Right bundle branch in ventricular septal defects

SUMMARY

This study aims to review the anatomical variations of the right bundle branch (RBB) in normal hearts and various ventricular septal defect (VSD) subtypes through a systematic literature review. Additionally, it seeks to propose hypotheses for optimizing surgical approaches to minimize conduction disturbances during VSD closure, based on anatomical evidence. We performed a systematic literature review of peer-reviewed articles published up to October 2024, focusing on the anatomy of the cardiac conduction system and its variations in association with VSD subtypes. The review encompassed 30 articles, analysing anatomical data from over 100 reported cases of normal and VSD hearts. In the normal heart, the RBB courses posterior to Lancisi’s muscle, which originates at the junction of the anterior-basal and posterior-basal limbs of the trabecular septomarginalis (TSM). In perimembranous inlet VSDs, the medial papillary muscle (MPM) does not reliably indicate the RBB’s course; instead, the RBB runs close to the membranous flap, positioning it on the edge of the VSD. In perimembranous outlet VSDs, the posterior limb of the TSM covers the branching and bifurcating bundles and the base of the RBB, causing these components to deviate towards the left ventricle beneath the defect’s edge, maintaining a distance of 3–5 mm. The RBB then courses intramurally, emerging at the base of the MPM. In tetralogy of Fallot cases with perimembranous outlet VSDs, the RBB consistently courses approximately 2 mm anterior to the MPM in 63–86% of cases. In normal hearts, the RBB runs posterior to Lancisi’s muscle; however, in perimembranous outlet VSDs (especially ToF), the RBB typically courses about 2 mm anterior to the MPM, a critical detail to consider during VSD repair to avoid conduction system injury.

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INTRODUCTION

Postoperative conduction disorders as complications of ventricular septal defect (VSD) closure are commonly reported, particularly in isolated VSD and tetralogy of Fallot (ToF) repairs. Among these complications, right bundle branch block (RBBB) (6.3–43.8%) [1–4], first-degree atrioventricular block (AVB) (14%) [5] and complete AVB (0.1–7.7%) [2, 4, 6, 7] are most often reported. The implications of postoperative RBBB extend to potentially adverse impacts on long-term outcomes, including diastolic dysfunction in the left ventricle (LV) and reductions in the fractional area change of the right ventricle [3, 8, 9].

In VSD closure, the suture lines and primary conduction pathways, such as the right bundle branch (RBB), are typically planned to avoid intersecting along the postero-inferior border of the VSD. After thoroughly examining the literature on anatomical considerations of the RBB and VSD subtypes, we herein propose a comprehensive technique for VSD closure that minimizes dysfunction of the RBB due to injury.

METHODS

To thoroughly review the relationship between the RBB and VSDs, we reviewed the existing literature. Our methodology involved a systematic analysis of anatomical studies, surgical observations and case reports, with a particular focus on the association between the RBB and various VSD subtypes, including perimembranous inlet and outlet defects and their implications in ToF (Table 1).

We performed an exhaustive search of electronic databases, including PubMed, MEDLINE and relevant cardiovascular surgery journals, using targeted search terms such as ‘right bundle branch’, ‘ventricular septal defect’, ‘conduction system’, ‘perimembranous’, ‘Tetralogy of Fallot’, ‘trabecula septomarginalis’, ‘septomarginal trabecula’, ‘Lancisi’s muscle’ and ‘medial papillary muscle’. Our search encompassed all relevant articles published up to October 2024.

The studies selected provided valuable insights into the anatomical considerations of the RBB and its proximity to different VSD subtypes. In addition, we critically examined the available surgical techniques for VSD closure, with a specific focus on strategies that minimize the risk of conduction disorders (particularly RBBB). We paid close attention to studies discussing suture placement, suturing techniques and their impact on the conduction pathways. This thorough analysis enabled us to propose an optimal approach to ensure the safety of the RBB during VSD closure.

RESULTS

Conduction systems in the normal heart

The sinus node, first described by Keith and Flack in 1907 [15], is positioned near the opening of the superior vena cava within the right atrium [16]. It sets cardiac pace via membrane-bound sodium Funny and intracellular calcium-mediate. The atrioventricular (AV) node, initially described by Tawara in 1906 as compact and spindle-shaped, connects directly to the His bundle [17]. The AV node functions as a low-pass filter/signal buffer, moderating rapid atrial rhythm transduction to the ventricles, but also assumes rate-setting of the ventricles during sinus bradycardia. It is located near the AV septum in the lower right atrium, within the Koch triangle, which is delineated by the coronary sinus ostium floor, the tendon of Todaro and the tricuspid valve septal leaflet [18, 19].

