Physiology of Left Ventricular Septal Pacing and Left Bundle Branch Pacing

Authors, Journal, Affiliations, Type, DOI

• Authors: Jesse Rijks, MD; Justin Luermans, MD, PhD; Luuk Heckman, MD; Antonius M.W. van Stipdonk, MD, PhD; Frits Prinzen, PhD; Kevin Vernooy, MD, PhD (corresponding), et al.
• Journal: Card Electrophysiol Clin 2022;14(2):181–9. © 2022 The Authors. Published by Elsevier Inc. Open access under CC BY
• Affiliations: Department of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Centre (MUMC+), the Netherlands; Department of Physiology, Maastricht University
• Type: Narrative review of the physiology underlying two conduction-system pacing modalities and the distinction between them. No systematic search, no evidence grading, no meta-analysis
• DOI: 10.1016/j.ccep.2021.12.010
• ⚠ Filename is misdated. The raw file is LVSP-LBBAP-CEPC-2021.md, reflecting the DOI's 2021 submission year, but the journal of record is 2022;14(2):181–9 and the copyright reads © 2022. The slug uses the correct year; raw_path still points at the 2021-named file

Overview

This review is organised around a single physiological distinction that the field sometimes blurs: "the difference between LVSP and LBBP is capture of the LBB in LBBP and only myocardial capture in LVSP." Left ventricular septal pacing places the lead on the left side of the interventricular septum and captures working myocardium near where the Purkinje system normally exits — giving near-physiologic activation without needing to prove conduction-system capture. Left bundle branch pacing aims at the specialised conduction system itself, which in theory yields more synchronous activation, but requires electrophysiological confirmation that the operator has actually achieved it. The review covers normal LV activation, the adverse effects of right ventricular pacing that motivated both techniques, the acute and long-term evidence for LVSP, LBBP in CRT, and then confronts the two directly. Its conclusion is deliberately unresolved: both appear to give (near-)physiologic activation, both show promise in CRT, and more long-term and more head-to-head studies are needed — stated twice in its Clinics Care Points.

Keywords

Left ventricular septal pacing · Left bundle branch pacing · Bradycardia pacing · Cardiac resynchronization therapy · Physiologic pacing

Key Takeaways

Key Points (the review's own)

1. Electrical activation of the left ventricle starts in the left bundle branch, followed by three endocardial areas at the left side of the interventricular septum
2. Right ventricular pacing is associated with adverse effects such as heart failure and atrial fibrillation
3. LVSP results in (near) physiologic activation of the LV and shows promising results in cardiac resynchronization therapy
4. LBBP maintains or restores (in LBBB) LV electrical and mechanical synchrony, with promising results in CRT
5. Implantation techniques for LVSP and LBBP are similar, although more advanced electrophysiological knowledge and equipment is needed to verify LBB capture
6. Theoretically LBBP leads to more synchronous LV activation because it captures the specialised conduction system

Physiologic Activation of the Left Ventricle

• Electrical activation begins in the left bundle branch and proceeds to three endocardial regions on the left side of the IVS — the anatomical basis for placing a lead there rather than at the RV apex
• Mechanical activation follows, and the review treats electrical and mechanical synchrony separately

Adverse Effects of Right Ventricular Pacing (the motivation)

• Pathophysiology of RV pacing and its clinical outcomes are reviewed as the case for physiologic alternatives: heart failure and atrial fibrillation are the named adverse associations
• The search for more physiologic pacing followed recognition of these effects

Left Ventricular Septal Pacing

• The hypothesis behind LVSP: because normal activation exits the Purkinje system at LV endocardial sites on the IVS, pacing near those exit sites should reproduce more physiologic activation
• The founding canine work (Little et al., 1982): pacing on the left side of the IVS reproduced several features of sinus rhythm — the IVS was activated from left to right, pre-ejection LV pressure exceeded RV pressure, and IVS motion was the same as in normal sinus rhythm. Invasively measured LV stroke volume and contractility (LV dP/dtmax) were better during LVSP than RVP in 7 anaesthetised open-chest dogs with healthy hearts
• Covered across acute effects, long-term effects, in the human heart, and in CRT

