1. The pulmonary veins and their ending into the left atrium

The pulmonary veins enter the venous component of the left atrium from behind. In the usual arrangement, two veins return from each lung, but neither the number of veins nor the pattern of their atrial endings is constant. A common left venous ending, produced by confluence of the superior and inferior left pulmonary veins before they reach the atrium, is frequent. On the right, separate or additional venous endings—often draining the middle lobe—are also encountered. These variants should be described from cross-sectional imaging or angiography rather than forced into a four-vein model. The superior venous endings are generally more cranial and anterior, whereas the inferior endings are more posterior and lateral. The right-sided endings lie close to the atrial septal surface; the left-sided endings are related to the left atrial appendage and the left lateral ridge [1–4].

The venoatrial junction is a transition rather than a sharply bounded anatomical ring. The ostium is often oval and changes its dimensions during the cardiac cycle. Endocardially, the smooth atrial wall continues into the venous lumen without a fixed circumferential landmark. For anatomical reporting, the ostium can be defined at the plane where the vein joins the atrial contour, while the antrum denotes the surrounding atrial tissue shared by one or more veins. This distinction matters during isolation: a wide antral lesion set lies in atrial myocardium and is not equivalent to a lesion placed at the venous ostium. On the posterior surface, the transition is related to epicardial fat, autonomic neural elements, and the reflections of the serous pericardium. On the endocardial surface, folds and ridges between adjacent endings create carinal regions whose thickness and muscular continuity vary.

Working cardiomyocytes extend for variable distances from the atrium onto the outer aspect of the pulmonary venous wall, forming myocardial sleeves. The sleeves are usually longest and most substantial around the superior veins, but there is marked interindividual and circumferential variation. They commonly taper distally and can end irregularly. Their architecture is not that of a single circular layer. Aggregates of cardiomyocytes can have circular, oblique, or longitudinal preferential orientation, with overlapping arrangements and abrupt changes in direction. Small gaps may separate neighbouring aggregates, and cardiomyocytes may bridge between ipsilateral veins across the carina. These features provide an anatomical basis for anisotropic conduction, nonuniform activation, and residual connections after an incomplete circumferential lesion [2–4].

The carina is not simply empty tissue between two circular ostia. It is a three-dimensional part of the venous atrium in which endocardial and epicardial cardiomyocyte alignments may take different courses. Epicardially placed aggregates can connect the sleeves of adjacent veins or join the posterior atrial wall outside an endocardially defined encirclement. Consequently, an apparently continuous endocardial line can coexist with viable intramural or epicardial conduction. Conversely, local delay recorded within a vein does not prove complete entrance and exit block. The anatomical endpoint remains electrical isolation, assessed independently in each venous component and interpreted with the known possibility of carinal or epicardial bridging.

Several neighbouring structures constrain ablation. The anterior aspect of the left superior venous ending is separated from the appendage by the left lateral ridge. The posterior wall and the venous endings are related to the oesophagus, whose course is mobile and not predicted safely by an assumed midline position. The right superior pulmonary vein is related anteriorly to the superior caval vein and right pulmonary artery, while the right inferior ending lies close to the posterior atrial septal surface. Outside the veins, ganglionated neural tissue is concentrated in variable epicardial fat pads. These relationships explain why the geometry and collateral-risk profile of each encirclement are patient-specific.

For atrial fibrillation ablation, anatomy therefore supports a regional rather than ostial conception of pulmonary venous isolation. Pre-procedural imaging should establish the number and confluence of venous endings, the size of the antra, the carinal configuration, and the relation of the posterior wall to the oesophagus. During mapping, the operator should expect nonuniform sleeve length, overlapping cardiomyocyte orientations, and connections that may not be accessible from a single endocardial point. Durable isolation depends on a continuous and sufficiently transmural lesion set placed in atrial tissue while respecting venous stenosis and extracardiac structures.

When recurrent conduction is identified, its location should be related to this anatomy rather than labelled only by clock position. A gap at a carina, a connection through a common venous vestibule, and a remote epicardial breakthrough are different mechanisms even if their activation appears in the same mapping sector. Likewise, dissociated venous potentials confirm local venous activity but do not by themselves describe every connection of a shared antrum. Precise reporting should name the vein or common ending, the anterior or posterior antral surface, the superior or inferior carina, and whether the recovered pathway was endocardial, intramural, or inferred to be epicardial. This vocabulary makes the anatomical reason for reconnection available for future procedures.

