The Role of Infarct Border Zone Remodelling in Ventricular Arrhythmias: Bridging Basic Research and Clinical Applications
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Updated: May 1, 2026

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples
Published on: April 21, 2014
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.
Abstract:
Patients who experience post-myocardial infarction (MI) and present with a left ventricular ejection fraction of less than 35% are classified as being at high risk for sudden cardiac death due to ventricular arrhythmias (VAs). The expansion of scar tissue and the extension of the infarct border zone (IBZ) following MI play critical roles in the progression of heart failure and the onset of VAs. Various aspects of structural remodelling, including cardiac fibrosis, along with electrophysiological changes such as alterations in gap junctions, ion channels, and autonomic nervous system function within the IBZ may contribute to abnormal impulse generation and conduction, thereby increasing susceptibility to arrhythmias. Currently, management strategies for VAs primarily encompass pharmacologic interventions (e.g., β-blockers, amiodarone), device-based approaches (e.g., ICD implantation), or catheter ablation techniques as outlined by ESC Guidelines. In this review, we systematically summarise both structural characteristics inherent in ischaemic myocardial substrates and clinical treatment strategies regarding VAs. We propose that early prevention strategies aimed at mitigating arrhythmogenic substrate formation represent an innovative approach to treating VAs following MI.
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