title: Electrophysiology of the A-V node in relation to A-V nodal reentry.
abstract: During A-V nodal reentry the impulse is supposed to travel through two distinct pathways in the A-V nodal junction, called slow and fast pathways. Clinically, catheter ablation of these pathways has been very successful in abolishing A-V nodal reentrant tachycardias. So-called double potentials have been used as a marker for the slow pathway, and the occurrence of accelerated junctional rhythms (AJR) following ablation is an indicator of successful destruction of the slow pathway. In Langendorff, blood-perfused porcine and canine hearts, extensive mapping of extracellular potentials, combined with microelectrode recordings, was carried out to answer the following questions: 1) what is the origin of double extracellular potentials? 2) what causes post-ablation AJR? 3) what is the activation pattern of the AV junction during ventricular echoes? 1) Two types of double potentials were found: a low-frequency component followed by a high-frequency deflection, the LH potential was caused by asynchronous activation of the sinus septum above the coronary sinus and the region between the coronary sinus orifice and tricuspid annulus, where the L component is a far field potential. HL potentials (high-frequency deflection followed by a low frequency component) were caused by asynchronous activation of atrial cells and cells with AV nodal characteristics at the same location. These cells were present around the entire tricuspid annulus, and were not part of the compact node. The proximity of LH potentials to the slow pathway is probably serendipity, HL potentials could represent the slow pathway. 2) Two types of AJR could be initiated both by application of radiofrequency energy and by heat: a regular rhythm that progressively accelerated and an irregular rhythm. The discrete sites where heat application induced AJR did not correlate with areas showing double potentials, nor with exit regions during ventricular pacing. They were close to the compact node and the underlying mechanism was accelerated phase 4 depolarization in single or multiple foci, the latter accounting for irregular AJR. The association between presence of AJR and successful slow pathway ablation is probably also serendipity. 3) During ventricular pacing, two separate areas of earliest atrial activity were found. When ventricular echoes were induced by premature stimulation, the retrograde impulse activated both atrial exit sites and still returned in the ventricles as an echo. Thus, no evidence was found that atrial tissue forms part of the reentrant circuit.
authors.affiliation: Department of Clinical and Experimental Cardiology, University of Amsterdam, The Netherlands.
authors.forename: M J
authors.initials: MJ
authors.lastname: Janse
authors.forename: M A
authors.initials: MA
authors.lastname: McGuire
authors.forename: P
authors.initials: P
authors.lastname: Loh
authors.forename: B
authors.initials: B
authors.lastname: Thibault
authors.forename: M
authors.initials: M
authors.lastname: Hocini
authors.forename: J M
authors.initials: JM
authors.lastname: de Bakker
mesh_terms: D000818:Animals; D001283:Atrioventricular Node / Q000502:physiology* / Q000601:surgery; D017115:Catheter Ablation; D004285:Dogs; D004594:Electrophysiology; D006329:Heart Conduction System / Q000503:physiopathology; D013611:Tachycardia, Atrioventricular Nodal Reentry / Q000503:physiopathology*; D013613:Tachycardia, Ectopic Junctional / Q000503:physiopathology