Evaluation of the Criteria to Distinguish Left Bundle Branch Pacing From Left Ventricular Septal Pacing

Authors, Journal, Affiliations, Type, DOI

• Authors: Shengjie Wu, MD; Xueying Chen, MD, PhD (these two contributed equally); Songjie Wang, MD; Lei Xu, MD; Fangyi Xiao, MD; Zhouqing Huang, MD; Rujie Zheng, MD; Limeng Jiang, MD; Pugazhendhi Vijayaraman, MD; Parikshit S. Sharma, MD; Lan Su, MD; Weijian Huang, MD
• Journal: JACC: Clinical Electrophysiology 2021;7(9):1166–1177. © 2021 by the American College of Cardiology Foundation, published by Elsevier. Manuscript received 17 November 2020; revised 26 January 2021; accepted 11 February 2021
• Affiliations: Department of Cardiology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China; the Key Lab of Cardiovascular Disease, Wenzhou; Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Disease; Geisinger Heart Institute, Wilkes Barre, Pennsylvania, USA; Rush University Medical Center, Chicago, Illinois, USA
• Type: Prospective single-centre study, n=30, with an invasive electrophysiological reference standard — a temporary His bundle pacing lead plus a multielectrode catheter in the left ventricle, used to define LBB capture directly rather than by ECG surrogate. IRB 2018-181
• DOI: 10.1016/j.jacep.2021.02.018
• Disclosures: Dr Vijayaraman — speaker/consultant with research and fellowship support from Medtronic; consultant for Abbott, Biotronik, Boston Scientific and Eagelpoint LLC; and holds a patent for a His bundle pacing delivery tool. Dr Sharma — speaker for Medtronic; consultant for Medtronic, Abbott Medical, Boston Scientific and Biotronik. All other authors report no relationships
• Funding: Key Research and Development Program of Zhejiang (2019C03012); Natural Science for Youth Foundation (81900345); Major Project of the Science and Technology of Wenzhou (ZS2017010); Clinical Research Plan of Shanghai Hospital Development Center (SHDC2020CR4003)
• Why it matters here: this is the only source in this wiki that validates LBB-capture criteria against direct electrophysiological evidence rather than an ECG surrogate. It is therefore the strongest reference standard in the LBBAP corpus, and it re-grades several criteria the wiki already presents (sources/lbb-capture-criteria-hrs-2021, sources/csp-ehra-2023, sources/ecg-lbbap-criteria-jaccep-2025)

Overview

Every other capture-criteria source in this wiki decides whether the left bundle was captured by reading the surface ECG — most often by watching for a QRS transition as output is decremented, a method available in barely a quarter of patients. This study instead placed three catheters: a temporary His bundle pacing lead, the LBBP lead, and a duodecapolar multielectrode catheter passed retrogradely across the aortic valve to map the left ventricular septum. LBB capture was then defined directly — by recording a retrograde His potential from the His lead after septal stimulation, and/or anterograde left conduction system potentials from the multielectrode catheter — and the validation is internal and elegant: the stimulus-to-retrograde-His interval (21.8 ± 5.9 ms) equalled the patient's own intrinsic His-to-LBB-potential interval (21.8 ± 6.9 ms), and stayed constant across selective, nonselective and high-output pacing. Against that standard, in 30 patients, the routinely used criteria are sorted into useful and not: abrupt shortening of Stim-LVAT by ≥10 ms and the characteristics of selective LBBP were the most valuable (both 100% specific), while a paced RBBB pattern proved necessary but not sufficient (present in 100% of LBB capture but also in 23.4–44.4% of LVSP), and paced QRS duration — counterintuitively longer during selective LBBP — was unhelpful. The paper's own caveat is that the technique is too complex for routine use and the sample too small for robust conclusions; its value is as the arbiter against which simpler criteria can be judged.

Keywords

(No author keyword list is printed. Abbreviations are listed in the article.)