The insulated AV junctions allow the conduction axis to traverse the crest of the muscular interventricular septum. When the right atrial wall is removed, the fibroadipose tissue of the inferior pyramidal space is seen interposing between the right atrial wall and the crest of the muscular ventricular septum. The fibrous tissue between the AV valves forms the roof of a recess within the left ventricular outflow tract, providing insulation for the conduction axis as it transitions from the atrial to ventricular components. This roof of the inferoseptal recess lies between the right fibrous trigone and the membranous septum, with these three fibrous structures collectively forming the central fibrous body [19]. The tricuspid valve is slightly displaced towards the ventricular side at the posterior ventricular septum, creating a gap between the tricuspid and mitral valves to form the AV membranous septum (AVMS), which serves as a divider between the right atrium and LV.

As the penetrating bundle advances through the central fibrous body, it moves anteriorly. During this course, the tricuspid valve annulus approaches the mitral valve annulus. This alignment creates the interventricular membranous septum (IVMS), dividing the right and left ventricular chambers. The penetrating bundle is situated within the inferior portion of the IVMS. It then transitions into the branching bundle, which gives rise to the left bundle branch (LBB) and, after further dividing into the bifurcating bundle, ultimately forms the RBB [20] (Fig. 1).

The landmark anatomies of the right bundle blanch

Trabecula septomarginalis

The trabecula septomarginalis (TSM) is derived from compression of apical trabeculations on the right ventricle’s (RV) septal surface. The posterior limb of the TSM terminates beneath the membranous septum, providing structural support in this region. Kurosawa et al. reported that the posterior limb of the TSM exhibited significant variability in its development, which directly influences the position and coverage of the conduction bundle at the AV junction [13]. In contrast, the anterior limb extends in a cephalad direction, reinforcing the surface of the sub-pulmonary infundibulum (Fig. 2A and B). The septal root of the supraventricular crest is situated between these limbs in the normal heart. This supraventricular crest is itself a muscle fold that anatomically separates the tricuspid and pulmonary valves within the roof of the RV [11].

Papillary muscle of the tricuspid valve

Historical and anatomical definitions

The prominent papillary muscle, typically found at the base of the sub-pulmonary infundibulum, was first noted by Lancisi and cited by Tandler in 1913. Luschka, in 1863, referred to this muscle as the papillary muscle of the conus. The presence of several ancillary muscles supporting it was highlighted by Wenink in 1977, who introduced the descriptive term ‘medial papillary complex’ for this group of muscles. The primary muscle within this complex is termed the ‘muscle of Lancisi’ and has a free-standing belly rooted in the septum at the bifurcation point of the TSM into its anterior-basal and posterior-basal limbs [11].

Definitions of the medial papillary muscle (MPM) vary among reports, with Kirklin et al. describing the MPM as the chord connecting both anterior and septal tricuspid valve leaflets to the ventricular septum [21] while Goor et al. position it between the inlet and outlet of the right ventricle, connecting it to the fusion site of the anterior and septal leaflets of the tricuspid valve [22]. According to Soto and Anderson et al., the MPM refers to the papillary muscles that support the commissure or cleft of the anterior and septal leaflets of the tricuspid valve, based on the posterior limb of the TSM [23].

Comparative role of papillary muscles in normal and VSD hearts

The papillary muscles are integral to developing the chordae tendineae and valve leaflets as the endocardial cushion interacts with the myocardium (initiating erosion with undermining) [24], and is connected to the papillary muscles. The chordae tendineae are arranged to support the valve leaflets during this process. In a normal heart, the substantial papillary muscle forms between the right dorsal conotruncal swelling (red-coloured leaflet in Fig. 3A and B) and the lateral endocardial cushion (light-blue-coloured leaflet in Fig. 3A and B), supporting the anterior leaflet of the tricuspid valve. This papillary muscle is referred to as Lancisi’s muscle and, although located between the anterior and septal leaflets, it usually does not cross the membranous septum. It primarily supports the anterior leaflet, which embryologically originates from the right dorsal conotruncal swelling (red-coloured leaflet) at the supraventricular crest (described by Netter [25]) and the lateral endocardial cushion (light-blue-coloured leaflet). The location of Lancisi’s muscle is typically at the base of the bifurcation of the TSM limb (Figs 1–3). Lancisi’s muscle extends few, if any, chordae tendineae to the septal leaflet since the septal leaflet originates from the superior endocardial cushion (yellow-coloured leaflet) and the inferior endocardial cushion (green-coloured leaflet), which embryologically differ from the anterior leaflet [26]. Consequently, Lancisi’s muscle primarily supports the anterior leaflet, while the small chordae tendineae in the inlet portion mainly support the septal leaflet (Fig. 3).

