Bidirectional atrioventricular reentrant tachycardia using bilateral accessory pathways

Abstract

Patients with Wolff-Parkinson-White (WPW) syndrome rarely have multiple accessory pathways (APs). Here, we present a case of a 21-year-old man with the manifest type B WPW syndrome who was experiencing multiple attacks of palpitations. The electrophysiological study revealed two APs located bilaterally: the anterolateral tricuspid annulus and lateral mitral annulus. Atrial/ventricular extrastimulations induced two types of wide QRS tachycardia conducting via two APs in the clockwise and counterclockwise direction. These two APs were eliminated with careful mapping and catheter ablation.

<Learning objective: It is extremely rare for patients with the Wolff-Parkinson-White syndrome to have multiple accessory pathways (APs) at the right and left lateral sides along with clinical tachycardia conducting via both pathways. The mechanism of such tachycardia may be due to the differences of effective refractory periods between two APs, long anatomical distance between APs, and no retrograde conduction via the atrioventricular node.>

Introduction

Atrioventricular reentrant tachycardia (AVRT) usually has a reentrant circuit through the atrioventricular node (AVN) and an accessory pathway (AP), and cases with multiple APs located at the right and left side are extremely rare. We treated a rare case of a bidirectionally-conducting reentrant tachycardia (through the bilateral APs) with no involvement of the AVN conduction.

Case report

The patient was a 21-year-old man without any structural heart disease. He had been experiencing palpitations during physical activity from the age of 12 years, and was diagnosed with the Wolff-Parkinson-White (WPW) syndrome on electrocardiogram (ECG). At the age of 13 years, he underwent catheter ablation at another hospital; however, it was unsuccessful. His symptoms worsened and he was referred to our hospital. No abnormal findings were detected during the physical examination, laboratory testing, and echocardiography. A 12-lead ECG revealed the manifest type B WPW syndrome (Fig. 1a); however, the ECG during a palpitation was unavailable.

Fig. 1.

12-lead electrocardiogram (ECG) before and after catheter ablation. 12-lead ECGs before ablation showed manifest type B Wolff-Parkinson-White (WPW) syndrome (a). Type A WPW syndrome was manifested after the right accessory (AP) pathway ablation (b). After both right and left AP ablation, no delta wave was present (c).

The electrophysiological study was performed after obtaining the patient’s written informed consent. The multipolar electrode catheters were placed on the right atrial appendage (RAA), tricuspid valve annulus (TVA), His bundle, right ventricle (RV), and coronary sinus (CS) through the right femoral vein and right subclavian vein. The intracardiac electrogram during sinus rhythm showed the AH interval of 82 ms, HV interval of −12 ms, and the earliest ventricular activation site (EVAS) was anterior lateral TVA (Fig. 2a, red arrow). The ventricular potentials at the distal CS were also relatively early (red dotted circle). During atrial pacing at a faster rate, the preexcitation conducting through the right AP was gradually manifested (Fig. 2b). The EVAS shifted to the distal CS without decremental conduction during atrial pacing at more than 200/min (Fig. 2c, red arrow), and elicited maximal preexcitation of type A delta wave during surface ECG. The ventricular potential at RV was the latest (dotted green arrow). During ventricular pacing, the earliest atrial activation site (EAAS) was at TVA (Fig. 2d, blue arrow). The atrial potentials at the distal CS were also relatively early (dotted blue circle). EAAS shifted to the distal CS at more than 180/min (Fig. 2e, blue arrow). These findings suggested the presence of bilateral APs and peculiar conduction properties; during relatively slow pacing rate, both APs were conducted (mainly right AP > left AP); however, the left AP alone was conducted during the rapid pacing rate. The effective refractory period (ERP) of the antegrade and retrograde right AP was longer than that of the left AP (the ERP of antegrade right AP was 310 ms, and that of retrograde right AP was 290 ms). The atrial extrastimulation induced a wide-QRS tachycardia (AVRT-1, Fig. 3a). The sequence of EVAS at distal CS and of EAAS at TVA during tachycardia indicated that the AVRT-1 conducted through the antegrade left AP and retrograde right AP in the clockwise direction. Furthermore, ventricular extrastimulation induced AVRT-2 (Fig. 3b). EVAS was at TVA and EAAS was at the distal CS during tachycardia; therefore, AVRT-2 conducted through the antegrade right AP and retrograde left AP in the counterclockwise direction. Tachycardia cycle length (TCL) was 350 ms on both AVRTs. The entrainment pacing from RAA during AVRT-2 revealed that the post-pacing interval (378 ms) was nearly equal to the TCL. In addition, the findings of antidromic atrial capture at TVA and orthodromic atrial capture at CS implied the tachycardia circuit using bilateral APs in a counterclockwise fashion (Fig. 2f). These findings excluded the tachycardia via AVN conduction, atrial, and ventricular tachycardia. Based on those observations, the tachycardia was diagnosed as two AVRTs via the right and left APs.