Key Takeaways

Abstract

• Objectives: to assess the predictive value of the proposed ECG and intracardiac electrogram characteristics for confirmation of LBB capture
• Background: "Previously proposed criteria to distinguish left bundle branch pacing (LBBP) and left ventricular septum (LVS) pacing (LVSP) have not been fully validated"
• Methods: a His bundle pacing lead, an LBBP lead, and a multielectrode catheter at the LVS were placed. Direct LBB capture was defined as demonstration of retrograde His potential on the His bundle pacing lead and/or anterograde left conduction system potentials on the multielectrode catheter during LBBP. The routinely used parameters — His, LBB potential, Stim-LVAT, and paced QRS morphology during LVSP and LBBP at various depths and outputs — were analysed
• Results: 30 patients (21 non-LBBB, 9 LBBB) who demonstrated direct LBB capture were included
  • The proportion of paced RBBB was 100% during LBB capture in all patients, compared to 23.4% in non-LBBB and 44.4% in LBBB during LVSP
  • "LBB potential was recorded in all patients during intrinsic rhythm (non-LBBB group) or His corrective pacing in LBBB" (⚠ contradicted within the paper — see Limitations)
  • Paced QRS duration was longer during selective LBBP than nonselective LBBP or LVSP only
  • All patients with characteristics of selective LBBP or abrupt decrease in Stim-LVAT of ≥10 ms demonstrated LBB capture
• Conclusions: "Direct LBB capture can be confirmed by recording retrograde His potential and anterograde left conduction system potentials. Abrupt decrease in Stim-LVAT of ≥10 ms and demonstration of selective LBBP could be used as simple criteria to confirm LBB capture"

Introduction — the gap

• The technique's premise: intraseptal LBB pacing captures the proximal LBB distal to the site of conduction delay, achieving "rapid and physiological left ventricular (LV) activation with a low pacing threshold and higher R-wave amplitudes"
• The criteria then in use, all indirect: the LBB potential; a paced RBBB pattern; Stim-LVAT; and selective LBBP defined by a discrete local EGM in the pacing lead with M or rsR′, and wide R′ with a notch in lead V1
• The problem stated bluntly: "However, these criteria provided an indirect guide, without direct evidence for LBB capture. Previous publications have incorrectly described LV septum (LVS) pacing (LVSP) as evidence of true LBBP, possibly because of the lack of standardized criteria"
• The design consequence: a lead at the His bundle and/or a high-density mapping catheter in the LV were used to record retrograde and/or anterograde potentials as direct evidence, and the previously described indirect criteria were assessed systematically against it

Methods

Population

• Prospective, patients referred for permanent pacemaker implantation or CRT
• Included: normal His-to-left Purkinje conduction (non-LBBB group) and typical LBBB strictly defined by Strauss criteria (LBBB group)
• Excluded: nonspecific intraventricular conduction defects, infra-Hisian atrioventricular block, and ischaemic cardiomyopathy — a set that matters for generalisability
• Informed consent obtained; IRB 2018-181

The instrumentation — three catheters

• Temporary His bundle pacing (HBP) lead (model 3830, Medtronic) at the His bundle, to stimulate and record the His potential
• Temporary curved multielectrode linear catheter (MEC) — duodecapolar 2-2-2 mm, Livewire, Abbott — placed across the aortic valve to map the LVS and record the anterograde left conduction system potential (PLCS) via a retrograde approach
  • Intravenous heparin given as a bolus to maintain an ACT >250 seconds during left septal mapping
• LBBP lead (model 3830, Medtronic) initially located 1 to 1.5 cm apical with regard to the HBP lead in the right ventricular septum, at an RAO 30° fluoroscopic view

How direct LBB capture was defined — the reference standard

• The physiological principle: when the LBB is stimulated, activation transmits quickly retrogradely to the His bundle (if His-LBB is intact) and anterogradely to the distal left conduction system
• Definition, in two alternative forms:
  1. stimulus to PHis = intrinsic His potential − PLBB, with Stim-His <35 ms — the normal His-to-ventricular interval being 35 to 55 ms — and/or
  2. demonstration of PLCS preceding the ventricular EGM on the multielectrode catheter during LBB pacing, when stimulation to the left conduction system is intact
• In the LBBB group, retrograde conduction testing was performed but no direct PHis could be recorded, because of the conduction block between LBB and His bundle. Instead a His potential behind the ventricular EGMs with a long Stim-His could be recorded from the HBP lead — explained by "long retrograde conduction from the stimulus via the left conduction system, myocardium, RBB, and to the His bundle"
• A recording advantage worth noting: the LBB potential concealed in LV activation could be observed from the MEC, which "can record more precise local activation than the LBB lead"

