachycardia transition was observed during ventricular overdrive pacing (VOP) (Figure 3). VA dissociation was seen in the upper panel and until the first cycle in the lower panel. Notably, the second atrial cycle in the lower panel shortened to 300 ms, followed by constant atrial cycles similar to those observed during the tachycardia after VOP. This suggests that the first stimulus, which retrogradely penetrated into the AVN circuit, terminated S/F AVNRT by provoking an antegrade block in the typical SP and the second stimulus captured the atria via the sup-SP, leading to the initiation of superior-type F/S AVNRT. VA dissociation was seen during VOP between the third and the last stimulus because of a repetitive retrograde block at the level of the lower common pathway (LCP), functionally developing and associated with the establishment of superior-type F/S AVNRT. SP ablation was subsequently performed in the posteroseptal region between the inferior aspect of the CS ostium and the tricuspid valve annulus. Loss of antegrade SP conduction was confirmed, indicating that the two tachycardias were no longer inducible.

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This case was characterized by three main findings. First, the EAAS during VES was reproducibly detected in the HB region, which was followed by a short AH anterograde conduction. Second, during VES, a smooth VA conduction curve with decremental properties was observed. Third, EAAS remained in the HB region during tachycardia, which was similar to VES findings; furthermore, a spontaneous transition with a gradual VA interval increase was observed. The differential diagnosis for tachycardia transitions with a Wenckebach-periodic VA prolongation observed during AVNRT, where EAAS was observed in the HB region, suggests two possibilities: S/F AVNRT with a decremental UCP; S/F AVNRT with a bystander sup-SP, where antegrade or retrograde conduction pathways within the AV node switch the tachycardia circuits. The former differential diagnosis is implausible for the following reasons: First, a two to threefold prolongation of the retrograde conduction time via an UCP, as illustrated in Figure 2, is not realistic. Such prolongation generally results in a Mobitz-type block.⁴ Second, a smooth VA conduction curve and an apparent similarity in the atrial activation pattern during VES do not always indicate a single retrograde pathway. It is possible to involve a retrograde conduction via a FP after VES not inducing a fast-slow echo. Third, a slight but significant difference in the TCL between short and long RP tachycardia suggests that the mechanisms of the two tachycardias may not be identical. We propose another mechanism responsible for the transition from short RP to long RP’ tachycardia, characterized by gradual VA prolongation and a constant CL, as follows: Short RP tachycardia (SVT1) can be diagnosed as S/F AVNRT based on its short RP appearance, induction with a jump in the AH interval, and successful elimination of the tachycardia following ablation of the typical SP. Moreover, retrograde conduction via a sup-SP functioning as a bystander during S/F AVNRT can be hypothesized,⁵ as VES demonstrated that the sup-SP had a retrograde effective refractory period shorter than that of the FP (Figure 1C). In summary, these two tachycardias represent a spontaneous and pacing-induced transition from S/F AVNRT to the F/S type, utilizing a sup-SP. Wenckebach-periodic VA prolongation and abrupt shortening of the HH/AA interval during tachycardia transition are crucial for diagnosing the mechanism of tachycardia.

FUNDING INFORMATION

None.

CONFLICT OF INTEREST STATEMENT

The authors declare no conflicts of interest.

ETHICS STATEMENT

Ethics approval to report this case was obtained from the institutional review board of Ogaki Municipal Hospital.

PATIENT CONSENT STATEMENT

Informed consent was obtained from the patient for the purpose of this report.

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