2. The true interatrial septum

The interatrial septum is often portrayed as the entire medial wall of the right and left atria. This is anatomically incorrect. A true septum is a partition that can be removed without entering extracardiac tissue. By that criterion, the true interatrial septum is limited essentially to the floor of the oval fossa, formed by the flap valve of the embryonic oval foramen, together with its immediate line of attachment. Most of the prominent rim seen from the right atrium is an infolding of atrial walls containing epicardial fat—particularly superiorly and posteriorly—not a muscular partition directly separating the two cavities [1,3,5,6].

From the right atrium, the oval fossa appears as a thinner central floor surrounded by a raised muscular rim. The anteroinferior margin approaches the vestibule of the tricuspid valve and the inferior pyramidal space. Superiorly, the apparent rim is continuous with the interatrial groove and the walls adjacent to the superior caval vein. Posteriorly, it reflects a fold between the atria. From the left atrium, the flap valve may be less conspicuous because its surface merges with the smooth septal aspect of the chamber. The left-sided view is bounded anteriorly by the aortic root, posteriorly by the right pulmonary venous component, and inferiorly by the mitral vestibule. These asymmetrical appearances explain why a puncture site that looks central from one chamber may appear eccentric from the other.

The thickness of the fossa floor is variable. It may be thin and translucent, thickened by overlapping tissue, or interrupted by a probe-patent oval foramen. The hinge of the flap valve can create a tunnel whose length and direction vary. The superior and posterior rims can contain fat within the interatrial fold, while the anterior relation is dominated by the transverse pericardial sinus and the non-coronary aortic sinus. These facts are important for transseptal access: tenting of a fold does not reproduce puncture of the true septum, and an excessively anterior trajectory can approach the aortic root. Likewise, an excessively posterior trajectory can place the needle near the posterior atrial wall and pericardial space.

The septal surface also has electrophysiological relevance. Activation recorded from this area may represent cardiomyocytes in the flap valve, adjacent right or left atrial walls, or far-field activity from nearby structures. Broad interatrial conduction does not occur through the whole apparent rim. Preferential interatrial routes include the anterior epicardial bridge formed by Bachmann’s bundle, posterior connections near the caval and pulmonary venous regions, and variable cardiomyocyte continuity at the margins of the oval fossa. These routes should not be conflated with the anatomical limits of the true septum.

For mapping and ablation of left atrial tachycardia, the term septal should therefore be used with precision. A circuit or focal source mapped to the broad medial left atrial wall may be paraseptal, anterior, posterior, or related to the right pulmonary veins rather than located in the true septum. This distinction changes the expected wall composition, thickness, extracardiac relations, and possible access from the contralateral atrium. It also prevents the oval fossa from being treated as a flat disc extending to the surrounding venous and atrioventricular junctions.

In practical terms, the fossa floor is the usual safe gateway to the left atrium, but the optimal puncture position depends on the intended target. Posteroinferior access can facilitate some pulmonary venous and mitral isthmus trajectories; a more anterior or superior puncture may suit other procedures. Intracardiac or transoesophageal echocardiography allows the tented tissue, aortic root, posterior wall, and pericardial space to be considered together. The guiding anatomical principle is simple: identify the true septum, recognise the surrounding folds, and describe neighbouring left atrial regions by what they actually are.

Previous transseptal punctures and surgical or catheter lesions can further alter this landscape. A residual defect may provide easy access but may be poorly aligned with the intended catheter trajectory; a thickened or scarred fossa can require greater force and can redirect the needle toward a fold. Closure devices occupy both surfaces and may leave only a limited true-septal margin. In these settings, reconstruction of the fossa together with the caval veins, aortic root, right pulmonary veins, and mitral vestibule is more informative than selecting a fluoroscopic point called “septal.” The same discipline should be retained when describing tachycardia: a scar beside a septal device is paraseptal unless the circuit demonstrably traverses the remaining floor of the oval fossa.