Left Bundle Branch Pacing in Cardiac Resynchronization Therapy

• LBBP produced a significant QRS shortening from 168 ± 38 ms to 119 ± 12 ms compared with baseline LBBB
• The mechanism of benefit is probably pacing beyond the site of conduction block in the left bundle — the correction of LBBB during LBBP is itself the evidence that it is useful in CRT
• Huang et al. performed LBBP in 63 patients with non-ischaemic cardiomyopathy
• Fig. 2 compares, across baseline LBBB, biventricular pacing, LVSP + RVP, LVSP alone, and HBP/LVSP: QRS duration (both onset-to-end and stimulus-to-end), QRS area by vectorcardiography, and SDAT by ECG belt — with significance markers against baseline, BVP versus LVSP, and LVSP + RV versus LVSP

LVSP or LBBP? — the central comparison

• Implantation technique barely differs, but LBBP demands more advanced electrophysiological knowledge and equipment to verify LBB capture
• Verification methods described: 12-lead ECG for QRS morphology plus LVAT (measured from the pacing spike to the peak of the R wave in V5 or V6); continuous pacing or fixation beats (ectopic ventricular beats caused by lead fixation) to assess morphology; a qR morphology in V1 indicating deep left-sided septal deployment; and septal contrast angiography
• The distinction restated: LVSP captures myocardium only; LBBP captures the LBB
• The number that matters most: actual LBB capture rates in the literature vary from 60% to 90%. So an "LBBP" cohort is never purely LBB capture — a substantial fraction may in fact be LVSP, which complicates every comparison between the two modalities

Clinics Care Points

• LVSP and LBBP both result in (near) physiologic electrical and mechanical activation of the left ventricle
• CRT studies show promising results for both
• More studies on the long-term effects of LVSP and LBBP are needed
• More studies comparing LVSP and LBBP are needed to evaluate and compare both strategies

Limitations of the document

Evident in the review itself

• This is a narrative review with no formal methodology — no search strategy, no inclusion criteria, no risk-of-bias assessment, no quantitative synthesis. Comparative statements rest on selected studies rather than a systematic body of evidence
• The review's own conclusion is that the comparison cannot yet be made. Its Clinics Care Points state twice that more long-term and more head-to-head studies are needed — so the paper is best read as a physiological framework and a statement of an open question, not as evidence favouring either modality
• The central confound is stated but not resolved: LBB capture rates in the literature vary from 60% to 90%. Every study labelled "LBBP" therefore contains an unquantified admixture of LVSP. Since the review's whole thesis rests on the distinction between the two, and the two cannot be reliably separated across published cohorts, comparisons between them are structurally unreliable. The review does not attempt to correct for this
• Much of the mechanistic evidence is from animal models — the foundational LVSP data (Little et al.) are from 7 anaesthetised open-chest dogs with healthy hearts, which cannot represent the failing or dyssynchronous ventricle the technique is deployed in
• The physiological argument is a hypothesis, not a demonstrated outcome benefit. "Theoretically LBBP leads to a more synchronous activation" is stated as theory, and the review supplies no outcome data resolving whether greater electrical synchrony translates into better clinical results
• No tables at all — the extracted file contains none, so the comparative content is entirely prose and figures, which limits how precisely the underlying numbers can be traced
• Conflict of interest: the review carries a dedicated Conflict of Interest section (not reproduced here); Frits Prinzen's department has long-standing research links with device manufacturers in this field

Key Concepts Mentioned

• concepts/Left-Bundle-Branch-Area-Pacing — one of the two modalities reviewed
• concepts/Conduction-System-Pacing — the umbrella category; LVSP is a distinct entity within it
• Left ventricular septal pacing (LVSP) — lead on the left side of the IVS capturing working myocardium near the Purkinje exit sites
• The capture-mechanism distinction — LVSP captures myocardium only; LBBP captures the LBB. The review's organising idea
• LBB capture rate variability (60–90%) — the confound that makes published LBBP cohorts heterogeneous
• LVAT — pacing spike to R-wave peak in V5/V6, the verification measure for LBB capture
• Fixation beats — ectopic ventricular beats caused by lead fixation, used to assess capture morphology
• qR in V1 — indicates deep left-sided septal deployment
• QRS area (vectorcardiography) and SDAT (ECG belt) — electrical synchrony measures used in the figure comparisons

Key Entities Mentioned

• concepts/Left-Bundle-Branch-Area-Pacing — primary concept page
• Maastricht University Medical Centre / CARIM — the authors' institution; Frits Prinzen is a long-standing contributor to ventricular activation and pacing physiology
• Little et al. (1982) — the founding canine LVSP experiments
• Huang et al. — LBBP in 63 patients with non-ischemic cardiomyopathy
• Elsevier Inc. — publisher; the article is open access under CC BY

Wiki Pages Updated

• Created: wiki/sources/lvsp-vs-lbbp-cepc-2022.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