In contrast, in perimembranous VSD, some papillary muscle structure is required to extend from the margins of the VSD to support the septal leaflet, as the normal chordae support is absent due to the defect in that area. This situation leads to a posterior positional shift of the substantial papillary muscles. In this case, these papillary muscles are referred to as the MPM, which then shifts posteriorly to support the defective area and, compared to Lancisi’s muscle in the normal heart, provides support to multiple parts of the tricuspid valve, including both the anterior and septal leaflets (Fig. 4). Consequently, the MPM in a heart with VSD bears a more significant functional burden than Lancisi’s muscle, resulting in differences in its position and role. Therefore, in the normal heart, the basement of Lancisi’s muscle is consistently located at the bifurcation of the anterior and posterior limbs of the TSM; conversely, in hearts with VSDs, MPM location is variable [14].

These differences highlight that Lancisi’s muscle and the MPM are distinct in both embryological development and anatomical function. Thus, in this article, we refer to the papillary muscle as Lancisi’s muscle in a normal heart and MPM in hearts with VSDs.

Right bundle branch in the normal heart

The RBB is a thin, cord-like structure that courses within the septum before emerging in the subendocardium of the RV. It becomes more superficial around its distal third within the TSM and then appears in the subendocardium of the RV at around the base of Lancisi’s muscle. The moderator band crosses the ventricular cavity, carrying part of the ramifications of the RBB (Figs 1 and 5A).

Several studies have provided detailed information about the course of the RBB. Tamiya et al. [27] examined the AV conduction system with 29 specimens, including both normal and malformed hearts. Their findings revealed that the conduction tissue travels below the membranous septum after passing through the dextrous area of the central fibrous body, often skewing into the LV. The bifurcation is located on the septum, approximately 2 mm proximal to the distal end of the membranous part. The RBB descends within the uppermost part of the septum, positioned slightly posterior to Lancisi’s muscle. On average, the RBB lies 0.1 mm anterior to the uppermost accessory papillary muscle (AcPM) and 4 mm posterior to Lancisi’s muscle. The RBB then continues through the moderator band within the TSM, moving towards the anterior papillary muscle and emerging into the subendocardium. Kurosawa et al. also reported on the anatomical course of the RBB, noting that, in 3 normal hearts ranging in age from 2 days to 19 years, the RBB runs posteriorly, approximately 5.3 mm posterior to Lancisi’s muscle [12]. Therefore, in the normal heart, the RBB consistently runs posterior to Lancisi’s muscle (Figs 1 and 5A).

Right bundle branch in ventricular septum defects

Perimembranous inlet VSD

According to the Soto criteria [23], perimembranous VSDs are adjacent to the IVMS remnant and, as such, when the anomalous VSD extends into the inlet muscular septum, it is covered by the septal leaflet of the tricuspid valve. The inferior rim of the VSD is also positioned away from the triangle of Koch and is attached to the tricuspid annulus at a right angle. The anterosuperior rim of this VSD is composed of the posterior limb of the TSM (Fig. 5B), meaning that the MPM, which originates from the posterior limb of the TSM, is based on the superior rim of the VSD (the surgeon’s left-hand border as visible through the right atrium and tricuspid valve). In this context, the location of the MPM can no longer reliably indicate the course of the RBB [21].

The posterior rim of the VSD consists of the fibrous continuity among the aortic, mitral and tricuspid valves, with the membranous flap being either small or absent. Consequently, the RBB runs close to the membranous flap and the AcPM, positioned just on the edge of the VSD [11]. It then continues without branching or penetration along the top of the ventricular septum, slightly covered by the RV muscle. Following this, it transitions into the branching bundle, with the RBB emerging at the base of the AcPM and spreading in a spindle form.

Milo et al. conducted a histological study of 3 cases of perimembranous inlet VSD [21], finding that the penetrating bundle shifted from the right atrium to the left ventricular outflow tract but remained 2 mm from the defect edge. In 2 of the observed hearts, the non-branching bundle was located 3 mm posterior to the defect’s edge when seen from the left ventricular outflow tract; however, the branching bundle and RBB were situated directly on the edge of the VSD.

