Unusual ventricular atrial conduction shift from the slow pathway to the fast pathway

Abstract

A 63-year-old woman underwent an electrophysiological study for a treatment of narrow QRS tachycardia, which was diagnosed as a slow-fast atrioventricular nodal reentrant tachycardia. She exhibited dual nodal retrograde conduction, with transitions from the fast pathway to the slow pathway and back to the fast pathway. After focal cryoapplications to the mid-septal region of the right atrial septum, both antegrade and retrograde slow pathway conduction were eliminated without affecting the antegrade fast pathway conduction. The mechanism of transition of retrograde conduction between the fast and slow pathways was explained by the following two scenarios: First, the slow pathway was initially concealed by the fast pathway and became evident only when the fast pathway was blocked due to a gap phenomenon. Second, the slow pathway conducted earlier than the fast pathway at a specific point between the ventricle and atrium, thereby masking fast pathway conduction. This could be attributed to the high levels of connexin 43 reported around the lower nodal bundle.

Learning objectives

When retrograde conduction transitioned from the fast pathway to the slow pathway and then back to the fast pathway, the mechanism was considered a gap phenomenon. This suggested that the slow pathway was initially masked by the fast pathway and could conduct only when the fast pathway was blocked. However, recent findings on the distribution of connexin 43 suggested another possibility that the slow pathway might also mask the fast pathway.

Introduction

In general, slower conduction is masked by faster conduction because the earlier-conducted impulse propagates through the surrounding tissue, creating a refractory period before the slower impulse reaches. As a result, slow pathway conduction is undetectable while the fast pathway is conducted. The slow pathway can only be assessed once the fast pathway is blocked except in the case of double response [1]. Usually, after the transition from the fast pathway to the slow pathway, atrioventricular nodal conduction is blocked when the slow pathway is blocked.

Here, we present a case in which retrograde conduction transitioned from the fast pathway to the slow pathway and then back to the fast pathway.

Case report

A 63-year-old woman was referred to the hospital because of symptomatic palpitations by narrow QRS tachycardia. An electrophysiological study was performed under local anesthesia after written informed consent was obtained. At baseline, the atrio-His and His-ventricular intervals were 72 and 44 ms, respectively. During ventricular extra-stimuli from the right ventricular apex, two types of ventricular atrial (VA) conduction were observed. The earliest atrial activation site of VA-1 was at the His region and of VA-2 at the coronary sinus (CS) ostium, respectively. Ventricular extra-stimuli were assessed three times, and we reproducibly found the following findings: As the stim1-stim2 interval shortened, the VA conduction shifted from VA-1 to VA-2, and then from VA-2 to VA-1 (Fig. 1). A para-Hisian pacing maneuver was performed at pacing cycle lengths of 600 ms and 400 ms to assess both VA-1 and VA-2 (Fig. 1). These findings were assessed in the absence of isoproterenol. A narrow QRS tachycardia with an A on V sequence was induced after a jump-up phenomenon during atrial extra-stimuli under isoproterenol infusion. The earliest atrial activation site during the tachycardia was at the His region. Atrial scan pacing from the CS ostium induced atrial ventricular block, which resulted in the termination of the tachycardia. The tachycardia was diagnosed as a slow-fast atrioventricular nodal reentrant tachycardia [2]. Focal cryoapplications on the mid-septum of the right atrial septum guided by “Jackman” potential [3] eliminated the antegrade slow pathway (Fig. 2). After the cryoapplications and 15 min following the cessation of isoproterenol, VA-2 disappeared, and VA conduction via VA-1 was continuously observed during ventricular extra-stimuli (Fig. 2).

Fig. 1.

Left: Intracardiac electrogram during extra-stimuli from the right ventricular apex. The earliest activation site during S1S2 350 ms was the His region, S1S2 340 ms, the CS ostium, and S1S2 320 ms, the His region. Middle: Conduction curve during extra-stimuli from the right ventricular apex. Right: Intracardiac electrograms recorded during para-Hisian pacing at cycle lengths of 600 ms and 400 ms. The earliest atrial activation sites were observed at the His region during pacing at 600 ms, and at the CS ostium during pacing at 400 ms. The atrial activation sequences remained identical between narrow and wide QRS complexes at both pacing cycle lengths. The interval between the stimulus and the earliest atrial activation differed by 56 ms at a cycle length of 600 ms, and by 40 ms at a cycle length of 400 ms.

CS, coronary sinus; Deca, decapolar catheter; HLRA, high lateral right atrium; LLRA, low lateral right atrium; RV, right ventricle.

Fig. 2.

Left: Fluoroscopic image of the successful cryoapplication. Right: Conduction curve during extra-stimuli after cryoapplication.

LAO, left anterior oblique; RAO, right anterior oblique.