Fig. 2.

The intracardiac electrogram during sinus rhythm and pacing. The red arrow indicates the earliest ventricular activation site, and the blue arrow indicates the earliest atrial activation site. The discrepancy between the earliest ventricular activation site at the sinus rhythm (a) and the earliest atrial activation site at slow RV pacing (b) may be due to the oblique location of the right AP.

AP, accessory pathway; AVN, atrio-ventricular node; CS, coronary sinus; d, distal; His, His bundle; HLRA, high lateral right atrium; Lt, left; LLRA, lower lateral right atrium; p, proximal; ppm, pacing per minute; RAA, right atrial appendage; Rt, right; RV, right ventricle; S, Stimulus; SR, sinus rhythm; TVA, tricuspid valve annulus.

Fig. 3.

The intracardiac electrogram during tachycardia. The red arrow indicates the earliest ventricular activation site, and the blue arrow indicates the earliest atrial activation site. The effective refractory period of the right AP was longer than that of the left AP. Therefore, the AES induced right AP block and reentrant tachycardia ensued in a clockwise direction (a). In contrast, VES induced right AP block and reentrant tachycardia ensued in a counterclockwise direction.

AES, atrial extrastimulation; AP, accessory pathway; AVN, atrioventricular node; AVRT, atrioventricular reentrant tachycardia; Lt, left; Rt, right; VES, ventricular extrastimulation.

First, right AP ablation was performed during the sinus rhythm. Atrial and ventricular potential on the ablation catheter was fused at the anterior lateral TVA, and P-QS pattern was confirmed on this site at a unipolar electrode. This site was the EAAS during the ventricular pacing. The right AP block was created by single radiofrequency application and then it elicited the manifest type A WPW morphology on surface ECG (Fig. 1b). Moreover, ablation of the left AP (lateral side of mitral annulus) was performed with the transaortic approach, as well as of the right AP. After ablation, there were no ventriculo-atrial conductions via the APs and AV node, and no tachycardia could be induced after the ablation. A 12-lead ECG after the ablation showed no delta wave (Fig. 1c). The patient has not had recurrence of tachyarrhythmia since.

Discussion

The incidence of multiple APs is reported to be 3% to 15% in patients with WPW syndrome [1], [2], [3], [4]; however, it is more common in pediatric patients, especially in patients with congenital heart diseases such as the Ebstein's anomaly [2], [3]. In the case presented here, the patient had no structural heart diseases; however, the presence of multiple APs was suspected because his symptoms started in childhood. According to a previous report based on the examination of 1010 patients with WPW syndrome [4], multiple APs were found in 31 of those patients (3.1%). While the two right APs (at the free wall and at the posterior wall of TVA) were most common (1.5%), the left and right APs were less frequent (0.6%). Thus, the presented case is extremely rare in terms of the localization of AP at both sides and the tachycardia conducting via both APs bidirectionally. Possible reasons behind the occurrence of such rare tachycardia include: (1) two APs with different ERPs, (2) a long anatomical distance between two APs, and (3) no ventriculo-atrial conduction via the AV node. According to a previous study reporting the relationship between the ERP and the location of AP, there are no differences of ERP in antegrade conduction between the right and left sides. However, ERP of the right AP is longer than that of the left AP in retrograde conduction [5]. Our case showed that the ERP of the right AP was longer than that of the left AP in both antegrade and retrograde conductions. These electrophysiological properties may have consequently caused the bidirectional tachycardias. The detailed ERP value of the left AP remains unknown because the pacing study was not performed after the right AP ablation. Additional electrophysiological study after an AP ablation would be necessary to elucidate the conduction property of the other AP, especially in case of multiple APs.

To conclude, we present here a case with bilateral APs and reentrant tachycardia conducting APs bidirectionally. The condition was fully treatable upon careful interpretation of the electrophysiological findings and mapping.

Conflict of interest

The authors declare that there is no conflict of interest.

Funding

None.