3. The atrial walls and their thickness

The left atrial wall has no uniform thickness. Measurements depend on the anatomical site, the phase of the cardiac cycle, tissue preparation, imaging resolution, and whether epicardial fat is excluded. Even within a named region, thickness changes over a few millimetres. The roof is generally more substantial than many parts of the posterior wall, whereas the anterior wall can become very thin where the atrium passes behind the ascending aorta. In anatomical series, the anterior wall in this relation may measure approximately 1–2 mm, while portions of the roof can reach several millimetres. Such ranges describe populations, not a safe lesion depth for an individual patient [1–3,7].

The posterior wall is especially heterogeneous. Its superior part blends with the roof and pulmonary venous antra; inferiorly it approaches the coronary sinus and the vestibule of the mitral valve. The wall between the pulmonary venous endings can be thicker than the tissue immediately surrounding some ostia, yet thin zones occur unpredictably. Externally, the posterior wall is related to pericardium, variable fat, and the oesophagus. The thickness of atrial myocardium alone therefore does not define the distance to the oesophageal lumen. The oesophagus can lie leftward, central, or rightward and can change position between imaging and the procedure [8].

The lateral wall is shaped by the appendage, left lateral ridge, and left pulmonary venous component. The ridge is often thick superiorly because it contains overlapping cardiomyocyte aggregates and epicardial structures, but its inferior end may narrow to a thin fold. The appendage itself has thick pectinate trabeculations separated by very thin membranous-looking areas. Inferiorly, the mitral vestibule is usually smooth on its endocardial surface, yet its myocardial thickness and the depth of the adjacent atrioventricular groove vary. The medial wall includes the thin oval-fossa floor but also much thicker surrounding folds and paraseptal tissue.

Wall thickness cannot be separated from muscular architecture. Aggregates of cardiomyocytes sharing a preferential orientation form overlapping layers rather than a set of discrete cables. At one depth the dominant orientation can be circumferential; at another it can be longitudinal or oblique. Interdigitation is prominent at the junctions between the roof, posterior wall, pulmonary venous antra, septal surface, and mitral vestibule. Histological and diffusion-based studies demonstrate that orientation can rotate across the wall, so an endocardial activation pattern need not reveal the course of deeper or epicardial cardiomyocytes [9,10].

This transmural heterogeneity has direct consequences for mapping. A broad wavefront on the endocardium may be driven by a narrower intramural route, while an epicardial aggregate can bypass an apparently complete endocardial line and re-enter through a breakthrough. Low bipolar voltage can reflect scar, poor contact, wavefront direction, thin viable myocardium, or cancellation between components; it is not a direct histological measurement. Similarly, delayed activation on one surface can coexist with more rapid conduction at another depth. High-density mapping improves spatial sampling but does not remove the need to interpret the wall as three-dimensional.

For ablation, a thick wall can prevent transmural injury, whereas a thin wall increases the risk of perforation and extracardiac damage. This apparent contradiction is resolved by regional planning rather than a uniform energy prescription. Imaging-derived thickness, local electrograms, contact assessment, lesion indices, and collateral anatomy should be combined. Repeated applications at a site of persistent conduction may be less rational than asking whether the pathway travels intramurally, epicardially, or through an adjacent structure. The left atrium must be treated as a wall with variable thickness and transmural organisation, not as a thin spherical shell.

Disease changes this normal regional pattern. Dilatation stretches the wall and alters curvature; fibrosis can separate surviving cardiomyocyte aggregates and increase directional dependence of conduction; fatty infiltration and previous lesions can create discontinuities at different depths. Atrial cardiomyopathy is therefore expressed not only as lower voltage but as a reorganisation of conduction within a pre-existing three-dimensional architecture. Comparison of voltage, activation, imaging, and wall thickness should be made region by region. This avoids interpreting every low-voltage area as equivalent scar and helps explain why apparently similar maps may support different tachycardia mechanisms.

4. The interpulmonary component and the atrial septal surface

The interpulmonary component is the posterior part of the left atrial venous component situated between the right and left pulmonary venous endings. It extends from the roof toward the inferior posterior wall and blends laterally with the pulmonary venous antra. It is not a separate embryological chamber and has no sharp borders on the endocardial surface. Its practical boundaries are defined by the venous ostia, the superior roof, and the inferior transition toward the coronary sinus and mitral vestibule. The term is useful because it identifies the tissue commonly designated as the posterior wall without implying uniform thickness or architecture.