The testing protocol

• Initial depth ≈ 6 to 8 mm into the septum, confirmed by the fulcrum sign or contrast injection, or inferred when the paced morphology was an RBBB pattern or PVCs with RBBB morphology were induced
• At that depth, low- and high-output pacing (usually >5 V/0.5 ms) was performed repeatedly:
  • Initial LBB capture = retrograde and/or anterograde potentials recorded from the HBP/MEC lead at first
  • LVSP without LBB capture = on reducing output, retrograde His and anterograde PLCS became absent or delayed at the same depth
• The lead was then advanced to the LV subendocardium adjacent to the LBB; the final site was where pacing at <1.0 V/0.5 ms demonstrated direct LBB capture
• At the final depth, outputs were tested in sequence: (1) lowest output capturing LBB or local myocardium; (2) increasing output to capture both LBB and local myocardium; (3) >5 V/0.5 ms
• If direct LBB capture could not be demonstrated, the lead was removed and the site reattempted, and the number of attempts was recorded
• Distinguishing equal thresholds: where the LBB capture threshold resembled the LVS myocardial threshold, the two were separated by changing output, pulse width, or pacing rate, or by programmed stimulation
• NS-LBBP→S-LBBP vs NS-LBBP→LVSP: during transition to S-LBBP the short Stim-LVAT remains unchanged; during transition to LVSP the Stim-LVAT is prolonged and no discrete local EGM follows the pacing stimulus in the LBBP lead
• Statistics: mean ± SD; Student's t-test and/or one-way ANOVA between groups; paired t-test and/or repeated-measures ANOVA within individuals; chi-square/Fisher exact between groups; Friedman and/or McNemar within individuals; significance p < 0.05; SPSS version 20.0

Results

Baseline

• Thirty patients, mean age 69.4 ± 9.5 years, enrolled December 2018 to August 2019
• Baseline QRSd: 85.5 ± 13.6 ms (non-LBBB) and 161.4 ± 14.3 ms (LBBB)
• Retrograde conduction testing in all 21 non-LBBB patients; anterograde assessment with the LV multipolar catheter in 7 non-LBBB and all 9 LBBB patients
• Successful LBBP with direct LBB capture was achieved in all 30 patients
• ⚠ Attempt counts, which bear on a live controversy: 2 patients required 2 attempts at deep septal positioning; in 28 patients only 1 attempt was required

The direct evidence, and its internal consistency

• With initial LBB capture, Stim-PHis was 21.8 ± 5.9 ms — the same as the intrinsic His-to-PLBB interval of 21.8 ± 6.9 ms. PHis was absent with decreasing output at that depth
• At the final depth, Stim-PHis was similar during S-LBBP, NS-LBBP at low output, and NS-LBBP at high output: 21.4 ± 6.3 vs 21.8 ± 5.9 vs 21.2 ± 5.9 ms (p = 0.759)
• PLCS was recorded in all 7 non-LBBB patients assessed and in all 9 LBBB patients. At the initial depth during low-output (LVSP) pacing, PLCS was not observed
• Shortest and longest Stim-PLCS were similar across initial LBB capture, S-LBBP and NS-LBBP at low and high output:

• In LBBB, PLCS could NOT be observed preceding the ventricular EGM during native conduction, but WAS present during LBB capture or His corrective pacing — i.e. the potential is unmasked by restoring conduction

Pacing morphology: what it does and does not prove

• Stim-QRSend of the paced W morphology during right ventricular septal pacing: 147 ± 13.2 ms (non-LBBB) and 151 ± 10.9 ms (LBBB)
• Paced RBBB pattern (incidence of R′ in V1): 100% during initial LBB capture in BOTH groups, falling to 23.4% (non-LBBB) and 44.4% (LBBB) during LVSP
• R′-wave amplitude and duration and the incidence of terminal S differed significantly between LVSP and LBBP in both groups (all p < 0.001)
• PLBB-to-LVAT during His corrective pacing: 65.1 ± 9.6 ms (non-LBBB) and 75.7 ± 7.2 ms (LBBB)
• Stim-LVAT fell significantly from LVSP to LBB capture: non-LBBB 90.8 ± 15.2 → 70.7 ± 7.7 ms (p < 0.001); LBBB 97.4 ± 13.1 → 81.7 ± 7.7 ms (p < 0.001)
  • In 53.3% of patients the Stim-LVAT during LBBP was at least 5 ms GREATER than the native PLBB-LVAT — so Stim-LVAT exceeding the native PLBB-LVAT cannot be used to rule out LBB capture
• Stim-LVAT during HBP was 87.8 ± 13.1 ms — the same as the intrinsic His-to-LV activation time of 87.2 ± 13.9 ms (p = 0.519), whereas "LBBP generally changes the initial LV activation sequence"
• The basis of the ≥10 ms criterion: the absolute change in Stim-LVAT from LVSP to LBB capture ranged 10 to 24 ms (non-LBBB) and 10 to 30 ms (LBBB)
• Absolute cut-offs, with their performance:

