Coexistence and spontaneous transition between orthodromic atrioventricular reentrant tachycardia and atrial tachycardia: The mechanism of atrial activation sequence

Abstract

The coexistence of multiple supraventricular tachycardias during electrophysiological study (EPS) is rare and can complicate diagnosis and treatment. We present a case of coexisting orthodromic atrioventricular reentrant tachycardia (AVRT) and atrial tachycardia (AT) with spontaneous transitions. A 15-year-old girl with palpitations underwent EPS revealing orthodromic AVRT via a left-sided accessory pathway (AP) and AT originating from the right atrium. The tachycardias had similar cycle lengths and exhibited spontaneous transitions. During AT, a unique cyclic atrial activation sequence was observed, hypothesized to result from fusion of antegrade AT conduction and retrograde conduction via a left-sided AP. Radiofrequency catheter ablation targeting the AP successfully terminated the arrhythmias, with no recurrence observed during follow-up. This case highlights the complex electrophysiological interplay between coexisting AVRT and AT, the mechanism of spontaneous tachycardia transitions, and the unique cyclic fusion atrial activation pattern resulting from combined antegrade AT conduction and retrograde conduction via a left-sided AP.

Learning objective

This case highlights the complex electrophysiological interplay between coexisting atrioventricular reentrant tachycardia and atrial tachycardia (AT), the mechanism of spontaneous tachycardia transitions, and the unique cyclic fusion atrial activation pattern resulting from combined antegrade AT conduction and retrograde conduction via a left-sided accessory pathway.

Introduction

Previous reports showed the coexistence of multiple types of supraventricular tachycardia (SVT) during electrophysiologic studies (EPS) [1], [2]. The coexistence of multiple tachycardias may present with atypical EPS findings and complicate SVT diagnosis. Here, we report a rare case of EPS with coexisting orthodromic atrioventricular reentrant tachycardia (AVRT) and atrial tachycardia (AT).

Case report

A 15-year-old girl with no relevant medical history presented to a local clinic with palpitations. Twelve‑lead electrocardiography (ECG) revealed narrow QRS tachycardia, with a heart rate of 217 beats/min. The patient was referred to our hospital for evaluation of EPS and catheter ablation. ECG revealed a heart rate of 77 beats/min in sinus rhythm, but no pre-excitation was found. Chest radiography revealed a cardiothoracic ratio of 40%. Echocardiography revealed no abnormalities.

During EPS, a decapolar catheter was placed in the coronary sinus (CS) and three quadripolar catheters were positioned in the right atrium (RA), right ventricle (RV), and His bundle areas (Fig. 1A). At baseline, the sinus cycle length was 690 ms. The atrio-His (AH) and His-ventricular intervals were 75 and 50 ms, respectively. Ventriculoatrial (VA) conduction was observed, with the CS mid-area identified as the retrograde earliest atrial activation site (EAAS) during RV pacing. Dual antegrade atrioventricular (AV) nodal physiology and decremental properties of AV conduction were observed during the atrial extra-stimulus. The Wenckebach rate during the atrial burst pacing was 160 bpm without isoproterenol (ISP) infusion. The retrograde decremental VA conduction was not observed before AP ablation; ventricular effective refractory period (ERP) was 240 ms during RV pacing. Para-Hisian pacing showed an AP/AP_L pattern according to a previous algorithm [3].

Fig. 1.

A) Catheter position in the EPS is shown in the RAO and LAO images. A decapolar catheter was placed deep into the CS because the existence of the left-sided AP was confirmed (yellow arrow).

B) Another narrow QRS tachycardia (SVT2) with the EAAS at the RA electrode was spontaneously induced during SVT1, transitioning from SVT1 to SVT2 (yellow arrow).

C) The variable atrial activation sequence was observed cyclically during SVT2 (yellow arrow).

D) A few minutes later, SVT2 re-transitioned to SVT1 spontaneously (yellow arrow).

EPS, electrophysiological study; LAO, left anterior oblique position; RAO, right anterior oblique position; CS, coronary sinus; AP, accessory pathway; SVT, supraventricular tachycardia; EAAS, earliest atrial activation site; RA, right atrium; RV, right ventricle.

