1. The aortic root within the cardiac base

The aortic root occupies a central position at the cardiac base. Its three sinuses are named right coronary, left coronary, and non-coronary according to their usual arterial origins, but the root is not supported by a complete circular muscular annulus. Each semilunar leaflet is attached along a crown-shaped hinge. Myocardium supports portions of the right and left coronary sinuses, whereas fibrous continuity between the aortic and mitral valves supports much of the non-coronary and adjacent left-coronary region. The interleaflet triangles extend toward the sinotubular junction and have relations that differ from those of the sinuses themselves [1–4].

The right–non-coronary interleaflet triangle is continuous inferiorly with the membranous septum and central fibrous body. The right coronary sinus overlies the muscular outlet septum and the crest of the ventricular septum, while the non-coronary sinus is related to the interatrial and atrioventricular septal region. These spatial relations place the aortic root beside the penetrating and branching atrioventricular conduction axis. A valve or prosthesis seated in the aortic root can therefore influence conduction tissue without directly entering a cardiac chamber containing that tissue [2–5].

2. Central fibrous body, inferior pyramidal space, and inferoseptal recess

The compact atrioventricular node lies at the apex of the inferior pyramidal space, a fibrofatty region enclosed by the diverging right and left atrial vestibules and the crest of the muscular ventricular septum. From this nodal position, the conduction axis passes superiorly and anteriorly into the central fibrous body. The inferoseptal recess of the left ventricle is the ventricular space beneath the aortic–mitral continuity and adjacent to the central fibrous body; it should not be confused with the inferior pyramidal space or with the inferoseptal process that contributes to its muscular boundaries [3–6].

These structures link the inferior atrioventricular junction to the aortic root. They explain why the conduction axis cannot be understood from the aortic annular plane alone. Proximally, the compact node is inferior and posterior to the root. The penetrating bundle then enters the fibrous tissues and approaches the lower border of the membranous septum. Distally, the branching bundle and proximal left bundle lie on or beneath the crest of the muscular septum, immediately below the right and non-coronary aortic sinuses. The entire relation is oblique and varies from heart to heart [2–6].

3. The membranous septum as an anatomical landmark

The membranous septum is formed by fibrous tissue at the junction of the aortic root, central fibrous body, and ventricular septum. The attachment of the septal tricuspid leaflet divides it into atrioventricular and interventricular components. Above the leaflet hinge, the atrioventricular component separates right atrium from left ventricle; below it, the interventricular component separates the ventricles. The proportions of the two components depend on the level and course of the tricuspid attachment [3,7].

Its lower border is a key landmark because the penetrating or non-branching His bundle commonly courses along this region before the axis branches. Yet neither the length of the membranous septum nor its lowest point defines the conduction axis precisely. The bundle may be deeply embedded, close to the endocardium, or displaced along the muscular crest. The first left-bundle ramifications can arise at different distances from the lower membranous border. Thus, computed tomographic measurement of membranous-septal length estimates the available separation between aortic implantation depth and the conduction tissues, but does not visualize the tissues themselves [2,3,7–10].

4. Penetrating and branching His bundle beneath the root

After losing the final atrial myocardial connection, the penetrating bundle enters the central fibrous body close to the rightward aspect of the aortic root. It then runs as the non-branching bundle beside or beneath the membranous septum before reaching the crest of the muscular ventricular septum. Here the branching component gives rise to the left bundle branch over the left septal surface and continues into the right bundle branch. The relationship is especially close to the nadir of the right coronary sinus and the commissural region between the right and non-coronary leaflets [2–5].

Histological variation is clinically decisive. A bundle protected by a thicker layer of fibrous tissue or myocardium may be relatively shielded from a prosthesis. A superficially placed axis along the membranous or muscular septal crest can be more exposed to radial compression or local trauma. The conduction system also has a blood supply that can be compromised by tissue injury or local oedema. These variables help explain why apparently similar prosthesis positions can produce different conduction outcomes [3,8–10].