• No significant difference in Stim-LVAT once the LBB was captured, within the same patient

The LBB potential — reported twice, with different values

• In one passage: "Intrinsic LBB potential was recorded in 76.3% of patients from the non-LBBB group, with an average amplitude of 0.08 ± 0.03 mV"
• In another: "The intrinsic LBB potential was recorded in all patients from the non-LBBB group, with an average amplitude of 0.3 ± 0.13 mV", adding that in LBBB the potential was recorded during His corrective pacing
• The abstract takes the second version ("recorded in all patients"). The two passages disagree on both the rate and the amplitude — see Limitations.
• From the group's own earlier work, cited here: "In patients with normal LBB activation, LBB potentials can be recorded in 98.3% (115/117) of patients with atrioventricular block or sick sinus syndrome (QRSd <120 ms)"
• The interpretive limits drawn by the authors: an LBB potential is "a good sign that the lead is anatomically adjacent to the LBB; however, it does not prove LBB capture". "It may require higher output to capture LBB in those without LBB potential, and LBB capture may be overestimated in these patients."

Selective capture — common at implant, and prone to inflation

• Selective conduction system capture was demonstrable in 18 non-LBBB patients and all 9 LBBB patients (27/30); in the remaining 3 non-LBBB patients, an NS-LBBP→LVSP transition was seen during threshold testing
• No selective LBBP was observed at the initial depth, because there the LBB capture threshold exceeded the local myocardial threshold. At the final depth, where the LBB capture threshold fell below the myocardial threshold, selective LBBP became observable
• 90% (27/30) demonstrated selective LBBP at implant in this study — "much higher than 39.6% to 54% in our previous studies, due to repeated testing". The authors attribute the increase to repeated testing during the waiting period for injury-current recovery, different pacing rates and pulse widths, and programmed stimulation
• And the yield does not persist: the large single-centre study they cite found 75.4% (460/618) with selective left bundle capture during the procedure but only 30.9% (191/618) at follow-up
• Thresholds are not stable even at one depth: "the LBB capture threshold and local myocardial capture threshold could vary even at the same depth"

Discussion — the four findings, in the authors' own numbering

1. Direct LBB capture can be confirmed by retrograde His potential and/or anterograde conduction of the distal left conduction system. Once the LBB is captured — irrespective of whether LVS myocardium is also captured — retrograde and anterograde intervals in the Purkinje system are unaffected, which is why the same Stim-PHis and Stim-PLCS values recur across initial capture, S-LBBP and NS-LBBP
2. At the initial depth, increasing output produced a transition from LVSP to LBBP accompanied by changes in several characteristics at once — abrupt change in Stim-LVAT, paced QRS morphology and QRSd, electrical axis, and transition zone
3. ⭐ "Abrupt shortening of Stim-LVAT by ≥10 ms and demonstration of selective LBB capture were the most valuable criteria for LBB capture." Once the LBB is captured, the absolute value of Stim-LVAT remains constant and can itself serve as a simple criterion in the same patient
4. ⭐ "A paced RBBB pattern was a necessary but not sufficient criterion to prove LBB capture because many patients with LVSP without LBB capture also demonstrated an RBBB pattern. Paced QRSd was also not sufficient to help distinguish LVSP from LBB capture."

On the RBBB pattern

• Useful "primarily as a screening tool", but several factors can produce or alter it: "the pacing site of the LBB, the depth of the pacing lead, intrinsic RBBB or LBBB, fusion with native RV activation, RBB activation via retrograde conduction by LBBP, existing conduction system disease, anodal capture, and selective or nonselective LBB capture"
• "A higher proportion of paced RBBB can be observed when the lead is fixed deeper into the LVS without LBB capture" — i.e. the pattern can arise from depth alone

On Stim-LVAT

• An abrupt ≥10 ms change was observed in ALL cases with transitions in either direction, so its specificity for confirming LBB capture was 100%
• Once LBB is captured, Stim-LVAT "abruptly shortens and then remains constant irrespective of increasing pacing output, no matter selective or non-selective"
• The absolute value is not transferable between patients — it "varies in patients and is dependent on the location of the pacing lead", and was longer in the LBBB group, attributed to enlarged LV and myocardial conduction delay
• The PLBB-LVAT comparator is impractical: it "is calculated by recording LBB potentials using an electrophysiology recording system, making it inconvenient to be used"

