Bi-ventricular Epicardial Activation in Left Bundle Area Pacing: a Comparison Study

Bradyarrhythmia Clinical Trial

— LBBAP  

Official title:

Bi-ventricular Epicardial Activation in Left Bundle Area Pacing: a Comparison Study

Clinical Trial Details — Status: Recruiting

Administrative data

• NCT number: NCT05401851
• Other study ID #: EC-2022-020
• Status: Recruiting
• Phase: N/A
• Start date: March 24, 2022
• Est. completion date: October 21, 2024

Study information

• Verified date: May 2023
• Source: Universitair Ziekenhuis Brussel
• Contact: Carlo de Asmundis, MD, PhD
• Phone: +32024763704
• Email: HRMC[@]uzbrussel.be
• Is FDA regulated: No
• Study type: Interventional

Clinical Trial Summary

Study of the ventricular activation patterns during left bundle area pacing and compare it with baseline activation during normal sinus rhythm in patients with and without baseline bundle branch conduction disorder.

Description:

Right ventricular (RV) pacing has long been the gold standard treatment for symptomatic brady arrhythmias. Right ventricular apical pacing has shown to cause electrical and mechanical desynchrony resulting in left ventricular (LV) dysfunction, and, in some cases, clinical heart failure together with other mechanical and arrhythmic complications. Hence, it was necessary to find a more physiologic method of pacing that ensures synchrony. His bundle pacing was first described in 2000, and is more recently adapted as a pacing method with less deleterious effects on the RV. However, lead dislodgement, high pacing thresholds, battery depletion, and difficulty identifying the exact location of His bundle were the most significant concerns related to this method. Subsequently, left bundle branch area pacing (LBB-AP), first described in 2017 by Huang et al, has emerged as safe alternative with excellent lead stability and capture threshold, and more ability to correct distal conduction disease as compared to His bundle pacing. Recent studies report promising mid-term outcome concerning left ventricular desynchrony. To the best of our knowledge, bi-ventricular activation was never studied in patients with LBB-AP.

Multiple tools have been used to assess biventricular (BiV) synchrony specially with chronic resynchronization therapy (CRT) including echocardiography and 12 lead ECG. Eschalier et al. found that epicardial noninvasive ECG mapping, was better at predicting clinical CRT response than QRS duration or the presence of LBBB. Activation patterns and timings with RV apical pacing, native LBBB, and BiV pacing have been well studied using this tool. With LBBP, however, these activation parameters have not yet been described.

This study aims to evaluate bi-ventricular activation in patients equipped with LBB-AP using non-invasive 3D mapping system in patients with or without baseline ventricular conduction disorder.

Recruitment information / eligibility

• Status: Recruiting
• Enrollment: 30
• Est. completion date: October 21, 2024
• Est. primary completion date: February 21, 2024
• Accepts healthy volunteers: No
• Gender: All
• Age group: 18 Years and older

Eligibility

Inclusion Criteria:

• 30 patients with a functional LBB-AP pacemaker

Exclusion Criteria:

• Age < 18 years

• Previous cardiac surgery

• Cardiomyopathy with documented ventricular scar

• Patients with prior pacemaker

Related Conditions & MeSH terms

• Bradyarrhythmia
• Bradycardia

Intervention

Device:
• Left Bundel Area Pacing
RV Lead will be placed deep in the interventricular septum

Locations

Country	Name	City	State
Belgium	UZ Brussel	Brussel

Sponsors (1)

Lead Sponsor	Collaborator
Universitair Ziekenhuis Brussel

Country where clinical trial is conducted

Belgium, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Epicardial map	Activation patterns (visual inspection) on non-invasive 3D ECG mapping	1 day
Primary	Epicardial map	Activation time (ms) on non-invasive 3D ECG mapping	1 day
Secondary	Echo parameters for resynchronization	LVEF (%)	90 days
Secondary	Echo parameters for resynchronization	intraventricular delay (ms)	90 days