The right side of this component approaches the atrial septal surface and the right pulmonary venous endings. The broad medial wall seen from the left atrium includes the flap valve of the oval fossa, folds around its margins, the anterior relation to the aortic root, and posterior tissue continuous with the right pulmonary venous antra. Only the flap valve and its immediate hinge constitute the true septum. The remainder should be described as septal surface, paraseptal tissue, or pulmonary venous wall according to its actual composition [5,6].

Across the interpulmonary component, cardiomyocytes are arranged in overlapping aggregates whose preferential orientation changes with location and depth. Superficial aggregates descending from the roof can fan over the posterior wall and pass between or around the pulmonary venous endings. Deeper, predominantly subendocardial aggregates may take more circumferential or oblique courses and merge with the venous sleeves or mitral vestibule. The boundaries between these patterns are gradual. Intersections and interdigitation create zones in which activation can separate transmurally and then reunite at endocardial or epicardial breakthroughs [9–11].

Anteriorly, the septoatrial region contributes cardiomyocyte alignments that arise near the atrial septal surface and sweep toward the left atrial roof and lateral wall. These alignments are not a discrete insulated tract. They overlap with adjacent myocardium and change orientation through the thickness of the wall. Superiorly and epicardially, they relate to the leftward extension of Bachmann’s bundle, the broad anterior interatrial bridge that crosses the interatrial groove. Bachmann’s bundle remains a valid name for that distinct bridge; it should not be used to imply that all left atrial myocardial alignments are separate conduction cables [12].

For posterior-wall isolation or linear ablation, the interpulmonary component must therefore be considered together with both carinae and the transmural architecture. Endocardial block across a line may be undermined by epicardial cardiomyocytes that pass around its end, by intramural survival within a thicker segment, or by reconnection through venous sleeves. Conversely, unnecessarily extensive ablation of a thin posterior zone increases oesophageal risk. Mapping should identify entrance and exit at the intended anatomical boundaries and should test for local capture rather than relying only on a visual lesion set.

The medial end of a posterior or roof-dependent tachycardia deserves equally precise description. A circuit that appears to involve the “septum” may actually rotate around the right pulmonary venous antrum, a prior transseptal scar, or a fold adjacent to the oval fossa. Comparing left- and right-atrial activation and integrating imaging can distinguish true transseptal participation from adjacent paraseptal conduction. The anatomical model is a continuous but regionally specialised venous atrium: interpulmonary posteriorly, paraseptal medially, and connected through overlapping cardiomyocyte arrangements.

The term “posterior wall” can obscure this continuity if it is treated as a rectangular plate. Superiorly, the interpulmonary component becomes the dome of the atrium; laterally it becomes the venous antra and carinae; inferiorly it blends with the vestibular and coronary-sinus regions. A roof-dependent circuit may therefore descend through one carina, while a posterior-wall circuit may use a narrow surviving channel at the inferior boundary of an isolation box. Labelling the actual anatomical boundary crossed by the wavefront is more informative than naming a geometric loop. It also directs testing to both sides and, when necessary, to the corresponding epicardial or venous relation.

5. The left atrial isthmus and vestibule of the mitral valve

The left atrial isthmus, commonly called the mitral isthmus, is the inferior left atrial corridor between the left inferior pulmonary venous ending and the hinge of the mural mitral leaflet. Its borders are functional rather than those of a discrete anatomical structure. Endocardially, it forms part of the smooth mitral vestibule. Epicardially, it is related to the left atrioventricular groove, the coronary sinus–great cardiac venous junction, the circumflex coronary artery, and variable fat. The corridor is therefore a complex three-dimensional region, not simply the shortest line drawn on an electroanatomical map [13–16].

The endocardial length varies with atrial size, venous anatomy, and the chosen endpoints. The wall is also nonuniform. A muscular shelf or pouch can occur near the pulmonary venous end; elsewhere, the atrial wall may be thin but separated from the coronary venous system by a substantial fat-filled groove. The mitral annulus itself is not a continuous fibrous ring. Along its mural aspect, the leaflet hinge, vestibular cardiomyocytes, fibrous tissue, and basal ventricular myocardium have variable relationships. A line that reaches an electroanatomically defined annulus may not yet have crossed every viable atrial connection.