The narrow QRS tachycardia (SVT1) was induced during programmed stimulation from the RA in the ISP loading setting. The tachycardia cycle length (TCL) was 300 ms. The retrograde EAAS was at the CS mid-area. His refractory premature ventricular contractions (PVC) did not reset either A-A or H—H interval. V-A-V activation sequence, correct post-pacing interval-TCL ≤110 ms, total pacing prematurity ≤125 ms, and antidromic His capture were observed during a ventricular overdrive pacing from the RV apex. The last entrainment sequence showed an H*-V*-A2 response during atrial overdrive pacing from the CS ostium [4]. Therefore, SVT1 was diagnosed as orthodromic AVRT via the left-sided accessory pathway (AP).

Another narrow QRS tachycardia (SVT2) with the EAAS at the RA electrode was spontaneously induced during SVT1, transitioning from SVT1 to SVT2 (Fig. 1B). The TCL was 280 ms. Moreover, the atrial activation sequences during SVT2 and RV pacing were significantly different. Therefore, SVT2 was diagnosed as an AT originating from the RA. Interestingly, a variable atrial activation sequence was observed cyclically during SVT2 (Fig. 1C). A few minutes later, SVT2 spontaneously re-transitioned to SVT1 (Fig. 1D). No pacing study could be performed during SVT2.

The AP was targeted. A three-dimensional electro anatomical mapping system (CARTO 3; Biosense Webster, Diamond Bar, CA, USA) was used, and open-window mapping of the left atrium and ventricle was performed using a multi-electrode catheter (Octaray; Biosense Webster) during AVRT, because AVRT was induced incessantly by catheter stimulation. The AP potentials were automatically annotated on the lateral wall of the mitral valve in the early meets-late gap. Radiofrequency ablation was performed, and tachycardia was immediately terminated with a VA block. Retrograde conduction of the AP disappeared. After AP ablation, VA conduction was not observed without ISP infusion. During ISP infusion, VA conduction with an EAAS at His area appeared, exhibiting retrograde decremental properties without evidence of dual retrograde AV nodal physiology. Moreover, no other tachycardia, including SVT2, was induced during any programmed stimulation in the ISP loading setting. The ablation procedure was completed successfully. Thereafter, the patient has had no arrhythmia recurrence.

Discussion

The unique characteristics of the present case are as follows; the coexistence of the orthodromic AVRT and AT was confirmed during EPS, the tachycardia transitions from SVT1 to SVT2 and re-transitions from SVT2 to SVT1 spontaneously, and a variable atrial activation sequence was observed cyclically during SVT2.

Previous reports have shown that dual SVTs with similar TCLs are prone to transition into each other [5]. This report showed that the cut-off point of the difference between the two TCLs of 25 ms had an 80% positive predictive value for the transition between double tachycardias. Moreover, the transition between tachycardia could occur because of spontaneous premature atrial contraction, conduction block at one limb of the tachycardia, or tachycardia-induced tachycardia. Here, the TCL of SVT1 and SVT2 was 300 and 280 ms, respectively. The ISP loading was performed during EPS, a situation that could easily induce tachycardia. Therefore, the tachycardia was vulnerable to transition. The transition from SVT1 to SVT2 appears to occur gradually, with fusion atrial activation sequence between the AT originating from the RA with a shorter cycle length and the orthodromic AVRT via the left-sided AP (Fig. 2A). In contrast, the re-transition from SVT2 back to SVT1 seems to result from spontaneous termination of SVT2, followed by induction of orthodromic AVRT from the last ventricular beat (Fig. 2B). During the transition between the two tachycardias, the RA recordings showed a distal-to-proximal activation sequence during AVRT, whereas the distal and proximal RA electrodes were activated almost simultaneously during AT. The morphology of the local electrograms also differed between the two tachycardias.

Fig. 2.

