Tracking Down the Anatomy of the Left Bundle Branch to Optimize Left Bundle Branch Pacing

Authors, Journal, Affiliations, Type, DOI

• Authors: José-Ángel Cabrera (corresponding); Andreu Porta-Sánchez; Roderick Tung; Damián Sánchez-Quintana
• Journal: JACC: Case Reports 2020;2(5):750–755. "Da Vinci Corner" — an anatomy editorial prompted by a case report in the same issue. Open access (CC BY-NC-ND)
• Affiliations: Unidad de Arritmias, Hospital Universitario Quirón-Salud Madrid and Complejo Hospitalario Ruber Juan Bravo, Universidad Europea de Madrid; Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid; University of Chicago, Center for Arrhythmia Care; Departamento de Anatomía Humana y Biología Celular, Universidad de Extremadura, Badajoz
• Type: Anatomical review / editorial, based on the authors' cadaveric dissection and histological series. No patient cohort, no outcomes, no systematic search
• DOI: 10.1016/j.jaccas.2020.04.004
• Disclosures: all authors report no relationships relevant to the paper

Overview

This paper answers a question the implanting literature usually assumes rather than examines: where, exactly, is the left bundle branch, and what does the lead pass through to reach it? Writing as a commentary on the first reported use of left bundle pacing for painful LBBB syndrome, Cabrera and colleagues — a cardiac anatomist's group — describe the variability of the His bundle's position within the triangle of Koch, the membranous septum's dimensions, and the origin, course and fascicular architecture of the left bundle. Their central argument is that the conventional 0–15 mm below the tricuspid annulus, apical to the His target is only a starting point: the transition from AV node to His is superior in 58.5% and inferior within the triangle of Koch in 41.5% of hearts, the membranous septum ranges from 1 to 9 mm, and the LBB origin ranges from <1 to 14 mm in width. They then enumerate the tissue layers a transseptal lead crosses — endocardium, fat, connective tissue, fibrous insulation, and a bundle 1–25 cell layers thick — and argue that multiple deployments risk permanent RBB injury, perforation, or septal artery damage.

Keywords

anatomy; cardiac electrophysiology; pacing

Key Takeaways

The clinical entry point — painful LBBB syndrome

• Painful LBBB syndrome is rate-related ventricular conduction aberrancy producing disabling chest pain; its true prevalence is unknown, it is confounded by coexisting coronary disease, and it is considered rare
• Described since 1946; treatments have varied and results are inconsistent, suggesting complex pathophysiology — probably dyssynchronous systolic septal motion (early septal radial inward thickening followed by late posterior inward thickening)
• HBP has been used successfully, because lesions causing intra-/infra-Hisian block are proximal and focal, and higher output can penetrate beyond the block to recruit the LBB (longitudinal dissociation). In this issue, Garg et al. reported the first 2 cases treated with left bundle pacing plus AV fusion, with complete symptom relief and marked QRS narrowing
• HBP's limitations, stated as the reason to look more distally: precise His location varies between patients; high and unstable thresholds; abnormal sensing; acute or chronic permanent His damage; and QRS cannot be normalised in almost half of patients in whom HBP is achieved

Locating the His bundle as the reference for LBB pacing

• Huang et al. (2017) placed the initial LBBP site 0–15 mm below the distal tricuspid valve annulus (ventricular aspect) and apical to the His position in RAO 30° — so the fluoroscopic His position is the critical landmark
• ⚠ The landmark itself moves. In the authors' anatomical studies the transition from AV node to His — defined by penetration into the insulating tissues of the central fibrous body, following Tawara — occurred superiorly in 58.5% of specimens and inferiorly within the triangle of Koch in the remaining 41.5%
• Consequently the axis penetrated on the atrial side of the hinge-line in just over half the hearts; in the rest the transition was at the hinge-line or on its ventricular aspect
• This variability also shifts the largest His bundle deflection relative to the septal leaflet and the angiographic vertex of the triangle of Koch — directly relevant to where the operator records His and therefore where they start

The LBB system

• The membranous septum is divided into atrioventricular and interventricular components at the base of the interleaflet triangle between the right and non-coronary aortic leaflets. Its length is 4.6 ± 1.5 mm (range 1–9 mm), and in almost three-fifths of specimens the interventricular component was very small or absent — in which case the LBB fascicles take off rapidly at the hinge of the septal tricuspid leaflet
• The target is wide, unlike HBP's. LBB fibres form a widely distributed subendocardial network — hence the intraseptal approach is easier than hitting the compact His
• The non-branching component runs along the septal crest for only 1–3 mm in 75–85% of cases before giving rise to the fascicles
• The LBB widens as it descends from base to apex; its origin width ranges from <1 to 14 mm, influenced by the His-to-septum relationship
• Three fascicles, not two. The classical bifascicular (anterior/posterior) description is incomplete: histopathology confirms three peripheral networks — a thin elongated anterior radiation, a wider posterior one, and a septal/middle branch that arises from the common LBB, from the anterior or posterior radiation, or from a plexus of both. Durrer's three synchronously activated LV endocardial islands within the first 5 ms are proposed as the terminal areas of these three parts
• The main LBB trunk extends 10–15 mm inferiorly toward the apex, so a transseptal lead usually penetrates the midseptal area — and often reaches the midseptal branch or even a wide posterior ramification
• Histology: the left branch is always subendocardial, related to the nadir of the non-coronary aortic leaflet; the right branch runs intramyocardially 1–2 mm from the RV endocardium. The LBB is separated from the endocardium by variable connective tissue, collagen and smooth muscle