Perimembranous outlet VSD

Perimembranous outlet defects extend from the central fibrous body and are delimited antero-superiorly by the insertion of the outlet septum into the muscular ventricular septum. Both aortic and tricuspid valves share a fibrous continuity as part of the defective rim and a thin, membranous septal remnant is often visible, appearing as a vestigial tricuspid septal leaflet.

The penetrating bundle is situated at the inferior part of the membranous septum and the top of the ventricular septum. Moving anteriorly, the branching bundle, bifurcating bundle and the base of the RBB are capped by the posterior limb of the TSM. Consequently, these conduction pathways deviate towards the LV. In the normal heart, Lancisi’s muscle is located at the bifurcation of the anterior and posterior limbs of the TSM (Fig. 5A), but in a heart with VSD, the MPM is located posterior to Lancisi’s muscle (though this may vary). The RBB runs intramurally and then emerges at the base of the MPM (Fig. 5C) [20]. Milo et al. studied 2 of these hearts histologically [21], noting that, in both cases, the triangle of Koch served as a landmark for the AV node and penetrating bundle. However, the bundle, which was unbranched, entered the left ventricular outflow tract significantly behind the defect. The branching bundles were located below the edge of the defect, maintaining a distance of 3–5 mm.

A critical consideration in both inlet and outlet defects is the presence of straddling and overriding of the tricuspid valve. Overriding of the tricuspid valve is almost always accompanied by straddling of its tension apparatus. The abnormal inferior insertion of the muscular ventricular septum to the AV junction, rather than the atrial septum, highlights the atypical positioning of the AV conduction axis. The conduction axis, located along the crest of the muscular ventricular septum, is deviated inferiorly due to the overriding. This deviation prevents it from maintaining contact with the regular AV node in the triangle of Koch. [28].

Juxta-arterial VSD

In juxta-arterial VSD, because of the absence of the muscularized cushions, the adjacent leaflets of the aortic and pulmonary valves are in fibrous continuity, producing a fibrous raphe that forms the superior rim of the defect [28]. The MPM arises from the posterior rim of the VSD while the penetrating bundle is located on the inferior part of the membranous septum and at the top of the ventricular septum. The bifurcating bundle and the origin of the RBB run within the muscle bar covered by the thin TSM, with the RBB emerging below the MPM. As a result, the relationship between the conduction system, including the RBB, and the papillary muscles remains similar to a normal heart [20]. According to reports by Tamiya, the position of the RBB in juxta-arterial VSD was observed to be 2 mm posterior to the MPM [27]. However, in certain cases, a juxta-arterial defect may extend to encompass the perimembranous region, becoming bordered by fibrous continuity between the leaflets of the mitral and tricuspid valves. This dual classification as both juxta-arterial and perimembranous positions the conduction axis much closer to the inferior corner of the defect, significantly elevating the risk of injury [28].

Tetralogy of Fallot

In ToF, the RV experiences pressure overload, leading to hypertrophy of the posterior limb of the TSM, which supports the MPM. Although Dickinson et al. found that the conduction axis to be potentially at risk in almost one-third of those having perimembranous defects [29], this hypertrophied posterior limb of the TSM basically covers the branching bundle and RBB, causing these conduction systems to deviate further towards the LV, and an interventricular part of the membranous septum is present in the posterior margin of the defect, the so-called membranous flap [30]. The VIF and infundibular septum are malaligned, deviating to the right side, creating a consequently malaligned VSD. Approximately, one-fifth of cases exhibit fusion of the caudal limb of the TSM with the VIF, leaving the interventricular membranous septum intact. This fusion results in the formation of postero-inferior myocardial tissue, commonly referred to as a ‘muscle bar’, which provides natural protection for the AV conduction tissue. The presence of this muscle bar reclassifies the defect from a perimembranous VSD to a muscular outlet VSD [28]. Notably, similar muscle bars that safeguard the conduction axis can also be found in cases of common arterial trunks.

The MPM is anatomically attached to the posterior limb of the TSM. Kurosawa et al. have made significant findings indicating that the RBB courses approximately 2.4 mm anterior to the MPM (Fig. 5), a relationship present in up to 63% of ToF cases [12, 20]. Tamiya et al. also reported a similar relationship, finding that the RBB took an anterior course of about 2 mm relative to the MPM in 86% of ToF cases [27]. On the other hand, the upper AcPM has more proximity to the RBB than MPM; the RBB reliably runs anterior or underneath the uppermost AcPM, no matter the type of VSD. Importantly, in conditions such as ToF with hypoplasia of the conus septum, the MPM exhibits morphological variations. Van Mierop [31] noted that the uppermost AcPM has often been mistaken for the MPM. Additionally, Kurosawa’s observation highlights that the location of the MPM does not strictly correlate with the precise location of the RBB, likely due to the diverse morphologies exhibited by the MPM [11].

