The Atrioventricular Node Revisited

In a previous publication with Bob Anderson, we compared the nature of the atrioventricular (AV) node (almost 120 years after Tawara’s original description in 1906), with the riddle of Sphynx.¹ In the great Sophoclean tragedy, the denouement of the riddle of Sphinx by mortal Oedipus was initially perceived by the Athenians as a form of hubris against the gods by a human, in the light of its insurmountable difficulty. We thought then that the accumulation of recent anatomical and electrophysiological evidence enabled us to provide the rationale for solving the nodal riddle without committing scientific hubris. However, myths and fiction still prevail in cardiology literature about the nature and conduction properties of the node both during sinus rhythm and tachycardia states.

The Atrioventricular Node does not Possess ‘Fast’ and ‘Slow’ Pathways

In the human heart, the transition between the atrial and ventricular components is found at the site where the apex of the inferior pyramidal space overlaps the inferior extent of the inferoseptal recess of the left ventricle.² This arrangement permits the inferior atrial inputs of the AV node, formed as inferior extensions within the vestibules of the tricuspid and mitral valves, to merge, producing the compact AV node at the apex of the inferior pyramidal space.^3,4 The right inferior extension is a combination of AV canal myocardium and the atrial component of the primary ring. Hence, it retains its ‘specialised’ histological characteristics, and is capable of both fast and slow conduction. The leftward extension is exclusively AV canal myocardium, and is not ‘specialised’ when assessed using standard histological stains, and is capable of only slow conduction.⁵ This notion is also supported by connexin genotyping studies that have shown that poor gap junction connectivity, due to differential expression of connexin isoforms, can result in substantially different conduction properties.^6,7 Thus, both extensions may act as the substrate of a ‘slow’ pathway for a re-entry circuit.^8–10

The cardiomyocytes of the central or right and left parts of the septum also provide inputs to the AV node before the node becomes insulated as the non-branching bundle (bundle of His; Figure 1). These atrial-nodal connections, such as the so-called ‘last connection’, are composed of ordinary working myocardium possessing atrial, or fast, conduction properties.¹¹ Preferential conduction to the node through these inputs provides the anatomical substrate of a ‘fast’ pathway. Thus, the atrial inputs to the node possess fast and slow conduction properties, not the node itself.

There is no Dual Atrioventricular Nodal Conduction

Studies have provided evidence on the conduction velocity in the area of the AV node and its inferior extension, calculating it to between 0.02 and 0.1 m/s in perfused canine and rabbit hearts.^12–14 In the human heart, mathematical modelling of the conduction velocity in these areas has provided a value of 0.04 m/s.¹⁵ For comparison, in the atrium, conduction velocities range from 0.5 to 0.8 m/s,^15–17 and in the His bundle 1.2–1.7 m/s.^15,18 Thus, slow, decremental conduction is a characteristic of the compact node itself and, perhaps, also of the inferior extensions, particularly the left. During sinus rhythm, or during ectopic or paced atrial rhythms, conduction to the node occurs through the fast-conducting, septal inputs (Figure 2). When the rates are fast enough to reach the refractoriness of these inputs, conduction travels through the inferior nodal extensions and jumps may be seen. All this is due to the difference in the conduction properties of atrial inputs; dual conduction of the AV node is a misnomer in scientific terms.

No Nodal Re-entry Exists

The AV node is a small structure, of an average length of 5 mm and width of 3 mm.^19,20 Mathematical modelling has allowed calculation of the length of the slow and fast pathways in typical AV nodal re-entry tachycardia, and indicates that the tachycardia uses a circuit from the AV node to the septal isthmus of an average size of 5–6 cm, confined within the pyramid of Koch.^21,22 These results have been verified by measurements of the relevant areas in histology specimens of human hearts.²² Thus, the tachycardia circuit is not contained within the AV node. It is junctional rather than nodal re-entrant tachycardia.

We do Not, Usually, Ablate the Node for Interruption of Atrioventricular Conduction

AV junctional ablation is perceived as implementing damage to the AV conduction axis by delivering radio frequency at a site where it is possible to record an atrial deflection with the earliest His bundle potential, followed by the ventricular deflection from the right or left septum.^23–29 Alternatively, alleged ‘specific’ ablation is achieved by simply targeting the site with the most prominent His bundle potential.^27,30–42 In patients with AF, in particular, the recording of a His bundle potential is the only feature guiding the chosen site of ablation. Both approaches, however, are unlikely to deliver lesions at the location of the AV node or its extensions.^11,29 Since mapping of the AV node is not yet possible in humans, specific ablation of the AV node can only be achieved by using specific anatomical landmarks in a dedicated procedure.⁴³