The risk of LBB injury and perforation — what the lead actually crosses

• Place the lead perpendicular to the septum to avoid an excessively apical position where the IVS thickens; this also speeds helical advancement to the left side
• Septal thickness is not a single number. The determinants of injury are:
  1. variable RV endocardial thickness
  2. fatty infiltration in the elderly
  3. connective tissue surrounding the LBB
  4. fibrous tissue related to the patient's conduction disorder
• The LBB itself ranges from 1 to 25 cell layers of specialised conducting myocardium, surrounded by a varying but considerable thickness of left subendocardial collagen and smooth muscle
• The consequence, stated plainly: "multiple lead deployments in this region can result in permanent RBB injury, cardiac perforation and/or damage to a septal artery"
• LBB current of injury may indicate that the tip is in close contact with the left-sided conduction system and possibly penetrating its fibrous insulation
• The intraprocedural guides remain paced ECG morphology, impedance trends and LBB-capture criteria at different outputs

Limitations of the document

Authors' own stated limitations

• None are stated. The paper is an editorial/anatomical review, not a study with a methods-and-limitations section

Additional limitations evident in the paper

• It is a narrative anatomy commentary, not a systematic anatomical study. The specimen counts, sampling method and selection criteria for the dissection/histology series are not given here — the numbers are drawn from the authors' prior publications and presented without denominators for some statements
• The clinical target it endorses (0–15 mm below the annulus, apical to His) is taken from Huang 2017, not derived from the anatomy; the paper's contribution is to explain why that target works on average and why it fails in a substantial minority
• No in vivo correlation. The fluoroscopic-anatomical relationships come from post-mortem hearts in simulated RAO/LPO views, without co-registration to live fluoroscopy, CT, or lead positions in patients
• No outcomes and no procedural data. The claims about perforation, RBB injury and septal artery damage are mechanistic inferences from histology; no rates, denominators or follow-up are supplied
• The "three fascicles" conclusion is contested — the paper itself notes that the size, number, location, configuration and distribution of LBB subdivisions "is still a matter of active debate", and that some authors describe an exclusively bifascicular structure. It presents the three-fascicle model as the histopathological consensus without adjudicating the disagreement
• The clinical case is not the authors' own. The two treated patients belong to Garg et al.; this paper is commentary on them, so the evidence for LBP in painful LBBB syndrome remains a two-case report
• Racial/ethnic and age composition of the specimen series is not reported, which matters for statements about fatty infiltration and fibrous tissue in the elderly
• The practical guidance is qualitative. "Perpendicular", "avoid excessively apical", "beware multiple deployments" — none is operationalised into a depth, angle or attempt limit, which is exactly what the implanting physician needs
• Rating rationale: rated medium. The anatomy is authoritative and directly useful — it supplies the variability data that explain why a fixed fluoroscopic target fails, and the tissue-layer account that underpins perforation risk. But it is a narrative editorial built on a cadaveric series with no denominators or outcomes, and its clinical recommendation is inherited from another paper. It informs technique; it does not test it

Key Concepts Mentioned

• concepts/Left-Bundle-Branch-Area-Pacing — the procedure whose anatomy this paper describes
• concepts/Conduction-System-Pacing — the umbrella category
• concepts/His-Bundle-Pacing — the proximal alternative and the anatomical reference point
• Painful LBBB syndrome — rate-related LBBB causing disabling chest pain; the indication in the index case
• Triangle of Koch / central fibrous body — the landmarks that define where the AV node becomes the His bundle
• Membranous septum — 4.6 ± 1.5 mm (1–9 mm); its interventricular component is minimal or absent in ~60%
• Left bundle branch fascicles — anterior, septal/middle, posterior; three networks rather than two
• Non-branching component — 1–3 mm in 75–85% before the fascicles arise
• LBB current of injury — a sign of contact with, and possible penetration of, the conduction system's fibrous insulation
• Longitudinal dissociation — the mechanism by which proximal pacing can bypass intra-Hisian block
• Septal artery — an additional structure at risk during multiple deployments

Key Entities Mentioned

• José-Ángel Cabrera; Damián Sánchez-Quintana — the anatomists whose dissection and histology series underpin the paper
• Roderick Tung; Andreu Porta-Sánchez — co-authors
• Sunao Tawara — the historical definition of the node-to-His transition used here
• Durrer et al. — the three LV endocardial activation islands within 5 ms
• Huang et al. — originator of the transseptal LBBP technique and its 0–15 mm target
• Garg, Master, Ellenbogen, Padala — the two-case report on LBP for painful LBBB syndrome that prompted this editorial
• Massing and James — right-sided His bundles and His–RBB junction anatomy
• JACC: Case Reports / American College of Cardiology Foundation / Elsevier — publisher

Wiki Pages Updated

• Created: wiki/sources/lbb-anatomy-jacccase-2020.md
• Updated: wiki/concepts/Left-Bundle-Branch-Area-Pacing.md
• Updated: wiki/concepts/Conduction-System-Pacing.md
• Updated: wiki/sourceindex.md
• Updated: wiki/wikiindex.md