The ongoing mystery of the atrioventricular node

Abstract

The first major insight into the mechanism of atrioventricular (AV) nodal reentrant tachycardia (AVNRT) was the identification of dual AV nodal physiology over 60 years ago.1 Since then, collaborative efforts by anatomists, cardiac surgeons, and electrophysiologists have paved the way for curative procedures ranging from surgical dissection of the AV node to catheter ablation of the “fast pathway” (FP) and later “slow pathway” (SP)—the latter being a mainstay technique of the last 25 years.2 Despite these advancements, however, the exact circuit of AVNRT remains unknown. One of the longstanding controversies regarding the circuit of AVNRT is the debate about the existence of upper (UCFP) and lower (LCFP) common final pathways (distinct AV nodal tissue linking the circuit to the atrium and ventricle, respectively).3,4 “Believers” cite the following to support existence of an UCFP: (1) cases of AVNRT with AV dissociation (complete UCFP block) or retrograde Wenckebach (partial UCFP block), (2) cases of AVNRT coexisting with atrial fibrillation, and (3) atrio-His (AH) intervals (atrial pacing@AVNRT cycle length) > AH intervals (AVNRT) (the ∆AH value reflecting the length of the UCFP).5 Similarly, evidence for a LCFP include: (1) cases of AVNRT with AV block above and below the His bundle recording site, (2) cases of AVNRT despite absence of ventriculoatrial conduction (and therefore inability to entrain tachycardia from the ventricle), and (3) positive ∆HA values. “Disbelievers,” on the other hand, refute existence of an UCFPbasedupon: (1) ability to entrainAVNRT from the coronary sinus with orthodromic capture of atrial electrograms at the His bundle region (indicating separate entrance and exit atrial sites into the circuit and not a single UCFP), (2) heterogeneous retrograde atrial activation patterns during AVNRT (not explainable by a single UCFP), and (3) lack of histological/anatomical data of an insulated tract (or “transitional cell envelope”) connecting FP and SP (both of which are believed to be anatomically discrete atrio-nodal pathways containing transitional cells linking the compact AV node to atrial myocardium).6–8 In this issue of PACE, Iqbal et al. present an interesting case in support of the “Believers”—a young man with AVNRT manifesting both persistent AV dissociation and transient AV block.9 Nodofascicular reentrant tachycardia with AV dissociation was excluded by the presence of AV block. Although an automatic junctional tachycardia was not definitively excluded (discriminating pacing maneuvers from the atrium such as delivery of His-refractory APDs or atrial overdrive pacing were not mentioned but would be unhelpful in the setting of AVdissociation), circumstantial evidence (induction after anAH jump) favored AVNRT. While LCFP block during AVNRT is relatively infrequent, UCFP block is extremely uncommon; and both occurring together is exceptionally rare. The debate between “Believers” and “Disbelievers” continues, but this nice contribution by Iqbal et al. is a welcome addition to the medical literature bringing us one step closer toward unraveling the mystery of the AV node.