1. Myoarchitecture of the ventricles

The ventricular walls form a continuous three-dimensional myocardial mass rather than a set of anatomically separable sheets, cords, or bands. Within that mass, cardiomyocytes are arranged in aggregates that share a preferential orientation over a limited distance. Adjacent aggregates overlap, branch, and interdigitate, and their dominant direction changes progressively from the epicardium toward the endocardium. The collagenous matrix maintains local alignment while coupling neighbouring aggregates mechanically. For this reason, a dissection plane or an imaging tract should not automatically be interpreted as the boundary of a discrete anatomical layer. The appropriate description is one of regional and transmural changes in orientation within a continuous wall [1–4].

In much of the left ventricular compact wall, the long axes of subepicardial cardiomyocytes follow an oblique trajectory, the mid-wall aggregates tend to become more circumferential, and the subendocardial orientation becomes oblique in the opposite sense. These directions vary continuously with depth and are modified around the base, apex, papillary muscles, ventricular septum, and valvar junctions. The familiar concept of a transmural rotation is therefore useful as a quantitative description, but it should not be converted into a literal model of nested shells. Likewise, helical trajectories describe the changing course of cardiomyocyte aggregates; they do not prove the existence of one isolated “myocardial band” that can be unwrapped from the ventricle without disrupting innumerable muscular connections [2–5].

The compact myocardium and the trabeculated component are also continuous. Trabeculations arise from the endocardial aspect of the wall and merge with papillary muscles, false tendons, and muscular bridges. Their orientation is not random: many follow the local direction of the underlying subendocardial cardiomyocytes, while others cross the cavity or join neighbouring trabeculations. The proportion of compact and trabeculated myocardium varies regionally and between individuals. This normal variability must be distinguished from pathological hypertrabeculation by integrating morphology, wall motion, chamber size, and clinical context rather than applying a single ratio in isolation [3,5,6].

The right ventricular wall is thinner and more coarsely trabeculated than the left. Epicardially, cardiomyocyte aggregates extend from the left ventricle across the anterior and inferior interventricular grooves into the right ventricular free wall. More deeply, longitudinally directed aggregates contribute to the inlet, septomarginal trabeculation, septoparietal trabeculations, moderator band, and papillary muscles. The subpulmonary infundibulum is a free-standing muscular sleeve and has a geometry different from that of the tricuspid inlet. These regional arrangements help the thin right ventricle shorten longitudinally and move its free wall toward the septum, while the left ventricle combines longitudinal shortening, circumferential constriction, and torsion [1,6].

The ventricular septum is not formed by two independent muscular walls placed back to back. It is a curved component of the ventricular myocardial mass, with a relatively smooth left ventricular surface and a markedly trabeculated right ventricular aspect. The septomarginal trabeculation and its continuities belong to the morphologically right ventricle, whereas the left surface is related to the branching atrioventricular conduction axis. At the base, the muscular septal crest approaches the membranous septum and the central fibrous body. At the apex, muscular continuity around the tip of the ventricles makes rigid assignment of every cardiomyocyte aggregate to a right-sided or left-sided “layer” anatomically artificial [2,5,6].

Myoarchitecture and activation are inseparable. The branching bundle system and subendocardial Purkinje network distribute activation rapidly to trabeculations and papillary muscles, after which propagation through working myocardium is influenced by local cardiomyocyte orientation, cell-to-cell coupling, wall thickness, scar, and loading. Conduction is generally faster along than across the prevailing myocardial orientation. A re-entrant circuit may therefore follow anisotropic corridors created by surviving aligned cardiomyocytes within fibrosis, and an apparently focal ventricular arrhythmia can have a deeper origin with more than one endocardial exit. The local electrogram represents this three-dimensional substrate, not merely the point touched by the catheter [3,7].

These principles have practical consequences for ablation. Lesion depth and direction should be judged against the local thickness and transmural architecture rather than a simplified layered diagram. The ventricular outflow tracts, septal summit, papillary muscles, moderator band, and false tendons all provide complex interfaces between compact and projecting myocardium. Catheter pressure can deform these structures, alter contact, and transiently suppress ectopy. Intracardiac echocardiography, computed tomography, or magnetic resonance imaging can show whether the catheter is on compact wall, a trabeculation, a papillary muscle, or an intracavitary bridge. Successful anatomical interpretation requires the electroanatomical map and the imaged substrate to use the same attitudinal coordinates [1,3,8].

