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

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.