Atrioventricular nodal reentrant tachycardia is sustained by functionally distinct inputs to the atrioventricular node and by the nodal axis itself. Its substrate cannot be understood as two isolated cables labelled fast and slow pathways, nor as a circuit confined within the compact node. Human histology, three-dimensional reconstruction, and electrophysiological observations instead support a network in which the inferior nodal extensions, multiple septal inputs, and working atrial myocardium forming the walls of the inferior pyramidal space contribute to the reentrant circuit. This anatomical model explains both the efficacy and the safety of slow-pathway ablation performed at a distance from the compact node and penetrating atrioventricular bundle. [1–8]

1  The atrioventricular node and the bundle of His

The atrioventricular conduction axis is the only normal myocardial connection across the insulating atrioventricular junctions. In the human heart, its atrial component is assembled within the atrial walls at the apex of the inferior pyramidal space. Cardiomyocytes from the tricuspid and mitral vestibules become histologically specialized as the rightward and leftward inferior nodal extensions. These extensions converge to form the compact atrioventricular node. Additional broad inputs arise from the muscular buttress at the base of the atrial septum. The rightward inferior extension is usually longer than the leftward extension, although their lengths, thicknesses, and exact relationships vary between individuals. [2–7,19]

The compact node is not a sharply encapsulated body with only two discrete entry points. Working atrial cardiomyocytes merge gradually with nodal cardiomyocytes. Transitional cells can be identified in some specimens, particularly in younger hearts, but are neither uniformly present nor arranged as a continuous insulated tract. Septal inputs are extensive and progressively diminish as a tongue of fibrous tissue separates the axis from the atrial myocardium. Once this fibrous insulation is complete, the axis becomes the nonbranching atrioventricular bundle. Standard histology shows continuity rather than an abrupt cellular boundary between the compact node and this bundle, although the bundle cells become more closely aligned and tightly packed. [2–7]

The terms node of Tawara and bundle of His have historical value, but the axis is best understood as a continuous structure whose components are defined by their relationships to the atrial myocardium and the plane of atrioventricular insulation. The compact node remains connected to atrial myocardium through its inferior extensions and septal inputs. The penetrating bundle is the short segment encircled by fibrous tissue as it crosses the insulating plane near the central fibrous body. It then continues as the nonbranching bundle along the inferior margin of the membranous septum before reaching the crest of the muscular ventricular septum and dividing into the bundle branches. [4–7,9,19]

The atrioventricular node lies centrally but is also related to epicardial fibrofatty tissues. This apparently paradoxical relationship is explained by its position at the apex of the inferior pyramidal space. The right atrial wall of that space is the region conventionally displayed as the triangle of Koch; the left atrial wall is formed by the mitral vestibule; and the ventricular boundary is produced mainly by the parietal wall of the left ventricle as the ventricular walls diverge towards the cardiac crux. Fibrofatty tissues of the inferior atrioventricular grooves fill the intervening space. Thus, structures that appear adjacent on an endocardial map may be separated by myocardium and extracardiac tissue in three dimensions. [3–7]

2  Anatomical substrate of nodal reentry

Dual atrioventricular nodal physiology describes different conduction and refractory properties, not necessarily two macroscopically visible pathways. The slowly conducting input is associated with the inferior nodal extensions and the atrial myocardium approaching them through the inferior paraseptal vestibules. The rapidly conducting input is related to multiple septal connections entering the compact node more superiorly. These functional domains overlap and vary. Their behaviour is influenced by anisotropy, cell-to-cell coupling, autonomic tone, activation direction, and the refractory properties of the nodal axis. [1,2,6–8]

In typical atrioventricular nodal reentrant tachycardia, antegrade activation usually reaches the node through the inferior slow input and returns to the atrium through the faster septal input. In atypical forms, the sequence and relative conduction times differ. Classification should be based on measured atrial-His and His-atrial relationships rather than assuming that every atypical tachycardia follows a single reversed circuit. The commonly used labels slow-fast, fast-slow, and slow-slow are electrophysiological descriptions; they should not be mistaken for proof of anatomically insulated limbs. [8,10]

Current evidence also argues against a circuit restricted to specialized nodal tissue. Working atrial myocardium within the walls of the pyramid of Koch can participate in the circuit, and multiple atrial breakthroughs may be present. All recognized variants can use the inferior nodal extensions as terminations of the slow input, while the broad septal inputs provide potential fast connections. The size and exact course of the circuit may therefore differ from patient to patient and even according to the direction in which the tachycardia is engaged. [2,6–8]