On selective pacing, and why QRSd fails

• Characteristics of selective pacing had a specificity of 100% for confirmation of LBB capture
• The QRSd argument, which is the most counterintuitive passage: "The paced QRSd reflects the fusion of LV and right ventricular (RV) electrical activation and may not be an ideal diagnostic value." LBBP gives rapid LV activation and delayed RV activation; during S-LBBP the RV activation is significantly delayed compared with NS-LBBP, wherein septal myocardial capture partially neutralises the delayed RV excitation — which is why S-LBBP has the longer QRSd. Paced QRSd was also longer in LBBB or RBBB than in narrow QRS, "possibly due to absent retrograde conduction to the RBB". Bipolar pacing with anodal capture can eliminate the paced RBBB pattern and shorten QRSd, but "may not be always feasible because of the high anodal capture threshold". Conclusion: "using the paced QRSd as 1 of the criteria for LBB capture was not accurate."

Study Limitations (the authors' own, in full)

• "This method is complicated and may not be practical for routine clinical use" — despite being, to their knowledge, the first systematic direct confirmation of LBB capture
• "The study population was small to draw robust conclusions"
• The findings "may not be applicable" in patients with infra-Hisian block, peripheral intraventricular conduction delay, or ischaemic cardiomyopathy with septal scar — all excluded from this study
• LVS pacing at sites far away from the conduction system was not performed — so the LVSP comparator is limited to near-conduction-system sites

Conclusions

• Direct evidence of LBB capture was demonstrated in all patients by recording retrograde and/or anterograde potentials
• Abrupt shortening of Stim-LVAT and/or characteristics of selective LBBP are useful and simple criteria to confirm LBB capture as INDIRECT evidence in clinical practice
• A paced RBBB pattern was necessary but not sufficient; paced QRSd was not helpful to distinguish LVSP from LBB capture

Limitations of the document

Authors' own stated limitations

• The reference standard itself is impractical: "this method is complicated and may not be practical for routine clinical use" — the very tool that makes the paper strong cannot be used to apply its conclusions
• "The study population was small to draw robust conclusions" — n=30, with the anterograde arm in only 7 non-LBBB + 9 LBBB patients, so several key comparisons rest on 7–9 patients
• Exclusions remove much of the real-world population: infra-Hisian block, peripheral intraventricular conduction delay, and ischaemic cardiomyopathy with septal scar — i.e. exactly the patients in whom capture adjudication is hardest
• The LVSP comparator is not representative: left septal pacing far from the conduction system was not performed, so the reported specificity of the criteria applies to a proximal comparator and may be optimistic for a lead placed apically

Additional limitations evident in the study

• ⚠ The LBB-potential rate and amplitude are each reported twice with different values, and the abstract picks one of them. One passage gives 76.3% of non-LBBB patients with amplitude 0.08 ± 0.03 mV; another gives the potential as recorded in all patients with amplitude 0.3 ± 0.13 mV. That is two different rates and two different amplitudes for one measurement, and the abstract states the "all patients" version. Given that the LBB-potential detection rate is already an unresolved contradiction in this wiki (see concepts/Left-Bundle-Branch-Area-Pacing), a paper that supplies both answers and does not reconcile them cannot be used to settle it. (The second amplitude also carries a residual extraction artefact — "0.3 ± + 0.13 mV".)
• Several "specificity 100%" claims are made from 30 patients, where that figure is imprecise. With n=30 and no observed false positives, the 95% confidence interval around "100% specific" still extends down to roughly 88% — and the subgroups are smaller still (the anterograde assessment in 7 non-LBBB patients). The paper reports point estimates without confidence intervals, so "100% specific" reads far more definitive than the data can support. The same applies to "all patients with characteristics of selective LBBP or abrupt decrease in Stim-LVAT of ≥10 ms demonstrated LBB capture" — sensitivity, not specificity, and from a cohort in which all 30 had capture by design, so the positive predictive value is definitionally uninformative (there were no non-capture patients to be misclassified)
• The cohort is selected so that the criteria's sensitivity is guaranteed. Every patient was required to demonstrate direct capture for inclusion ("successful LBBP was achieved with evidence for direct LBB capture in all 30 patients"). A study that includes only confirmed captures cannot estimate sensitivity — it can only describe how often each feature appeared among captures. The 100% RBBB-pattern figure is therefore a description of the captured state, and the meaningful comparison (23.4%/44.4% during LVSP) comes from the within-patient output manipulations
• The 90% selective-capture figure is inflated by the protocol and the authors say so. It is "much higher than 39.6% to 54% in our previous studies, due to repeated testing" — and the same passage cites a study in which procedural selective capture of 75.4% fell to 30.9% at follow-up. So the paper documents that its headline selectivity figure is a product of intensive testing, and that the state is transient. Any inference that "selective capture is common" must carry both qualifications
• The clinical value of achieving selective capture is left unexamined. The paper establishes that selective LBBP is 100% specific for capture — but given that S-LBBP has a longer paced QRSd, that routine outputs post-implant capture local myocardium anyway (as sources/lbbap-implant-jce-2019 also argues), and that selective capture largely disappears by follow-up, the question of whether pursuing it changes any outcome is not addressed
• No clinical outcomes, no follow-up, and no comparison against the criteria in the population that needs them. The study is an acute implant-time validation. It does not report whether using these criteria changes success rates, attempt counts, perforation, or resynchronisation response — so the practical gain from the re-grading remains inferred
• Single centre and a highly specialised protocol (three catheters, transaortic mapping, ACT >250 s, programmed stimulation) — reproducible only in an experienced research EP lab. The n=30 cohort's uncomplicated passage (28 of 30 needed a single attempt) suggests an operator skill level that itself limits generalisability
• Rating rationale: rated medium. The reference standard is genuinely the strongest in this corpus — direct electrophysiological evidence, with an elegant internal check (Stim-PHis equalling the patient's own intrinsic His-PLBB) — and the findings are consequential, correcting two criteria the wiki carries. But n=30, no confidence intervals on 100% claims, a cohort selected so sensitivity cannot be estimated, four exclusion criteria that strip out the difficult substrate, and an internal contradiction on the LBB-potential rate. It is a methodologically important, small, single-centre study — medium, not high

