Propagation in the AV node: A model based on a simplified two-dimensional structure and a bidomain tissue representation

Abstract

A model is proposed to explain mechanisms of propagation in the atrioventricular (AV) node of the heart. The model is based on a simplified two-dimensional anatomic description of the central node region and on a bidomain tissue model for the propagation. The central region is described as a three-tissue compartment model; the proximal tissue composed of ANL cells, the central tissue composed of N cells and the distal tissue composed of NH cells. The central N region is outlined as an unexcitable gap by forcing these cells to behave as depressed cells for which the fast ionic currents are inactivated. This model has allowed the authors to test the electrotonic gap hypothesis, which explains the time-delay properties of the AV node. Typical conduction curves have been obtained, as well as common patterns of Wenckebach blocks. Premature stimulus and resulting mapping of cell responses in the N region of the model show typical membrane potential dissociation in two components. The model has also been submitted to several programmed stimulation protocols in documented anterograde and retrograde conduction. The results show that the model is valid and covers several well known dynamic properties of the AV node.

Progress and Gaps in Understanding the Electrophysiological Properties of Morphologically Normal Cells From the Cardiac Atrioventricular Node

“…Mathematical simulations have been used to investigate important aspects of AVN activity, generally focusing on conduction phenomena such as slowed or blocked A-V conduction, or electrotonic inhibition (e.g. [Urushibara et al, 1987;Ikeda et al, 1990;LeBlanc & Dube, 1993;Liu et al, 1993;Sun et al, 1995;Meijler et al, 1996]). However, whilst such models may have simulated effectively some aspects of AVN function, either they can reproduce macroscopic AVN behavior without the incorporation of single cell activity, or valuable cellular electrophysiological information has emerged since their inception.…”

Conduction delays across the specialized conduction system of the heart: Revisiting atrioventricular node (AVN) and Purkinje-ventricular junction (PVJ) delays

“…Studies of human AVN attributed Wenckebach periodicity to a step-delay mechanism ( 30 , 31 ), and intracellular microelectrode studies on rabbit AVN indicated that the increase in AVN delay with decreasing cycle length could not be explained by decremental conduction but a step-delay located centrally in the AVN ( 32 ). Mathematical models of AVN propagation and Wenckebach behavior included step-delays localized within the node ( 33 , 34 ). These studies expressed the compelling requirement of a step-delay mechanism despite speculation about the nature of and precise location of this component of AV delay.…”

Inherited and Acquired Rhythm Disturbances in Sick Sinus Syndrome, Brugada Syndrome, and Atrial Fibrillation: Lessons from Preclinical Modeling

“…The numerous cellular types composing the AVN are very heterogenous with only the midnodal cells similar to SAN pacemaker ones in terms of HCN4, L-type Cav1.2/1.3, and T-type Cav3.1/3.2 channels. In the peripheral regions, cells organize in multiple, separated bundles with few gap junction connections (specific regional repertoire of Cxs) and voltage-gated Nav1.5 channels (responsible for I Na current), characteristics that likely contribute to the AVN delay onset and maintenance [69,80,[85][86][87][88][89].…”