This model explains why successful ablation usually does not require recording a specialized slow-pathway potential or delivering energy directly to the compact node. The lesion is placed in working atrial myocardium of the inferior paraseptal vestibule, where it interrupts or modifies access to the rightward inferior nodal extension. Junctional acceleration during radiofrequency delivery is a useful physiological response, but it is not a direct image of the node and does not prove that the catheter is touching nodal cardiomyocytes. [1–3,8,11]

3  The membranous septum

The membranous septum is the fibrous component of the cardiac septal structures. It lies at the superior part of the muscular ventricular septum and forms part of the central fibrous body. Viewed from the left ventricular outflow tract, it is usually located at the base of the fibrous interleaflet triangle between the right and noncoronary aortic sinuses. Its shape and dimensions vary substantially. It is continuous with the right fibrous trigone and with the fibrous tissues surrounding the inferoseptal recess of the left ventricular outflow tract. [4,5,7,9,12,19]

The hinge of the septal leaflet of the tricuspid valve divides the membranous septum into atrioventricular and interventricular components. The atrioventricular component separates the right atrium from the left ventricle, whereas the interventricular component separates the two ventricles. These designations depend on the relationship of the tricuspid hinge and should not be inferred from an isolated two-dimensional view. Transillumination and cross-sectional imaging demonstrate both the small size of the structure and its variable position relative to the aortic root and the virtual basal ring. [4,9,12]

At the superior end of the triangle of Koch, the compact node becomes the penetrating bundle as the axis enters fibrous insulation close to the junction of the membranous septum and right fibrous trigone. The nonbranching bundle then courses along the inferior margin of the membranous septum. More distally, the branching bundle is sandwiched between the membranous septum and the crest of the muscular ventricular septum before the left bundle branch spreads subendocardially and the right bundle branch continues within the ventricular septum. This relationship makes the membranous septum a powerful landmark, but not a direct outline of the conduction axis: the length of the nonbranching bundle and its position relative to the septum vary. [4–7,9,12,13]

For ablation of nodal reentry, the membranous septum marks the region that should be respected rather than targeted. A catheter positioned near its right atrial aspect is close to the penetrating axis and carries a greater risk of permanent atrioventricular block. The same anatomy explains conduction injury during surgery, transcatheter aortic valve implantation, and interventions within the left ventricular outflow tract. The adjacency of the aortic root also means that an apparent right paraseptal location may have a close anatomical counterpart in the noncoronary aortic sinus or left ventricular outflow tract. [5,9,12–14]

4  The triangle of Koch

The triangle of Koch is an endocardial landmark on the right atrial wall. Its anterior boundary is the hinge line of the septal leaflet of the tricuspid valve. Its posterior boundary is the tendon of Todaro, a fibrous continuation of the Eustachian valve within the central fibrous body. Inferiorly, the boundaries diverge around the vestibular tissue related to the coronary sinus ostium. The superior apex points towards the central fibrous body and the site at which the conduction axis penetrates the atrioventricular insulating plane. [1–5,19]

The tendon of Todaro is not always visible from the endocardial surface. The Eustachian ridge may be prominent, but its continuation as the tendon frequently requires palpation or knowledge of its expected course. The tricuspid hinge is similarly not identical to the electrically defined tricuspid annulus on a mapping system. The coronary sinus ostium varies in size and may be partly covered by the Thebesian valve. Consequently, the apparent dimensions and orientation of the triangle change with catheter projection, atrial dilation, age, and the morphology of its component landmarks. [1,3,15]

The triangle should not be interpreted as a flat container holding the node immediately beneath every point of its surface. It forms the right atrial wall of the three-dimensional inferior pyramidal space. The compact node occupies the superior apex within the anteroinferior buttress of the atrial septum, while the inferior nodal extensions descend towards the right and left atrial vestibules. The coronary sinus and its ostium are surrounded by the fibrofatty tissues filling the base of the space. This explains why the inferior part of the triangle provides access to the slow input while remaining separated from the compact node. [2–7]

The inferior paraseptal region is sometimes called posteroseptal. In attitudinal orientation it is inferior, not posterior, and much of it is not a true septum. The right and left atrial vestibules are separated from each other and from the ventricular myocardium by the fibrofatty tissues of the inferior pyramidal space. The term septal is therefore useful as an electrophysiological convention but must not be taken to imply a simple shared wall. Inferior paraseptal is a more accurate description when the location is judged within the body. [3–5,16]