The proximal left bundle spreads from the branching axis immediately below this region. Damage need not cause complete atrioventricular block: it may produce new left bundle branch block, fascicular disturbance, or progression of pre-existing right bundle branch block to complete block. The electrical phenotype depends on the longitudinal and transverse extent of injury and on the patient’s baseline conduction reserve.

5. Mechanisms of conduction injury during aortic-valve intervention

Surgical aortic-valve replacement can injure the axis through sutures, debridement, direct trauma, haemorrhage, or oedema near the membranous septum and right–non-coronary commissural region. Transcatheter implantation adds sustained radial force from the frame, displacement of calcified native tissue toward the septum, and interaction of the sealing skirt with the ventricular outflow tract. Balloon predilatation or postdilatation may add transient or permanent trauma. The site of injury is therefore not confined to the final lower edge of the frame [3,8–12].

Conduction disturbance may appear during valve crossing, balloon inflation, release of the prosthesis, or after the procedure. Immediate block suggests direct mechanical interaction, whereas delayed disturbance can reflect evolving oedema, inflammation, haematoma, continued frame expansion, or progressive injury in tissue already diseased. Recovery is possible when the mechanism is transient, but persistent injury to the penetrating or branching axis may require permanent pacing. The timing of an electrocardiographic change should consequently be interpreted as evidence about mechanism, not simply as a binary procedural complication [9–12].

6. Anatomical determinants of risk in TAVI

Implantation depth relative to the membranous septum is one of the most useful anatomical predictors. A frame extending below the aortic annular plane into the left ventricular outflow tract approaches the branching bundle and proximal left bundle. When implantation depth exceeds the membranous-septal length, the prosthesis is more likely to overlap the estimated level of the conduction axis. The relationship is continuous rather than governed by a universal cut-off, and measurement depends on the computed tomographic plane and the point chosen on the prosthesis [8–12].

Risk is modified by the type and radial characteristics of the prosthesis, oversizing, the depth and symmetry of deployment, and the need for postdilatation. Calcification in the basal septum or below the right and non-coronary sinuses can transmit force toward the conduction tissues. A prominent muscular septal crest or short membranous septum may reduce the available margin. Conversely, a long membranous septum does not guarantee safety if the device is implanted deeply or eccentric calcium concentrates pressure on the septum [8–12].

Pre-existing right bundle branch block is clinically important because new injury to the left-sided axis may eliminate the remaining route for ventricular activation. Baseline first-degree atrioventricular block, fascicular disease, or a broad QRS can indicate reduced reserve. These electrical factors do not change the anatomy, but they change the consequence of an anatomically similar lesion. Procedural risk assessment should therefore combine root and septal imaging, planned device geometry, implantation depth, calcium distribution, and the baseline electrocardiogram.

7. Imaging, procedural orientation, and pacing implications

Pre-procedural computed tomography should identify the nadirs of the aortic sinuses, annular plane, membranous septum, muscular septal crest, left ventricular outflow tract, and distribution of subannular calcium. Measurements should be made in reproducible multiplanar reconstructions. The predicted conduction axis can be represented as a three-dimensional zone extending from the inferior border of the membranous septum onto the left septal surface, rather than as a point. This conveys uncertainty honestly and is better suited to procedural planning [8–10].

Fluoroscopic cusp-overlap or other deployment views can help control depth, but the projected annular plane remains a surrogate for a complex crown-shaped root. Intraprocedural electrocardiography and rapid pacing responses supply functional information not visible on imaging. When conduction injury occurs, knowledge of the likely level helps plan pacing: His-bundle capture above or within the lesion may fail, whereas left bundle branch area pacing distal to the injured segment may recruit preserved specialized tissue. After TAVI, however, the frame can alter access, fluoroscopic landmarks, and lead orientation [11–13].

No anatomical metric should be presented as a guarantee. Membranous-septal length, implantation depth, and calcium burden improve prediction at population level, while individual outcomes remain influenced by microscopic bundle position and tissue response. The purpose of anatomy is to define the vulnerable zone, reduce avoidable overlap, and interpret conduction changes—not to imply that the conduction axis can always be seen directly.