A porcine large animal model of radiofrequency ablation-induced left bundle branch block.

CRT CSP LBBB cardiac resynchronization therapy conduction system pacing large animal model left bundle branch block

Journal

Frontiers in physiology
ISSN: 1664-042X
Titre abrégé: Front Physiol
Pays: Switzerland
ID NLM: 101549006

Informations de publication

Date de publication:
2024
Historique:
received: 12 02 2024
accepted: 27 03 2024
medline: 6 5 2024
pubmed: 6 5 2024
entrez: 6 5 2024
Statut: epublish

Résumé

Electrocardiographic (ECG) features of left bundle branch (LBB) block (LBBB) can be observed in up to 20%-30% of patients suffering from heart failure with reduced ejection fraction. However, predicting which LBBB patients will benefit from cardiac resynchronization therapy (CRT) or conduction system pacing remains challenging. This study aimed to establish a translational model of LBBB to enhance our understanding of its pathophysiology and improve therapeutic approaches. Fourteen male pigs underwent radiofrequency catheter ablation of the proximal LBB under fluoroscopy and ECG guidance. Comprehensive clinical assessments (12-lead ECG, bloodsampling, echocardiography, electroanatomical mapping) were conducted before LBBB induction, after 7, and 21 days. Three pigs received CRT pacemakers 7 days after LBB ablation to assess resynchronization feasibility. Following proximal LBB ablation, ECGs displayed characteristic LBBB features, including QRS widening, slurring in left lateral leads, and QRS axis changes. QRS duration increased from 64.2 ± 4.2 ms to 86.6 ± 12.1 ms, and R wave peak time in V6 extended from 21.3 ± 3.6 ms to 45.7 ± 12.6 ms. Echocardiography confirmed cardiac electromechanical dyssynchrony, with septal flash appearance, prolonged septal-to-posterior-wall motion delay, and extended ventricular electromechanical delays. Electroanatomical mapping revealed a left ventricular breakthrough site shift and significantly prolonged left ventricular activation times. RF-induced LBBB persisted for 3 weeks. CRT reduced QRS duration to 75.9 ± 8.6 ms, demonstrating successful resynchronization. This porcine model accurately replicates the electrical and electromechanical characteristics of LBBB observed in patients. It provides a practical, cost-effective, and reproducible platform to investigate molecular and translational aspects of cardiac electromechanical dyssynchrony in a controlled and clinically relevant setting.

Sections du résumé

Background UNASSIGNED
Electrocardiographic (ECG) features of left bundle branch (LBB) block (LBBB) can be observed in up to 20%-30% of patients suffering from heart failure with reduced ejection fraction. However, predicting which LBBB patients will benefit from cardiac resynchronization therapy (CRT) or conduction system pacing remains challenging. This study aimed to establish a translational model of LBBB to enhance our understanding of its pathophysiology and improve therapeutic approaches.
Methods UNASSIGNED
Fourteen male pigs underwent radiofrequency catheter ablation of the proximal LBB under fluoroscopy and ECG guidance. Comprehensive clinical assessments (12-lead ECG, bloodsampling, echocardiography, electroanatomical mapping) were conducted before LBBB induction, after 7, and 21 days. Three pigs received CRT pacemakers 7 days after LBB ablation to assess resynchronization feasibility.
Results UNASSIGNED
Following proximal LBB ablation, ECGs displayed characteristic LBBB features, including QRS widening, slurring in left lateral leads, and QRS axis changes. QRS duration increased from 64.2 ± 4.2 ms to 86.6 ± 12.1 ms, and R wave peak time in V6 extended from 21.3 ± 3.6 ms to 45.7 ± 12.6 ms. Echocardiography confirmed cardiac electromechanical dyssynchrony, with septal flash appearance, prolonged septal-to-posterior-wall motion delay, and extended ventricular electromechanical delays. Electroanatomical mapping revealed a left ventricular breakthrough site shift and significantly prolonged left ventricular activation times. RF-induced LBBB persisted for 3 weeks. CRT reduced QRS duration to 75.9 ± 8.6 ms, demonstrating successful resynchronization.
Conclusion UNASSIGNED
This porcine model accurately replicates the electrical and electromechanical characteristics of LBBB observed in patients. It provides a practical, cost-effective, and reproducible platform to investigate molecular and translational aspects of cardiac electromechanical dyssynchrony in a controlled and clinically relevant setting.

Identifiants

pubmed: 38706948
doi: 10.3389/fphys.2024.1385277
pii: 1385277
pmc: PMC11066324
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1385277

Informations de copyright

Copyright © 2024 Wiedmann, Jamros, Herlt, Paasche, Kraft, Beck, Prüser, Erkal, Harder, Zaradzki, Soethoff, Karck, Frey and Schmidt.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The first author declared that he was an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Auteurs

Felix Wiedmann (F)

Department of Cardiology, University Hospital Heidelberg, Heidelberg, Germany.
DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg/Mannheim, University of Heidelberg, Heidelberg, Germany.
HCR (Heidelberg Center for Heart Rhythm Disorders), University Hospital Heidelberg, Heidelberg, Germany.

Max Jamros (M)

Department of Cardiology, University Hospital Heidelberg, Heidelberg, Germany.

Valerie Herlt (V)

Department of Cardiology, University Hospital Heidelberg, Heidelberg, Germany.

Amelie Paasche (A)

Department of Cardiology, University Hospital Heidelberg, Heidelberg, Germany.
DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg/Mannheim, University of Heidelberg, Heidelberg, Germany.

Manuel Kraft (M)

Department of Cardiology, University Hospital Heidelberg, Heidelberg, Germany.
DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg/Mannheim, University of Heidelberg, Heidelberg, Germany.

Moritz Beck (M)

Department of Cardiology, University Hospital Heidelberg, Heidelberg, Germany.

Merten Prüser (M)

Department of Cardiology, University Hospital Heidelberg, Heidelberg, Germany.
DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg/Mannheim, University of Heidelberg, Heidelberg, Germany.
HCR (Heidelberg Center for Heart Rhythm Disorders), University Hospital Heidelberg, Heidelberg, Germany.

Atilla Erkal (A)

Department of Cardiology, University Hospital Heidelberg, Heidelberg, Germany.

Maren Harder (M)

Department of Cardiology, University Hospital Heidelberg, Heidelberg, Germany.

Marcin Zaradzki (M)

Department of Cardiac Surgery, University Hospital Heidelberg, Heidelberg, Germany.

Jasmin Soethoff (J)

Department of Cardiac Surgery, University Hospital Heidelberg, Heidelberg, Germany.

Matthias Karck (M)

Department of Cardiac Surgery, University Hospital Heidelberg, Heidelberg, Germany.

Norbert Frey (N)

Department of Cardiology, University Hospital Heidelberg, Heidelberg, Germany.
DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg/Mannheim, University of Heidelberg, Heidelberg, Germany.
HCR (Heidelberg Center for Heart Rhythm Disorders), University Hospital Heidelberg, Heidelberg, Germany.

Constanze Schmidt (C)

Department of Cardiology, University Hospital Heidelberg, Heidelberg, Germany.
DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg/Mannheim, University of Heidelberg, Heidelberg, Germany.
HCR (Heidelberg Center for Heart Rhythm Disorders), University Hospital Heidelberg, Heidelberg, Germany.

Classifications MeSH