Atrioventricular Nodal Reentry; What Have We Learned from Ablation Techniques?

Abstract

While atrioventricular (AV) nodal modification is highly successful in curing AV nodal reentry controversy remains as to the functional and/or anatomical nature of the reentrant circuit. The concept of dual AV nodal pathways as the underlying physiology of AV nodal reentry has focused attention on the fact that successful selective “fast” and/or “slow” pathway ablation can be accomplished by delivering radiofrequency (RF) energy at spatially separate sites (the apex and base of the triangle of Koch). The ability to selectively ablate these two pathways has led to the concept that the fast pathway and slow pathway are discrete anatomical structures with the intervening atrium required to complete the circuit. The proposed route would be from the compact AV node to the atrium over the fast pathway with sequential atrial activation from the fast to the slow pathway and then back to the compact node at the apex of the triangle of Koch. However, much evidence is available to suggest that this construct is too simplistic and that AV nodal reentry is far more complex. As will be noted below, there has never been documentation of sequential activation of the atrium that is compatible with this simple construct. The purpose of this chapter is to review the data obtained over the past decade during mapping and ablation of AV nodal tachycardia and experimental studies of the AV junctional region that suggest the need to reconsider our concepts of AV nodal reentry and to accept the fact that, just because ablation at apparently disparate sites is successful, this provides limited information as to the underlying mechanism of the arrhythmia. Recent data to be reviewed below suggest the primacy of the roles that atrionodal coupling and non-uniform anisotropy must play in the mechanism of AV nodal reentry.