COMMENT

RBB in normal heart vs VSD heart

In a normal heart, Lancisi’s muscle is positioned at the bifurcation of the TSM between its anterior-basal and posterior-basal limbs. The RBB emerges 2.0–5.3 mm posterior to Lancisi’s muscle within the subendocardium, following a consistent course across the RV [12, 27]. This anatomical configuration provides a predictable pathway for the RBB, minimizing the risk of injury during surgical procedures.

In contrast, the course of the RBB in hearts with perimembranous VSD is significantly influenced by the defect’s subtype and area [10, 30]. In perimembranous inlet VSDs, the RBB is positioned near the edge of the defect, particularly close to the membranous flap and AcPM. This proximity increases the risk of RBB injury during surgical repair as the MPM is based on the superior rim of the VSD, a location that does not reliably predict the RBB’s pathway [11, 21].

In perimembranous outlet VSDs, the conduction system deviates towards the LV, with the posterior limb of the TSM covering the base of the RBB. In this scenario, the RBB runs intramurally and eventually emerges at the base of the MPM, presenting a unique set of challenges during surgical interventions.

As discussed, in the normal heart, the base of Lancisi’s muscle is consistently located at the bifurcation of the anterior and posterior limbs of the TSM. However, in hearts with VSDs, the location of the MPM can vary [14]. In short, while the anatomical course of the RBB does not change, the location of the major papillary muscles—Lancisi’s muscle and the MPM—shifts, altering the positional relationship of the RBB’s emergence and major papillary muscle (Fig. 5A and C). The deviation of the RBB in these cases requires careful consideration to prevent conduction system damage during VSD closure [20, 21].

In ToF, the position of the RBB is variable and depends on MPM morphology. Despite this variability, studies show that, in 63–86% of cases, the RBB courses approximately 2 mm anterior to the MPM [12, 20]. This consistent anatomical relationship indicates that, while the RBB’s course is affected by the hypertrophied posterior limb of the TSM in ToF, it still follows a relatively predictable path in relation to the MPM, although variations must be accounted for during surgical repairs.

VSD closure for perimembranous inlet VSD

In the context of perimembranous inlet VSD, the location of the MPM does not reliably indicate the running course of the RBB [21]. The RBB is positioned close to the membranous flap and the AcPM, resting just at the edge of the VSD [11], while the non-penetrating, non-branching bundle is located at the top of the ventricular septum. As the bundle progresses, it transitions into the branching bundle (with the RBB emerging at the AcPM base) and spreads in a spindle-like formation.

When closing this type of VSD, it is crucial to carefully consider the position of the RBB to avoid iatrogenic injury. The suture line should be placed sufficiently away from the edge of the defect to minimize the risk of damaging the conduction system, particularly the RBB, which is vulnerable due to its proximity to the VSD margin.

VSD closure for perimembranous outlet VSD

In perimembranous outlet VSDs, the conduction system components—including the branching bundle, bifurcating bundle and the base of the RBB—are covered by the posterior limb of the TSM. This anatomical configuration causes these structures to deviate towards the LV, positioning them below the edge of the defect at a distance of 3–5 mm [21]. After this deviation, the RBB continues intramurally and emerges at the base of the MPM [20].