Cardiomyocyte aggregates in the vestibule tend to follow the atrioventricular junction circumferentially, but oblique and longitudinal alignments enter from the lateral and posterior walls. Their preferential orientation can change between endocardial and epicardial depths. Near the coronary sinus, atrial cardiomyocytes may connect with the myocardial sleeve surrounding the venous wall. These overlapping arrangements can create an epicardial or intramural bypass around an endocardial lesion. The phenomenon is not evidence for an isolated tract; it follows from ordinary working cardiomyocytes arranged across a thick, folded, and variably fatty junction.

The circumflex artery is a major constraint. Its course relative to the coronary sinus and mitral hinge varies, and in some patients it lies close to the intended line. The coronary sinus is likewise not a fixed surrogate for the mitral annulus. Ablation from within the venous lumen may reach epicardial cardiomyocytes or complete a line, but it adds risks of venous injury and thermal damage to the neighbouring artery. Coronary imaging is appropriate when the artery–vein–line relationship is uncertain or when energy delivery within the coronary sinus is being considered.

Bidirectional block across the line is the desired electrophysiological endpoint, yet its proof can be difficult. Differential pacing and activation sequence changes should be interpreted with the possibility of slow residual conduction, epicardial bypass, and far-field venous signals. A very long conduction time around the mitral annulus is supportive but not equivalent to complete block. High-density mapping on both sides of the line can identify a gap; persistent endocardial block with continued passage may point toward the coronary venous sleeve or another epicardial connection.

This anatomy also shapes perimitral tachycardia. The protected central obstacle is not the leaflet alone but the entire atrioventricular junction, and the circuit can use endocardial, intramural, or epicardial levels. The most rational line is not invariably the geometrically shortest: catheter stability, wall thickness, pouches, venous and arterial proximity, and the likelihood of transmural continuity all matter. Successful ablation requires integration of the vestibule with the atrioventricular groove rather than treating them as independent surfaces.

Alternative lines, including an anterior route from the mitral junction toward a pulmonary venous or roof lesion, cross a different architecture and exchange one set of constraints for another. They may avoid the coronary sinus but approach the aortic root, Bachmann-related anterior myocardium, and thicker anterior wall. The choice between an inferior isthmus line and an anterior line should thus follow the demonstrated circuit, existing scars, wall geometry, and neighbouring structures. In either case, block must be proven across the entire three-dimensional line; termination of tachycardia at one point is not sufficient evidence that the anatomical corridor has been durably interrupted.

6. Gross anatomy and architecture of the left lateral ridge

The left lateral ridge is the fold separating the left pulmonary venous component from the left atrial appendage. It is also known clinically as the left atrial ridge or coumadin ridge. Superiorly, it usually begins between the left superior pulmonary venous ending and the appendage; inferiorly, it tapers toward the left inferior vein and mitral vestibule. Its apparent width and prominence depend on the relative size and spacing of the appendage and veins. In some hearts it is broad and rounded, while in others it is narrow or sharply crested [1,3,13].

The ridge is a fold, not a solid muscular bar. Its core can contain epicardial fat, the oblique vein of the left atrium or its ligamentous remnant, autonomic nerves, small vessels, and variable myocardial connections. The endocardial surfaces facing the appendage and pulmonary vein can approach one another closely at the crest while diverging toward the base. This geometry affects catheter contact: an electrode may sit on the crest, slide into the appendage, or engage the venous antrum while appearing similar in a single projection.

Muscular architecture changes from surface to depth. Superficially, cardiomyocyte aggregates related to the leftward extension of Bachmann’s bundle can pass toward the appendage and lateral wall. More deeply and toward the endocardium, alignments associated with the septoatrial region sweep across or into the ridge. Other cardiomyocytes encircle the pulmonary venous ending or continue into pectinate muscles of the appendage. These populations overlap and interdigitate. Their preferential orientations are not separated by insulating planes and should not be represented as several independent cables [9,12,13].

The superior ridge is often thicker because of its myocardial content and the breadth of the fold. The inferior part can be much thinner, even when the endocardial silhouette remains prominent. Consequently, electrogram amplitude and lesion depth can change along a short distance. The transmural course of cardiomyocytes also allows activation recorded on the appendage-facing surface to differ from that on the venous-facing surface. This is relevant when a pulmonary venous encirclement crosses the ridge or when a tachycardia channel is mapped between the appendage and a prior lesion set.

