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How to Diagnose, Map, and Ablate AVRT Due to Atriofascicular Conduction Fibers

Babak Nazer, MD; David S. Kwon, MD, PhD; Melvin M. Scheinman, MD

Introduction

In 1938, Ivan Mahaim presented the first description of specialized conduction fibers connecting the atrioventricular node (AVN) or His bundle to ventricular myocardium.¹ These connections have since become known as nodoventricular (NV) or fasciculoventricular (FV) fibers. In 1971, Wellens presented the first electrophysiologic characterization of these tracts,² describing decremental conduction properties associated with these fibers. Several years later, Becker et al.³ identified an AVN-like structure in the tricuspid valve annulus, from which emerged an accessory connection to the anterior right ventricle in a patient with Ebstein’s anomaly. We now understand that fibers may originate from the AVN proper and insert into ventricular muscle (NV) or into either the left or right fascicles (NF) (true Mahaim tracts). However, atriofascicular fibers usually arise from the lateral tricuspid annulus and insert into or are adjacent to the right bundle branch at the right ventricular apex (Figure 10.1). Independently, the Jackman and Haïssaguerre labs have defined these pathways with meticulous mapping studies, following the fibers from their atrial origin to the ultimate ventricular insertion.^4,5 An understanding of these connections, the diagnostic criteria, and EP ablation techniques will be the focus of this chapter.

Surface Electrocardiogram

The ECG for atriofascicular tachycardias typically reveals a left bundle morphology with a late transition and leftward axis (Figure 10.2). In sinus rhythm, the ECG may exhibit only minimal preexcitation. In 2004, Sternick et al. noted a consistent rS or rsR pattern in lead III among patients diagnosed with atriofascicular tachycardias (Figure 10.3).⁶ Although this pattern may be present in some normal ECGs, the atriofascicular tachycardias were never associated with a Q wave in lead I, where subtle preexcitation may be observed. Moreover, the rS pattern changed after successful ablation of the atriofascicular pathway.

Electrophysiology Study

Atriofascicular pathways have special properties. These tracts have decremental conduction properties, and they respond to vagal stimulation and to adenosine administration like the AVN. In fact, dual conduction with double fire due to longitudinal dissociation has also been reported.7 Atriofascicular pathways are unidirectional in the anterograde direction, and, thus, support only antidromic AVRT.

An understanding of these particular properties of atriofascicular pathways is required to correctly diagnose and treat the arrhythmia. In sinus rhythm, the 12-lead ECG manifestation depends on the relative conduction properties between the atriofascicular pathway and the AVN. Consequently, with atrial pacing at faster rates, especially on the lateral right atrial (RA) wall closer to the pathway, a greater degree of preexcitation will emerge with a left bundle branch block (LBBB) pattern. Depending on the relationship between the AVN and the atriofascicular pathway conduction and refractory characteristics, preexcitation is revealed by simple atrial overdrive pacing and also with single atrial extrastimuli. During the transition from AVN conduction to accessory pathway (AP) conduction, the AH-AV interval lengthens while the H-V interval shortens. Once antidromic tachycardia is initiated, the H-V relationship is reversed, and the His bundle recording may be found after the QRS with a constant V-H interval.⁶ In addition, there is reversal of the normal His-to-right bundle branch activation. During preexcitation over the atriofascicular pathway, the right bundle branch precedes the His depolarization, and it is this change in the electrogram that proves conduction over the atriofascicular pathway.

Interestingly, tachycardia variations have been noted. Sternick et al. have reported two distinct cycle lengths (CLs) of atriofascicular tachycardias eliminated by ablation at a single point.⁸ Their findings were explained by either retrograde conduction via dual AVN pathways or by retrograde block in the right bundle branch. Changes in the V-H interval explain the mechanism of variation in TCL, with an increase in V-H interval suggestive of retrograde block in the right bundle branch.⁹

An important maneuver for patients with antidromic APs is to introduce a premature atrial stimulus near the atrial insertion of the AP (on the lateral tricuspid annulus in the case of atriofascicular tachycardia) at a time when the septal atrium has been depolarized.¹⁰ Analogous to the His-refractory ventricular extrastimulus, an atrial premature contraction (APC) delivered when the septal A is committed would be expected to advance the ensuing ventricular depolarization and reset the tachycardia. If this maneuver results in ventricular capture and consequent resetting of the tachycardia, then an atriofascicular pathway is present and participates in the tachycardia (Figure 10.4). Once established, the retrograde limb must be confirmed, whether retrograde via the normal conduction pathway or utilizing a different septal AP. For such a determination, parahisian pacing would reveal the presence of such a septal pathway.

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