E Patterson1, B J Scherlag. 1. Department of Medicine, College of Medicine, University of Oklahoma Health Sciences Center and Department of Veterans Affairs Medical Center, Oklahoma City, Okla 73104, USA. eugene-patterson@uokhsc.edu
Abstract
BACKGROUND: Longitudinal dissociation of an anatomic pathway into 2 electrophysiologically distinct pathways has been hypothesized as a basis for localized AV nodal reentry and supraventricular arrhythmias. METHODS AND RESULTS: Extracellular bipolar and intracellular microelectrodes were used to record activation in the superfused rabbit AV junction. A subset of rabbit hearts (n=19 of 72) demonstrated dissociation of the posterior AV nodal input into >/=2 functional pathways. Antegrade AH conduction was maintained by a pathway just inferior to the tendon of Todaro. Rate-dependent conduction block was observed in a second pathway just superior to the tricuspid annulus, allowing retrograde activation of the distal portion of the inferior posterior AV nodal input and leading to the formation of apparent "dead-end" pathways. The superior (antegrade) and inferior (retrograde) pathways were separated by a band of well-polarized but poorly excitable transitional cells. Additional decreases in the atrial cycle length progressively increased the AH interval, further delaying retrograde activation of the inferior pathway, and progressively moved the site of conduction block in the inferior pathway proximally, thus extending the length of the retrograde conduction pathway and allowing circus movement within the transitional cells of the posterior AV nodal connection. CONCLUSIONS: Longitudinal dissociation within the posterior AV nodal input can give rise to localized reentry and AV nodal reentrant tachycardia.
BACKGROUND: Longitudinal dissociation of an anatomic pathway into 2 electrophysiologically distinct pathways has been hypothesized as a basis for localized AV nodal reentry and supraventricular arrhythmias. METHODS AND RESULTS: Extracellular bipolar and intracellular microelectrodes were used to record activation in the superfused rabbit AV junction. A subset of rabbit hearts (n=19 of 72) demonstrated dissociation of the posterior AV nodal input into >/=2 functional pathways. Antegrade AH conduction was maintained by a pathway just inferior to the tendon of Todaro. Rate-dependent conduction block was observed in a second pathway just superior to the tricuspid annulus, allowing retrograde activation of the distal portion of the inferior posterior AV nodal input and leading to the formation of apparent "dead-end" pathways. The superior (antegrade) and inferior (retrograde) pathways were separated by a band of well-polarized but poorly excitable transitional cells. Additional decreases in the atrial cycle length progressively increased the AH interval, further delaying retrograde activation of the inferior pathway, and progressively moved the site of conduction block in the inferior pathway proximally, thus extending the length of the retrograde conduction pathway and allowing circus movement within the transitional cells of the posterior AV nodal connection. CONCLUSIONS: Longitudinal dissociation within the posterior AV nodal input can give rise to localized reentry and AV nodal reentrant tachycardia.