A final distinction is important for the atlas. “Orientation” describes the dominant direction of cardiomyocytes within a sampled region; it does not imply that every cell is parallel or that sharp borders exist between directions. “Transmural” describes change through the wall; it does not mean three histologically detachable layers. This vocabulary accommodates dissection, histology, diffusion imaging, and electromechanical observations without forcing them into a single oversimplified model. It also explains why ventricular mechanics remain coordinated despite marked regional differences: local aggregates are mechanically and electrically continuous with their neighbours throughout the myocardial mass.

Apparent architectural planes also depend on the method of observation. Blunt dissection tends to follow cleavage planes within connective tissue and can create smooth surfaces that seem more discrete than they are histologically. Histological sections sample only one plane, whereas diffusion-based imaging estimates dominant orientations within voxels and is affected by resolution and modelling assumptions. These methods are complementary when their limits are acknowledged. A convincing anatomical interpretation should persist across adjacent sections and three-dimensional reconstruction and should preserve the observed continuities between compact wall, trabeculations, septum, and papillary structures [3–5].

2. The inferoseptal process and recess

Three neighbouring structures must be distinguished in the inferoseptal heart: the inferoseptal process of the left ventricle, the inferoseptal recess of the left ventricular outflow tract, and the inferior pyramidal space. The process is myocardium; the recess is an intracavitary extension of the left ventricle; and the pyramidal space is an extracavitary fibro-adipose compartment. Their superior and inferior extremities approach and partly overlap in three-dimensional space, but they are neither synonyms nor subdivisions of one structure. Confusing them obscures the relations of the atrioventricular conduction axis and produces misleading descriptions of “posteroseptal” anatomy [5,7–9].

The inferoseptal process is the basal prominence of left ventricular myocardium at the inferior aspect of the ventricular septal region. It projects between the right and left atrioventricular junctions and forms the muscular ventricular floor beneath the inferior pyramidal space. Its prominence and contour vary. On the left ventricular side, it contributes to the inferoseptal wall near the mitral vestibule and the inferior end of the outflow tract. On the epicardial side, fibro-adipose tissue of the inferior atrioventricular groove lies against it. The term “process” is preferable to treating this myocardium as a true atrioventricular septum, since much of the adjacent region does not directly separate atrial from ventricular cavities [7,9].

The inferoseptal recess is a pocket-like, inferior extension of the left ventricular outflow tract. It descends from the rightward end of the aortic–mitral continuity between the skirt of the aortic leaflet of the mitral valve and the smooth inferoseptal surface of the left ventricle. Its roof is formed largely by fibrous tissue derived from the fused atrioventricular cushions and includes the fibrous continuity between the mitral and tricuspid valvar leaflets. The atrioventricular component of the membranous septum contributes to its rightward boundary. The recess is therefore inside the left ventricular cavity even though, in some sections and projections, its deepest portion lies immediately beside atrial and extracavitary structures [5,8,9].

The inferior pyramidal space is entered from the inferior atrioventricular groove and narrows superiorly toward the central fibrous body. Its walls are formed by the diverging vestibules of the right and left atrioventricular junctions, while its floor is provided by the inferoseptal process. It contains fibro-adipose tissue, the artery to the atrioventricular node, and variable small vascular and neural elements. The coronary sinus and the ostium of the middle cardiac vein are close to its inferior base. The compact atrioventricular node lies at its superior apex, where the conduction axis becomes the penetrating bundle. Thus, the pyramidal space belongs to the epicardial and atrioventricular groove continuum, not to the left ventricular cavity [7,9].

Superiorly, the pointed apex of the inferior pyramidal space approaches the inferiorly directed end of the inferoseptal recess. The fibrous roof of the recess and the muscular crest beneath it create the setting in which the non-branching atrioventricular bundle penetrates the central fibrous body. The bundle then reaches the crest of the muscular ventricular septum and gives rise to the branching component and the right and left bundle-branch systems. Individual variation in the depth of the recess, the height of the inferoseptal process, the length of the membranous septum, and the rotation of the aortic root changes the distance between endocardial targets and the conduction tissues [8–10].