5  The septal isthmus and the target for ablation

The usual right-sided target is the septal isthmus: the inferior paraseptal vestibular myocardium between the coronary sinus ostium and the hinge of the septal tricuspid leaflet. Ablation in this region modifies the atrial approach to the rightward inferior nodal extension. A more inferior lesion is generally farther from the compact node and penetrating bundle. Progressive movement superiorly towards the apex of the triangle increases the probability of encountering rapid-pathway inputs and the conduction axis. [1–3,8,11]

The precise target cannot be reduced to a fixed distance from the coronary sinus ostium. The size of the ostium, the position of the tricuspid hinge, the length of the rightward nodal extension, and the dimensions of the inferior pyramidal space differ among patients. Electrograms must be interpreted in this anatomical setting. A small atrial and larger ventricular signal often confirms proximity to the vestibule, but signal ratios alone do not locate the inferior nodal extension. Likewise, a discrete potential in the region may represent complex local atrial architecture rather than a histologically specialized tract. [1–3,6,11]

When right-sided ablation is ineffective, the substrate may be approached from the left atrial mitral vestibule or, in selected circumstances, from within the coronary sinus. This does not imply a separate left-sided disease. The rightward and leftward inferior nodal extensions converge on the same compact node, and both atrial vestibules form walls of the inferior pyramidal space. A left-sided approach can therefore interrupt access to the leftward extension or reach a circuit situated closer to the left vestibular input. The coronary sinus musculature and adjacent coronary arteries must be considered before energy is delivered within the venous lumen. [2,3,6–8]

6  Mapping endpoints and anatomical safety

The procedural objective is durable elimination of inducible clinical nodal reentry while preserving normal atrioventricular conduction. Complete abolition of every sign of dual nodal physiology is not always necessary. A residual single echo beat may be compatible with a successful result when sustained tachycardia is no longer inducible under an appropriate stimulation protocol. Conversely, disappearance of a previously observed slow-pathway potential is not by itself a validated endpoint because such potentials are not specific anatomical markers. [8,11,17]

Junctional rhythm during radiofrequency application reflects engagement of tissue connected to the nodal axis and is commonly observed at effective sites. Rapid junctional acceleration, loss of ventriculoatrial conduction during junctional beats, prolongation of atrioventricular conduction, or new conduction block should prompt immediate reassessment. Cryothermal energy offers the possibility of testing a reversible effect before a permanent lesion, which can be useful when the estimated target is close to the compact node, especially in smaller hearts. The energy source does not remove the need for anatomical localization. [11,17]

The atrioventricular nodal artery most often arises from the dominant coronary artery at the crux and enters the inferior pyramidal space. Its course is variable and brings it close to the nodal region and, in some hearts, to the inferior paraseptal ablation field. The coronary sinus and small venous tributaries, the central fibrous body, and the tricuspid and mitral vestibules complete the local three-dimensional environment. These relationships help explain why apparently small changes in catheter position may alter both efficacy and risk. [1,3,4]

A His bundle electrogram identifies a functional recording site, not the entire anatomical extent of the penetrating and nonbranching bundle. The recording may include far-field components, and the largest His potential does not necessarily lie directly over the narrowest segment of the axis. Anatomical and clinical observations show that the penetrating bundle and the corresponding recording site can lie inferior to the visually estimated apex of the triangle. Nevertheless, tagging the His recording region provides a practical superior safety landmark. Combining it with the coronary sinus ostium, tricuspid hinge, fluoroscopic orientation, and, when available, intracardiac echocardiography produces a more reliable map than any single landmark. [3–5,9,19]

7  Variability and limits of anatomical extrapolation

Age, atrial enlargement, fibrofatty infiltration, ischaemic disease, congenital malformations, and previous intervention can alter the dimensions and tissue composition of the region. The compact node and its extensions retain the same general plan, but their precise location within the triangle of Koch is variable. Ebstein malformation and some congenitally malformed hearts can show unusual nodal extensions or persisting nodoventricular connections. In such settings, the landmarks and pathways described for the normally structured adult heart cannot be transferred without modification. [6,7]

Marked species differences are equally important. The length and course of the nonbranching bundle, the development of the inferior pyramidal space and inferoseptal recess, and the arrangement of nodal cardiomyocytes differ between humans and commonly studied mammals. Experimental findings from rabbit, dog, pig, ox, or mouse hearts can illuminate conduction physiology but should not be mapped directly onto human procedural anatomy. Current human histology and high-resolution phase-contrast tomography provide the most appropriate structural reference. [6,7,18]