New insights into atrioventricular nodal anatomy, physiology, and immunochemistry: A comprehensive review and a proposed model of the slow-fast atrioventricular nodal reentrant tachycardia circuit in agreement with direct potential recordings in the Koch’s triangle area

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most frequent regular tachycardia in humans. In this review, we describe the most recent discoveries regarding the anatomical, physiological, and molecular biological features of the atrioventricular junction that could underlie the typical slow-fast AVNRT mechanisms, as these insights could lead to the proposal of a new theory concerning the circuit of this arrhythmia. Despite several models have been proposed over the years, the precise anatomical site of the reentrant circuit and the pathway involved in the slow-fast AVNRT have not been conclusively defined. One possible way to evaluate all the hypotheses regarding the nodal tachycardia circuit in humans is to map this circuit. Thus, we tried to identify the slow potential of nodal and inferior extension structures by using automated mapping of atrial activation during both sinus rhythm and typical slow-fast AVNRT. This constitutes a first step toward the definition of nodal area activation in sinus rhythm and during slow-fast AVNRT. Further studies and technical improvements in recording the potentials of the atrioventricular node structures are necessary to confirm our initial results.

Introduction

In 1906, Sunao Tawara,¹ a young Japanese pathologist working in the laboratory of Ludwig Aschoff, provided an excellent morphological description of the atrioventricular (AV) node (AVN), His bundle, and the surrounding atrial myocardium. Three years later, the German pathologist Walter Koch² described the triangle where the AVN lies, which bears his name. In 1909, Lydia DeWitt,³ a pathologist at the University of Michigan, published an article titled “Observations on the sinoventricular connecting system of the mammalian heart.” Using Tawara’s description as her guide, she created an elaborate 3-dimensional wax model that was the first, and most complete, reconstruction of the conduction system of several mammalian species at that time.³ More than 100 years later, however, the structure and function of the AV conduction axis have still not been completely elucidated and, despite numerous investigations and debates among anatomists and electrophysiologists, are still highly controversial.

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most frequent regular tachycardia in humans and is strongly related to the anatomy and physiology of the AV nodal and junctional area. Although AVNRT has been extensively studied, our understanding of its exact mechanism, its precise anatomical site, and the pathways involved in the circuit that sustains the arrhythmia is still incomplete.

However, since the initial description by Tawara,¹ there have been many new insights into the fields of anatomy, embryology, physiology, molecular biology, and electrophysiological mapping of the AV junction. If properly integrated, these could suggest a new hypothesis regarding not only the complex anatomical and functional arrangement of the AVN but also the precise anatomical site of the circuit and the nature of the pathways involved in human AVNRT (Figure 1).

This review describes the most recent discoveries regarding the anatomical, physiological, and molecular biological features of the AV junction that could underlie the typical slow-fast AVNRT mechanisms and that could lead to the proposal of a new theory concerning the circuit of this puzzling and intriguing arrhythmia.