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(Circulation. 1998;98:164-174.)
© 1998 American Heart Association, Inc.

Basic Science Reports

Anatomic and Functional Characteristics of a Slow Posterior AV Nodal Pathway

Role in Dual-Pathway Physiology and Reentry

Djamila Medkour, MD; Anton E. Becker, MD; Karim Khalife, BSc; ; Jacques Billette, MD, PhD

From the Department of Physiology, Faculty of Medicine, University of Montreal, Montreal, Canada (D.M., K.K., J.B.) and the Department of Cardiovascular Pathology, Academic Medical Center, University of Amsterdam, the Netherlands (A.E.B.).

Correspondence to Dr Jacques Billette, Pavillon Desmarais #2135, Départ physiologie (Médecine), Université de Montréal, CP 6128, Succ CV, Montréal (Québec), Canada, H3C 3J7. E-mail billettj{at}ere.umontreal.ca

Background—The AV node is frequently the site of reentrant rhythms. These rhythms arise from a slow and a fast pathway for which the anatomic and functional substratum remain debated. This study proposes a new explanation for dual-pathway physiology in which the posterior nodal extension (PNE) provides the substratum for the slow pathway.

Methods and Results—The anatomic and functional properties of the PNE were studied in 14 isolated rabbit heart preparations. A PNE was found in all studied preparations. It appeared as an elongated bundle of specialized tissues lying along the lower side of Koch's triangle between the coronary sinus ostium and compact node. No well-defined boundary separated the PNE, compact node, and lower nodal cell bundle. The electric properties of the PNE were characterized with a premature protocol and surface potential recordings from histologically controlled locations. The PNE showed cycle-length–dependent posteroanterior slow activation with a shorter refractory period (minimum local cycle length) than that of the compact node. During early premature beats resulting in block in transitional tissues, the markedly delayed PNE activation could propagate to maintain or resume nodal conduction and initiate reentrant beats. A shift to PNE conduction resulted in different patterns of discontinuity on conduction curves. Transmembrane action potentials recorded from PNE cells in 6 other preparations confirmed the slow nature of PNE potentials.

Conclusions—The PNE is a normal anatomic feature of the rabbit AV node. It constitutes a cycle-length–dependent slow pathway with a shorter refractory period than that of the compact node. Propagated PNE activation can account for a discontinuity in conduction curves, markedly delayed AV nodal responses, and reentry. Finally, the PNE provides a substratum for the slow pathway in dual-pathway physiology.

Key Words: atrioventricular node • tachycardia • reentry • electrophysiology

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