The Role of Infarct Border Zone Remodelling in Ventricular Arrhythmias: Bridging Basic Research and Clinical

Jin Ma1, Qiuxiong Chen1,2, Dongqun Lin1

  • 1Guangdong Provincial Hospital of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.

Insights

Patients with low ejection fraction after myocardial infarction (MI) face high risk of sudden cardiac death from ventricular arrhythmias (VAs). Targeting scar tissue and infarct border zones may prevent these life-threatening arrhythmias.

Area of Science:

  • Cardiology
  • Electrophysiology
  • Cardiac Pathophysiology

Background:

  • Post-myocardial infarction (MI) patients with ejection fraction <35% are at high risk for sudden cardiac death due to ventricular arrhythmias (VAs).
  • Scar tissue expansion and infarct border zone (IBZ) remodeling are key drivers of heart failure progression and VA development.
  • Structural changes (fibrosis) and electrophysiological alterations (ion channels, gap junctions, autonomic dysfunction) in the IBZ promote abnormal impulse conduction.

Purpose of the Study:

  • To systematically review structural characteristics of ischemic myocardial substrates.
  • To summarize current clinical treatment strategies for VAs post-MI.
  • To propose novel prevention strategies targeting arrhythmogenic substrate formation.

Main Methods:

  • Systematic review of literature on myocardial infarction, ventricular arrhythmias, and cardiac remodeling.
  • Analysis of structural and electrophysiological changes in the infarct border zone.
  • Evaluation of current pharmacological, device-based, and catheter ablation therapies for VAs.

Main Results:

  • Identified critical roles of scar tissue and IBZ in VA pathogenesis.
  • Detailed structural and electrophysiological substrate modifications contributing to arrhythmias.
  • Summarized established treatment modalities including beta-blockers, amiodarone, ICDs, and ablation.

Conclusions:

  • Current VA management relies on treating established arrhythmias.
  • Early prevention strategies targeting substrate modification offer a promising innovative approach.
  • Mitigating arrhythmogenic substrate formation could reduce VA incidence and sudden cardiac death post-MI.

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