The ridge is a common source of fractionated or multicomponent electrograms. Such signals can result from anisotropic activation through intersecting cardiomyocyte alignments, sequential activation of the two sides of the fold, far-field appendage or pulmonary venous activity, or scar from previous ablation. Fractionation does not by itself identify an arrhythmogenic focus. Pacing, activation timing, local capture, and three-dimensional contact information are needed to determine which tissue is being recorded.

For ablation, the ridge is simultaneously a possible conduction route and a region of procedural constraint. Thick superior tissue can hinder transmurality, while the thin inferior fold can be vulnerable to excessive heating. The appendage must not be inadvertently isolated unless that is an intended and carefully considered endpoint. Epicardial Marshall structures within or beside the fold may sustain conduction despite an endocardial lesion. Recognition of the ridge as a folded, transmurally organised region explains why endocardial geometry alone can underestimate its complexity.

The ridge also provides an important landmark when interpreting left pulmonary venous reconnection. A potential recorded on its venous-facing aspect may belong to antral myocardium, whereas a signal a few millimetres anteriorly may arise from the appendage or a deeper cardiomyocyte alignment. Pacing from both sides of the fold can clarify local capture and direction of conduction. If the ridge participates in a narrow channel after previous ablation, the entrance and exit may lie at different depths or at opposite surfaces. The target should be defined by activation and entrainment evidence, with imaging used to confirm that catheter pressure is applied to tissue rather than to the appendage ostium or venous lumen.

7. Gross anatomy and architecture of the left atrial appendage

The left atrial appendage is the trabeculated component of the morphologically left atrium. It arises from the anterolateral chamber, overlies the left atrioventricular groove, and wraps variably around the left side of the pulmonary trunk. Its ostium lies between the left lateral ridge posteriorly and the mitral vestibule inferiorly. Unlike the smooth venous component, its endocardial surface is dominated by pectinate muscles. External shape is highly variable, with one or more lobes and bends; descriptive shape categories can aid imaging communication but do not replace direct measurement of the ostium, landing zone, depth, and neighbouring structures [2,3,17].

The ostium is usually oval rather than circular. Superiorly and posteriorly it approaches the left pulmonary venous antrum across the lateral ridge. Inferiorly it is related to the mitral vestibule and circumflex coronary artery. The left phrenic nerve descends on the pericardial surface of the left atrium and ventricle and may approach the appendage. The appendage is also close to the pulmonary trunk and left ventricular free wall. These relations are relevant not only to occlusion but also to ablation at the ostium or within the appendage.

Pectinate muscles are branching ridges composed of working cardiomyocytes. They arise from a complex network near the ostium and extend toward the distal lobes. Between them, the wall can be extremely thin. Additional pectinate trabeculations can extend outside the anatomical appendage onto the adjacent left atrial wall, blurring a simple ostial boundary. At the ridge and roof, pectinate cardiomyocytes overlap with broader subepicardial and subendocardial alignments. The result is a three-dimensional architecture in which preferential orientation changes abruptly around trabecular branches and across the wall [9,13].

This architecture affects electrical behaviour. Rapid conduction may follow the long axis of a pectinate muscle, while transverse passage between trabeculations is slower and less uniform. Complex electrograms can represent sequential activation of neighbouring trabeculae or far-field signals from the ridge, mitral vestibule, or left superior pulmonary vein. Scar or ablation at the ostium can create narrow surviving channels capable of sustaining localised re-entry. The appendage can also act as a focal source or as part of a larger macroreentrant circuit.

Electrical isolation of the appendage is therefore a major anatomical intervention, not simply another linear lesion. The ostial circumference includes the lateral ridge, anterior wall, and mitral vestibular relations, each with different thickness and transmural organisation. Epicardial cardiomyocytes can bypass an endocardial line, and incomplete lesions may be proarrhythmic. Complete isolation also removes mechanical activation from a chamber already predisposed to stasis, so the consequences for thromboembolism and the need for anticoagulation or occlusion must be considered in the clinical strategy.