The anatomy is clinically important on several surfaces. From the right atrium, the triangle of Koch overlies the inferior pyramidal space and provides an approach to the atrioventricular node. From the left ventricle, the inferoseptal recess provides an intracavitary route toward the fibrous roof and penetrating axis. From the aortic root, the region is approached through the non-coronary and right coronary sinuses and the myocardium beneath them. From the coronary venous system, the coronary sinus and middle cardiac vein define the inferior epicardial neighbourhood. These routes are close in three dimensions but cross different tissues and carry different risks [1,7–9].

For mapping and ablation, a label such as “inferoseptal” should identify a region, not substitute for structural analysis. An early signal may arise from ventricular myocardium of the process, from tissue beside the recess, from an accessory connection crossing the inferior atrioventricular junction, or from the specialized conduction system. Energy delivered from the left ventricular recess can be separated from the compact node by fibrous tissue yet remain close to the penetrating bundle. Energy within the coronary sinus or middle cardiac vein may be close to the atrioventricular nodal artery or a coronary branch. The safest effective surface is therefore determined by three-dimensional relations rather than by fluoroscopic proximity alone.

The distinction also matters for imaging and surgery. Multiplanar and virtual dissection should show whether a space contains contrast and is continuous with the left ventricular outflow tract, which identifies the recess, or contains fat and vessels outside the cavities, which identifies the inferior pyramidal space. The muscular tissue separating these spaces is the inferoseptal process. This simple tissue-based definition—cavity, myocardium, and extracavitary fat—provides a reproducible framework across specimens, computed tomography, magnetic resonance imaging, and procedural mapping.

The region should not be described as part of the true atrial septum. The floor of the triangle of Koch overlies extracavitary tissue, and the offset between the mitral and tricuspid hinges creates atrioventricular relations without requiring a muscular septum between the right atrium and left ventricle. Likewise, the term central fibrous body should be used for the fibrous complex around the right fibrous trigone and membranous septum, while recognising that the fibrous roof of the inferoseptal recess is a major part of the same continuity. Naming each tissue explicitly prevents a schematic “septal” plane from replacing the real anatomy [5,8–10].

3. Right ventricle and right papillary muscles

The morphologically right ventricle is recognised by its coarse apical trabeculations, septomarginal trabeculation, moderator band, and tricuspid valve with chordal attachments to the ventricular septal surface. In the normally arranged heart it is predominantly anterior and wraps around the rightward aspect of the left ventricle. Its cavity is usefully divided into inlet, apical trabecular, and outlet components. The inlet extends from the tricuspid junction to the papillary muscles; the apical component is heavily trabeculated; and the outlet is the free-standing subpulmonary infundibulum. These parts merge without sharp internal borders, but the distinction clarifies catheter trajectories and the relation of the tricuspid and pulmonary valves [1,2,6].

The septomarginal trabeculation is a broad Y-shaped muscular complex on the right ventricular septal surface. Its superior limbs extend toward the infundibulum and the membranous septal region, while its body descends toward the apex. Septoparietal trabeculations arise from this complex and pass toward the parietal wall of the outflow tract. The moderator band is not the whole septomarginal trabeculation. It is a variable intracavitary bridge extending from the septal complex to the anterior papillary muscle or adjacent free wall. It may be thick or slender, single or branching, and can insert at different levels [6,11].

The tricuspid subvalvar apparatus is more variable than a three-papillary-muscle diagram suggests. A large anterior papillary muscle usually arises from the anteroinferior free wall and commonly receives the moderator band. An inferior papillary muscle or group arises near the diaphragmatic wall. Small medial papillary muscles—also termed septal or conal papillary muscles according to position—arise from the septal surface near the supraventricular crest and membranous septal region. Some hearts show several small medial muscles, while others have direct chordal attachments from the septum with little intervening papillary tissue. The number of muscles, heads, and chordal origins is therefore highly variable [1,6,11].