Discussion

It is common for the VA conduction via the fast pathway to convert to that via the slow pathway, as the stim1-stim2 interval is shortened during ventricular extra-stimuli. The slower VA conduction is masked by the earlier VA conduction because the atrial tissue at the earliest activation site of the slower conduction is activated by the earlier VA conduction and is in the refractory period when the slower conduction reaches the atrial tissue (Fig. 3, Upper panel). In the present case, during VA-2 conduction, VA-1 conduction was not observed, and again the VA conduction via VA-1 returned as the extra-stimulus interval was shortened. There were two possible explanations. First, VA-1 exhibited a gap phenomenon [4]. During the gap of the VA-1 conduction, VA-2 was unmasked and observed. However, after focal cryoapplications to eliminate the antegrade slow pathway conduction, VA-1 conduction was continuously observed, and no gap phenomenon was observed. With this first explanation, it was difficult to account for the disappearance of the gap phenomenon in the fast pathway following focal cryoapplications, which eliminated both the antegrade and retrograde slow pathways. The key issue is whether a single, localized cryoapplication could reasonably affect all three pathways: the retrograde fast, antegrade slow, and retrograde slow pathways. However, the S2A2 interval became shorter than at baseline. The fast pathway conduction might have been altered by local autonomic changes induced by cryotherapy or residual effects of isoproterenol. Second, both VA-1 and VA-2 were diagnosed as nodal conduction according to the results of the para-Hisian pacing. Recent reports have suggested that the slow pathway does not fully conduct slowly from assessing the distribution of connexin 43 [5]. It was possible that the slow pathway conducted earlier than the fast pathway somewhere in between the ventricular and atrium and masked the fast pathway conduction (Fig. 3, Middle panels). There are two possible mechanisms of conduction block in the retrograde fast pathway. First, conduction via the retrograde slow pathway may reach the fast pathway through a connection between the slow and fast pathways, as seen in slow-fast atrioventricular nodal reentrant tachycardia (Fig. 3, Middle left). Second, electrotonic inhibition from a coexisting retrograde slow pathway could interfere with retrograde conduction in the fast pathway. This may occur through subthreshold depolarizations that prolong the refractory period of adjacent cells (Fig. 3, Middle right) [6]. After slow pathway elimination, the retrograde fast pathway could conduct continuously. In a previous report [7], the efficacy and safety of cryoablation for slow pathway ablation at adjacent sites where transient atrioventricular block was observed during cryoablation were shown and the authors suggested the possibility that cryoablation targeted the connection between the AV node and the slow pathway, which could be considered the lower nodal bundle. Simultaneous elimination of both the antegrade and retrograde slow pathways supported the influence on the common pathway. From this second hypothesis, it was reasonable that after the slow pathway elimination, the fast pathway continuously conducted. The drawback of the second hypothesis was explanation of the fast pathway conduction between S1S2 intervals of 350 ms and 400 ms. We speculated that until the S1S2 interval was below 340 ms, the difference in conduction velocity between the retrograde fast and slow pathways was not large enough for the retrograde slow pathway to affect the conduction of the fast pathway. Electrical conduction in the atrioventricular node is not solely determined by connexin 43. Connexin 40 is abundantly expressed in both the compact node and the inferior nodal extension [8]. However, its presence does not consistently correlate with increased conduction velocity [8]. This discrepancy may be due to post-translational modifications affecting gap junctional coupling or to the co-expression of isoforms such as connexin 45 [9], which is also present in nodal tissues. Moreover, conduction velocity is influenced not only by connexin isoform distribution, but also by architectural and electrotonic properties of the pathway, including cellular morphology, ion channel expression, and fiber orientation [10]. This hypothesis could not be confirmed without observation of the electrogram of the atrioventricular node and transitional cells.

Fig. 3.

Upper: A schema describing the mechanism that the slow pathway is masked by the fast pathway. Middle: The slow pathway is possible to be activated faster than the fast pathway in the lower nodal bundle according to the connexin 43 distribution. The earlier activated slow pathway could affect the conduction of the fast pathway, causing a conduction block. There are two possible mechanisms of conduction block in the retrograde fast pathway. First, conduction via the retrograde slow pathway may reach the fast pathway through a connection between the slow and fast pathways, as seen in slow-fast atrioventricular nodal reentrant tachycardia (Middle Left). Second, electrotonic inhibition from a coexisting retrograde slow pathway could interfere with retrograde conduction in the fast pathway. This may occur through subthreshold depolarizations that prolong the refractory period of adjacent cells (Middle Right). Lower: After focal cryoapplications (highlighted by the orange circle) at the slow pathway, the retrograde fast pathway could conduct continuously.

CN, compact node; INE, inferior nodal extension; LNB, lower nodal bundle; TC, transitional cells.

Patient permission/consent statement

This study was approved by the Institutional Review Board of Osaka Rosai Hospital (IRB No. 2024-124). Written informed consent was obtained from the patient for publication of this case and any accompanying images.

Funding

None.

Declaration of competing interest

None.