A) The mechanism of the findings in Fig. 1B is shown in the laddergram. The transition from SVT1 to SVT2 appears to occur gradually, with fusion atrial activation sequence between the AT originating from the RA with a shorter cycle length and the orthodromic AVRT via the left-sided AP (yellow arrow).

B) The mechanism of the findings in Fig. 1D is shown in the laddergram. The re-transition from SVT2 back to SVT1 seems to result from spontaneous termination of SVT2, followed by induction of orthodromic AVRT from the last ventricular beat (yellow arrow).

SVT, supraventricular tachycardia; AVRT, atrioventricular reentrant tachycardia; AT, atrial tachycardia; RA, right atrium; CS, coronary sinus; RV, right ventricle; AVN, atrioventricular nodal; AP, accessory pathway; SP, slow pathway; FP, fast pathway; ERP, effective refractory period.

A variable atrial activation sequence was observed cyclically during SVT2. The mechanism of the variable atrial activation sequence was speculated to be a fusion beat between antegrade conduction due to AT originating from the RA and retrograde conduction via the left-sided AP (Fig. 3). The transient shortening of the atrial activation cycle via the retrograde AP can cause the decremental antegrade conduction via the fast pathway or antegrade conduction via another slow pathway. As shown in Fig. 3, AH interval was prolonged from 170 ms to 260 ms immediately after the atrial activation cycle via the retrograde AP. Fig. 2B shows that AH interval was prolonged from 140 ms to 240 ms without the atrial activation cycle via the retrograde AP. This finding can be explained by switching of antegrade conduction via AV nodal fast pathway to that slow pathway during SVT2 if the ERP for antegrade conduction via AV nodal fast pathway is close to the TCL of SVT2.

Fig. 3.

The mechanism of the findings in Fig. 1C is shown in the laddergram. The mechanism of the findings is speculated as a fusion beat between antegrade conduction due to the AT originating from the RA and retrograde conduction via the left-sided AP.

AT, atrial tachycardia; RA, right atrium; AP, accessory pathway; CS, coronary sinus; FP, fast pathway; SP, slow pathway; ERP, effective refractory period; AVN, atrioventricular nodal.

We believe that the variable EPS findings in this case can occur under several specific conditions: (i) the coexistence of two SVTs with similar TCLs, (ii) an SVT using a retrograde atrioventricular AP, (iii) an SVT with antegrade decremental conduction or existence of dual AV nodal physiology, (iv) a case in which the AT originates on the opposite side from the retrograde atrioventricular AP, and (v) the timing of the ERP of AP.

There are limitations to this case. First, SVT2 was observed only once during EPS. Therefore, pacing study and three-dimensional mapping were not performed during SVT2. A detailed evaluation of SVT2 could not be performed. However, as shown in Fig. 2A, four beats were observed prior to the complete transition from AVRT to AT. Moreover, the arrhythmic activity exhibited a waxing and waning pattern during SVT2. Therefore, even within the context of orthodromic AVRT, the diagnosis of AT seems justified.

Second, right AT was induced only during AVRT via the left AP. The initiation of right AT may require retrograde conduction via the left AP. Right AT was spontaneously induced during AVRT without any specific trigger. Atrial burst pacing from the CS mid-area and ventricular burst pacing were also performed during the EPS session; however, right AT could not be induced under these conditions. It should be noted that this patient exhibited retrograde conduction via the AV node under ISP infusion. Because these pacing maneuvers do not exactly replicate the atrial activation sequence during AVRT, it is possible that right AT could only be induced in the context of AVRT. Furthermore, as AT spontaneously transitioned a few minutes after the onset of AVRT, a relatively prolonged period of rapid atrial activation may have been necessary. The occurrence of AT under ISP infusion also suggests that the drug may have facilitated its induction.

This case highlights the complex electrophysiological interplay between coexisting AVRT and AT, the mechanism of spontaneous tachycardia transitions, and the unique cyclic fusion atrial activation pattern resulting from combined antegrade AT conduction and retrograde conduction via a left-sided AP.

Informed consent

Written informed consent was obtained from the parents of the patient.

Funding

None.

Declaration of competing interest

None.