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Updated: Feb 16, 2026

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
12:45

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

Published on: December 11, 2017

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Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch

Jingfeng Wang1, Zhenning Nie1, Haiyan Chen2

  • 1Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University.

Journal of Visualized Experiments : Jove
|December 30, 2017
PubMed

Insights

Researchers developed a new canine model for heart failure with left bundle branch block to study cardiac resynchronization therapy. This model shows CRT effectively reverses heart dysfunction and remodeling.

Area of Science:

  • Cardiology
  • Biomedical Engineering
  • Animal Models

Background:

  • Left bundle branch block (LBBB) predicts significant benefits from cardiac resynchronization therapy (CRT) in heart failure (HF) patients.
  • Existing HF models lack stable LBBB and show rapid reversal of left ventricular (LV) dysfunction, limiting CRT research.

Purpose of the Study:

  • To establish a chronic, stable canine model of asynchronous HF with isolated LBBB for studying CRT.
  • To validate the model's suitability for assessing CRT's structural and biological reverse remodeling effects.

Main Methods:

  • Induction of asynchronous HF via left bundle branch (LBB) ablation and 4 weeks of rapid right ventricular (RV) pacing in canines.
  • Implantation of pacing leads for CRT and use of radiofrequency (RF) catheter ablation.
  • Validation using 2D speckle tracking imaging and aortic velocity time integral (aVTI) to assess LV asynchrony and CRT efficacy.

Main Results:

  • Successful establishment of a chronic, stable HF model with LV asynchrony.
  • CRT demonstrated effectiveness in coordinating ventricular activation, improving LV pump function, and reversing LV dilation.
  • Histopathological analysis revealed CRT-induced reverse remodeling, including restored cardiomyocyte diameter and collagen volume fraction (CVF).

Conclusions:

  • A feasible and valid method for developing a chronic asynchronous HF model with LBBB was established.
  • This model is suitable for investigating the structural and biological reverse remodeling induced by CRT.
  • The model provides a platform for further research into CRT mechanisms and optimization.

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