When the appendage participates in tachycardia, activation mapping should distinguish ostial, ridge-related, and distal trabecular sources. Catheter stability is limited by lobes and thin intertrabecular walls, and aggressive manipulation carries perforation risk. Intracardiac echocardiography can define the ostium and catheter relation to the pectinate network. The anatomical objective is to understand whether the appendage is the origin, a passive bystander, or a necessary limb of the circuit before committing to isolation.

The appendage also changes with rhythm and loading. Its ostial dimensions and lobe relationships are dynamic, and atrial enlargement can flatten the ridge or broaden the junction with the atrial body. Thrombus must be excluded before instrumentation, especially when function is impaired. Previous surgical ligation or percutaneous closure can leave a residual neck, an electrical connection, or peri-device tissue capable of supporting tachycardia. Such cases require separate assessment of mechanical exclusion and electrical continuity: one cannot be inferred from the other. Any lesion near a closure device should also take account of device position, residual flow, adjacent circumflex artery, and the thin atrial wall.

8. The septopulmonary and septoatrial regions

The septopulmonary and septoatrial regions describe recurring patterns within the continuous muscular architecture of the left atrium. They are not insulated tracts and should not be depicted as isolated cords. Each consists of aggregates of ordinary working cardiomyocytes that share a preferential orientation over part of their course, overlap neighbouring aggregates, and interdigitate at their margins. The names are topographical: they identify relationships with the atrial septal surface, pulmonary venous component, roof, posterior wall, and mitral vestibule [9–11].

The septopulmonary region is most evident on the epicardial aspect of the left atrial roof and posterior wall. Cardiomyocyte aggregates can arise near the anterior interatrial groove and roof, pass posteriorly, and fan between or around the pulmonary venous endings. Some descend toward the inferior posterior wall and meet circumferentially oriented cardiomyocytes of the mitral vestibule. The arrangement varies markedly between hearts: the dominant alignment may divide around venous ostia, cross the interpulmonary component, or merge with carinal and sleeve myocardium. Its limits are therefore regional rather than those of a dissectible structure [11].

The septoatrial region is expressed more strongly in deeper and subendocardial layers. Cardiomyocyte aggregates arise from the atrial septal surface and adjacent anterior wall and sweep toward the roof, lateral wall, appendage, and mitral vestibule. At the left lateral ridge they can intersect with cardiomyocytes related to the leftward extension of Bachmann’s bundle and with venous or appendage alignments. Around the oval fossa, these arrangements must not be confused with the true septum: most of the surrounding tissue is folded or paraseptal wall.

The two regions overlap extensively. Their apparent separation in a dissection depends on the depth and direction from which the wall is viewed. Across the atrial thickness, preferential orientation can rotate from a more longitudinal or fan-shaped epicardial pattern to a circumferential or oblique endocardial pattern. Intersections may occur without a sharp boundary, and cardiomyocytes from one alignment can merge with those of another. “Transmural architecture” therefore describes both change through depth and continuity between layers; it does not imply the existence of stacked, independently insulated sheets [9–11].

Bachmann’s bundle should be distinguished from these regional patterns. It is a broad, recognisable subepicardial interatrial bridge crossing the anterior interatrial groove. Its cardiomyocytes are tightly aggregated and predominantly parallel as they connect the right and left atria. Once its leftward extension spreads into the roof, appendage, and lateral wall, however, it overlaps the regional left atrial architecture. The name “bundle” remains appropriate for the defined interatrial bridge, but it should not be transferred to the septopulmonary or septoatrial regions [12].

These arrangements provide an anatomical basis for anisotropy, transmural dissociation, and breakthrough. A wavefront can travel rapidly along a preferential orientation but slowly across it. Endocardial activation may therefore be driven by an epicardial route in the septopulmonary region, then appear suddenly at a breakthrough where transmural connections converge. Conversely, an endocardial route associated with the septoatrial region can bypass a lesion whose epicardial surface appears intact. Fibrosis, dilatation, and prior ablation accentuate discontinuities between surviving cardiomyocyte aggregates.

For atrial fibrillation and tachycardia ablation, the practical lesson is to interpret lines and maps in three dimensions. A roof line, posterior box, anterior line, or mitral line crosses different preferential orientations at different depths. Persistent conduction should prompt a search for intramural or epicardial passage and remote breakthrough, not repeated energy at a single endocardial point by default. Describing these structures as regions preserves their anatomical continuity and avoids the misleading expectation of a single cable that can be transected at one site.