Key Concepts Mentioned

• concepts/Left-Bundle-Branch-Area-Pacing — the technique; this paper supplies its strongest capture validation
• concepts/Conduction-System-Pacing — the umbrella category
• concepts/Cardiac-Refractoriness — not addressed, but the programmed-stimulation workaround for equal thresholds relies on the same refractoriness differential
• Direct LBB capture — defined here by retrograde His potential and/or anterograde left conduction system potential (PLCS), not by ECG
• Stim-PHis — stimulus-to-retrograde-His interval; <35 ms (normal His-ventricular interval 35–55 ms), and equal to the patient's intrinsic His-PLBB
• PLCS — anterograde left conduction system potential, recorded from a duodecapolar catheter across the aortic valve
• Stim-LVAT — stimulus to peak LV activation; abrupt shortening ≥10 ms = 100% specific for LBB capture
• Selective vs nonselective LBBP — with the crucial and counterintuitive finding that paced QRSd is LONGER in selective LBBP, because RV activation is more delayed when septal myocardial capture is not there to fuse with it
• Paced RBBB pattern — necessary but not sufficient; can occur with deeper LVS placement without capture
• PLBB-LVAT — the LBB-potential-to-LV-activation comparator, measured from the patient's own intrinsic conduction
• Anodal capture — can abolish the RBBB pattern and shorten QRSd, but has a high threshold
• Strauss criteria — used to define the LBBB group strictly

Key Entities Mentioned

• concepts/Left-Bundle-Branch-Area-Pacing — primary concept page
• Medtronic SelectSecure 3830 — used for both the His bundle lead and the LBBP lead; the standard lumenless lead in this wiki
• Abbott Livewire duodecapolar 2-2-2 mm multielectrode catheter — the transaortic mapping catheter that provides the anterograde half of the reference standard
• First Affiliated Hospital of Wenzhou Medical University and the Key Lab of Cardiovascular Disease, Wenzhou — the investigating centre; the Wenzhou/Huang group is one of the originators of LBBP
• Geisinger Heart Institute (Vijayaraman) and Rush University Medical Center (Sharma) — co-authoring centres
• Pugazhendhi Vijayaraman — co-author on both this paper and the JACCEP 2025 criteria paper; holds a patent for a His bundle pacing delivery tool, and discloses Medtronic research funding
• American College of Cardiology Foundation / Elsevier — publisher (JACC: Clinical Electrophysiology)

Wiki Pages Updated

• Created: wiki/sources/lbbp-vs-lvsp-criteria-jaccep-2021.md
• Updated: wiki/concepts/Left-Bundle-Branch-Area-Pacing.md
• Updated: wiki/sourceindex.md
• Updated: wiki/wikiindex.md