Chordal support crosses simplistic leaflet territories. Chords from the anterior papillary complex usually reach both the anterior and inferior tricuspid leaflets; the inferior complex contributes to the inferior and septal leaflets; and medial papillary muscles or direct septal chords support the septal and anterior leaflets near their commissure. Commissural chords may arise from small papillary projections between the principal groups. The leaflets themselves are best defined by their hinge lines and zones of apposition rather than by assuming that one papillary muscle belongs exclusively to one leaflet. This interconnected tension apparatus distributes systolic load across the irregular right ventricular geometry [1,6].

The myoarchitecture of the papillary complexes is continuous with the wall and trabeculations from which they arise. Subendocardial cardiomyocyte aggregates sharing a predominantly longitudinal direction pass into the septomarginal and septoparietal trabeculations, through the moderator band, and toward the anterior papillary muscle. The moderator band frequently carries a distal ramification of the right bundle branch, allowing early activation of the anterior papillary muscle and free wall. Smaller Purkinje ramifications spread over other trabeculations and papillary structures. This arrangement explains why mechanical and electrical behaviour cannot be assigned to the muscle alone without considering its septal, parietal, and conduction-system connections [6,11].

Right ventricular papillary muscles, the moderator band, and adjacent trabeculations can generate premature ventricular complexes or ventricular tachycardia. Activation may emerge at the apparent attachment of the moderator band, the body of the band, the anterior papillary muscle, or the adjacent free wall. Because specialized conduction tissue may participate, the surface breakout can be remote from the initiating focus and the QRS may be narrower than expected for ordinary working myocardium. Multiple muscular insertions can also create more than one exit. A focal electroanatomical label should therefore be supported by imaging of the complete intracavitary structure [11,12].

Mapping is technically demanding. A mobile papillary head or moderator band moves rapidly during the cardiac cycle, while coarse trabeculations create recesses that can be mistaken for stable contact. Catheter pressure may suppress ectopy mechanically and obscure the target. Intracardiac echocardiography is particularly valuable for confirming whether the electrode contacts the septal origin, mid-portion, papillary insertion, or free wall. The proximity of the right bundle branch requires caution when energy is delivered near the septal origin of the moderator band or superior septomarginal trabeculation. Repeated lesions based only on an early signal, without defining the structure, risk ineffective treatment or conduction injury [11,12].

The same anatomy affects pacing and structural procedures. Trabeculations may entangle or deflect a lead, and a lead that appears “septal” in one fluoroscopic view may lie on the anterior wall or within a trabecular recess. The moderator band and anterior papillary complex can prevent a catheter from reaching the true apical cavity. During tricuspid intervention, chordal and papillary attachments determine leaflet mobility and device interaction. Cross-sectional imaging, multiple fluoroscopic projections, and intracardiac or transoesophageal echocardiography should therefore be used to translate the two-dimensional silhouette into the actual three-dimensional right ventricular cavity.

Papillary morphology must also be interpreted together with the tricuspid junction. The hinge of the septal leaflet is displaced toward the apex relative to the mitral hinge, while the anterior and inferior hinges follow the irregular right atrioventricular junction. Papillary muscles draw the leaflet zones of apposition toward the ventricular cavity during systole without actively closing the valve. Annular dilatation, right ventricular remodelling, or displacement of papillary attachments can therefore produce regurgitation even when the leaflets and chords remain intact. For device planning, the relevant geometry includes the hinge, commissures, chordal fan, papillary bases, moderator band, and right coronary artery in the atrioventricular groove.

4. Left ventricle and left papillary muscles

The morphologically left ventricle has fine apical trabeculations, a smooth septal surface, extensive fibrous continuity between the aortic and mitral valves, and two principal papillary-muscle groups. Its inlet, apical trabecular, and outlet components share a common cavity. The aortic leaflet of the mitral valve separates inflow from outflow dynamically, but there is no muscular partition comparable with the supraventricular crest of the right ventricle. The outlet narrows between the septum and the aortic leaflet toward the aortic root, while the apical trabecular component continues from the inlet toward the apex without a sharp anatomical boundary [1,2,5].