This regional model also improves interpretation of activation direction. The same anatomical area may conduct differently when approached from the septal surface, pulmonary veins, appendage, or mitral vestibule because the wavefront meets preferential cardiomyocyte orientations at different angles. Rate and prematurity can further expose functional block at intersections that conduct during sinus rhythm. Thus, a map acquired in one rhythm is not a static portrait of the architecture. Comparing activation during pacing from several sites can reveal the directional behaviour expected from overlapping and transmurally changing orientations.

9. The Marshall structures and their relationships

The Marshall structures occupy the epicardial aspect of the left lateral atrium between the left pulmonary venous component and the appendage. The venous element is the oblique vein of the left atrium, also called the vein of Marshall. These are two names for the same structure and should not be listed as separate veins. The vein descends from the region of the left superior pulmonary vein along the lateral ridge and inferior left atrial wall, joining the coronary sinus near its transition to the great cardiac vein. When the lumen is obliterated, the remnant is described as the ligament of Marshall [13,18,19].

Patency, calibre, length, branching, and exact course are highly variable. A patent vein can be short or can extend cranially with several atrial branches. Its angiographic appearance represents only the venous lumen, not the full Marshall complex. The surrounding fold contains variable fat, small arteries, lymphatics, autonomic nerves and ganglia, and working cardiomyocytes. Even when the venous lumen is absent, neural and myocardial relationships can persist within the ligamentous and fatty remnant.

Cardiomyocyte aggregates around the Marshall vein or ligament have variable connections to the coronary sinus myocardial sleeve, left atrial wall, pulmonary venous region, left lateral ridge, and mitral vestibule. They do not form a universally continuous isolated tract. Some connections are broad, others narrow, and their orientation can change along the cranio-caudal course. Epicardial cardiomyocytes may cross the mitral isthmus or enter the atrium at sites remote from the endocardially earliest signal. These relationships explain how the Marshall complex can participate in focal activity, local re-entry, or an epicardial limb of perimitral tachycardia [18,19].

The autonomic component is also relevant. Sympathetic and parasympathetic nerves and small ganglia accompany the vein and adjacent epicardial fat. Neural activation can modulate atrial refractoriness and pulmonary venous activity, but the density and distribution of these elements vary. The Marshall region should therefore be understood as a neurovascular–muscular complex. A venous intervention can affect several components at once, and its electrophysiological result cannot be attributed automatically to a single mechanism.

The vein crosses the epicardial aspect of the left atrial isthmus before reaching the coronary sinus–great cardiac venous junction. It is related to the circumflex coronary artery, although the order and distance between vein, artery, coronary sinus, and mitral hinge vary. Superiorly it lies within or beside the left lateral ridge, close to the left pulmonary venous antrum and appendage. These relationships account for both its usefulness as an epicardial route and the need to define neighbouring coronary anatomy.

Ethanol infusion into the vein of Marshall can create injury along venous branches and can facilitate interruption of epicardial connections at the mitral isthmus. Its distribution is determined by venous anatomy and cannot be assumed to cover the entire endocardial line. A non-visualised vein may be absent, occluded, too small, or inaccessible; collateral filling may also redirect ethanol. The procedure therefore complements rather than replaces anatomical mapping and demonstration of bidirectional block.

The Marshall region summarises the central message of left atrial ablation anatomy. Endocardial surfaces are only one aspect of a wall whose cardiomyocytes, veins, arteries, nerves, fat, and pericardial relations vary through depth. A residual connection after pulmonary venous, ridge, or mitral isthmus ablation may be intramural or epicardial and may emerge remotely. Atrial cardiomyopathy and prior lesions further remodel this substrate [20,21]. Durable treatment follows from defining the structure that carries conduction and choosing the safest surface from which it can be interrupted.

Terminology should remain equally disciplined in procedural reports. “Vein of Marshall” identifies the patent or cannulated oblique vein; “ligament of Marshall” identifies its obliterated remnant; “Marshall complex” or “Marshall region” includes the accompanying cardiomyocytes, nerves, vessels, fat, and their connections. Failure to distinguish these meanings can make an anatomical observation appear contradictory. A patient may have no usable venous lumen yet retain an electrically important Marshall region, whereas successful venous cannulation does not prove that every associated myocardial connection has been reached.