During the surgical closure of perimembranous outlet VSDs, it is crucial to ensure that the suture line, particularly along the VSD postero-inferior rim, is placed away from the edge of the defect. The stitches should be placed superficially, maintaining a 2–3 mm buffer, as measured from the inner VSD margin at the postero-inferior rim. Meanwhile, within the RBB danger zone located below the endocardium underneath the MPM, especially when using the interrupted closure technique, two adjacent mattress stitches should be placed with a 2–3 mm gap to avoid injury to the RBB. The stitches should resemble an ‘inverted Y’ to further minimize the risk of conduction system injury (Fig. 4). When a patient presents with a ‘muscle bar’ consisting of postero-inferior myocardial tissue and fusion of the caudal limb of the TSM with the VIF, leaving the interventricular membranous septum intact, the fundamental principles of VSD closure remain applicable. In such cases, the muscle bar serves as a reliable anchoring line for sutures, providing effective protection to the conduction axis and minimizing the risk of trauma [28]. Recent advances in 3D imaging, such as phase-contrast computed tomography, have proved valuable for surgeons during the closure of perimembranous VSDs and Yoshitake et al. demonstrated that this imaging technique could accurately locate the AV conduction axis [32]. In their study, which involved 8 specimens from infants weighing less than 4 kg, all with outlet-type perimembranous VSDs, the images visualized the course of the conduction system from the AV node to the RBB and LBB. The study concluded that placing a longitudinal suture line at least 3 mm from the RV endocardial surface should effectively avoid trauma to the conduction system during VSD repair. In addition, Tretter et al. presented an article exploring advancements in understanding the AV conduction axis using Hierarchical Phase-Contrast Tomography (HiP-CT), a groundbreaking imaging technology. HiP-CT provides unmatched 3D, cellular-level resolution, effectively addressing the limitations of traditional 2D histologic studies and invasive mapping techniques [33].

‘Shallow-bite’ suturing technique for VSD closure

In 2021, we conducted a study comparing the postoperative conduction disorders between continuous and interrupted suturing to repair perimembranous outlet VSD in both ToF and isolated VSD cases [34]. In this study, we reported a continuous ‘shallow-bite’ suturing technique based on holding to the innermost margin of the VSD to close while avoiding interference with any conduction pathways, including the RBB and AVB (Fig. 6). This approach is particularly beneficial in cases of perimembranous outlet-type VSDs, which often have a well-developed posterior TSM limb, as seen in ToF cases.

The traditional interrupted suturing technique involves mattress stitches at fixed horizontal distances from the VSD margin to provide a reliable margin from the conduction system. However, at the location where the RBB approaches the endocardial surface, inadvertent impingement on the RBB by at least some mattress stitches may increase the risk of postoperative RBBB. Anderson et al. [35] further emphasized this risk, noting that sutures placed through the septal crest could potentially damage the conduction axis, particularly in cases where the conduction system branches directly onto the septal crest. The continuous ‘shallow-bite’ suturing technique, on the other hand, is designed to minimize this risk by keeping the suture line separated from the critical conduction pathways.

In our previous study, the implementation of the shallow-bite continuous suturing technique to close outlet-type VSDs in ToF was associated with a reduced incidence of postoperative RBBB compared to the traditional interrupted suturing technique. Later, in 2023, Kim et al. published an article with the same concept as ours, presenting a shallow-bite suturing technique for closing perimembranous VSDs, which reduces the occurrence of RBBB and tricuspid valve regurgitation compared to traditional methods [36].

CONCLUSIONS

In normal hearts, the RBB runs posterior to Lancisi’s muscle while, in perimembranous outlet VSDs (especially in ToF), it typically courses about 2 mm anterior to the MPM. Understanding these anatomical details is crucial for surgeons to avoid conduction system injury during VSD closure.

FUNDING

None.

Conflict of interest: None.

ACKNOWLEDGEMENTS

None.

DATA AVAILABILITY

The data underlying this article are available in the article.

Author contributions

Fumiya yoneyama: Conceptualization; Data curation; Formal analysis; Funding acquisition; Visualization; Writing—original draft. Hideyuki Kato: Supervision; Validation; Writing—review & editing. Bryan J. Mathis: Investigation; Supervision; Writing—review & editing. Fuminaga Suetsugu: Conceptualization; Formal analysis; Investigation. Yuji Hiramatsu: Conceptualization; Formal analysis; Investigation; Supervision; Writing—review & editing.

Reviewer information

European Journal of Cardio-Thoracic Surgery thanks Robert H. Anderson, Nabil Hussein and the other anonymous reviewers for their contribution to the peer review process of this article.

REFERENCES

ABBREVIATIONS

ABBREVIATIONS
 
• AcPM

  Accessory papillary muscle

 
• AVB

  Atrioventricular block

 
• AVMS

  Atrioventricular membranous septum

 
• DORV

  Double outlet right ventricle

 
• IVMS

  Interventricular membranous septum

 
• LBB

  Left bundle branch

 
• LV

  Left ventricle

 
• MPM

  Medial papillary muscle

 
• RBB

  Right bundle branch

 
• RBBB

  Right bundle branch block

 
• RV

  Right ventricle

 
• ToF

  Tetralogy of Fallot

 
• TSM

  Trabecular septomarginalis

 
• VIF

  Ventriculo-infundibular fold

 
• VSD

  Ventricular septal defect