In attitudinal orientation, the principal mitral papillary-muscle groups are inferoseptal and superolateral. The traditional names “posteromedial” and “anterolateral” describe the heart removed from the body and standing on its apex; they do not accurately represent the muscles in the living thorax. Each group may consist of one trunk, several trunks, or a broad base dividing into multiple heads. Their tips project toward the ventricular cavity, and their bases commonly merge with a network of trabeculations before those trabeculations join the compact wall. It is therefore inaccurate to assume that every papillary muscle attaches directly and uniformly to a smooth solid wall [5,13,14].

Both principal papillary groups provide chords to both mitral leaflets. The leaflet adjacent to the aortic root is best termed the aortic leaflet, and the opposite leaflet the mural leaflet. Chords inserting at the free edge limit prolapse; intermediate or “strut” chords attach to the ventricular surface of the aortic leaflet and transmit substantial load; and basal chords attach closer to the hinge, particularly on the mural leaflet. Commissural chords arise from papillary heads directed toward the two zones of leaflet apposition. This crossed support means that papillary anatomy cannot be reduced to a one-muscle–one-leaflet scheme [5,13].

Cardiomyocyte aggregates of the papillary muscles are continuous with those of the adjacent subendocardial wall and trabecular network. Their preferential orientation follows the long axis of each papillary trunk but fans and interdigitates at the base. False tendons may connect a papillary muscle to the septum, opposite wall, apex, or another papillary muscle. Some are predominantly muscular, some contain fibrous tissue, and some carry ramifications of the left bundle-branch and Purkinje system. The specialized conduction network spreads as a branching subendocardial mesh rather than as two invariant cables. Its variable relations help explain the rapid activation of papillary structures and the diversity of ventricular exits [3,5].

The inferoseptal and superolateral groups differ in their vascular environment, but broad rules should not be mistaken for individual anatomy. The superolateral group often has access to more than one arterial source, whereas the inferoseptal group more often depends on branches associated with the inferior interventricular or circumflex circulation. Coronary dominance and intramyocardial branching substantially modify this pattern. Ischaemia or infarction can therefore produce papillary dysfunction, elongation, fibrosis, or rupture, but mitral regurgitation is frequently caused by displacement of an intact papillary complex during ventricular remodelling rather than by isolated papillary necrosis [13,14].

Left ventricular papillary muscles are recognised sources of premature ventricular complexes and ventricular tachycardia. The arrhythmogenic substrate may be focal, related to the Purkinje system, or associated with scar at the papillary base. Because the muscle has several heads, trabecular attachments, and a broad intramural base, activation can reach the endocardium through different exits and the QRS morphology may change spontaneously or during ablation. The earliest accessible electrogram may lie on one surface while the true focus is deeper within the muscle or at its attachment. A unipolar QS pattern and local prematurity are useful, but neither alone proves that the complete substrate has been reached [15].

Catheter stability is a central challenge. A papillary muscle moves in translation, rotates, and changes shape during systole; an electrode can slide from a head to an adjacent chord or ventricular wall while appearing stable fluoroscopically. Intracardiac echocardiography allows direct identification of the target head, confirms contact, and distinguishes the papillary muscle from neighbouring trabeculations and false tendons. Three-dimensional imaging can also show whether a lesion set is being applied circumferentially around a base or focally to one exit. Excessive energy near chordal insertions should be avoided because structural injury may impair valve competence [13,15].

Papillary-muscle anatomy should be interpreted as a functional complex comprising ventricular wall, trabecular base, papillary trunks and heads, chordae tendineae, mitral leaflets, and the subendocardial conduction network. Alteration of any component changes tension, activation, or both. For the electrophysiologist, the useful unit is consequently larger than the apparent intracavitary prominence. For the imager and surgeon, the same principle prevents a normal multiple-headed muscle or false tendon from being misclassified as a mass. Attitudinal naming, definition of the individual morphology, and integration of imaging with electrograms provide the most reproducible description.

Normal variants include bifid or multiheaded papillary muscles, accessory papillary projections, direct chordal origins from the ventricular wall, and muscular or fibromuscular false tendons. Their significance depends on function and context. A broad papillary base may contain an arrhythmic focus that is inaccessible from a single head, whereas a thin accessory projection may be a bystander. In mitral intervention, the height and separation of the muscles influence the chordal corridor and the risk of left ventricular outflow obstruction. Describing the individual architecture is therefore more informative than forcing every heart into a two-conical-muscle model [5,13,14].