Post-infarct ventricular tachycardia is driven by progressive multicellular remodeling of the infarct border zone, challenging the view of VT corridors as purely passive fibrotic channels.
This review reconceptualizes post-MI VT circuits as dynamic, multicellular environments rather than passive fibrotic channels, with implications for electroanatomical mapping and ablation.
Abstract Ventricular tachycardia (VT) in the post‐myocardial‐infarction heart is sustained by re‐entry arising from slow and heterogeneous impulse propagation within the infarct border zone. Seminal histological and electrophysiological studies demonstrated that re‐entry is enabled by conduction corridors of surviving myocardial bundles embedded within fibrotic scar. However, growing experimental and clinical evidence indicates that this structural concept alone does not fully account for the complex electrophysiological behaviours observed in infarct‐related VT. In this review, we examine the evolution of the arrhythmogenic substrate following myocardial infarction and the development of the critical slow‐conducting pathway known as the ‘diastolic isthmus’. Post‐infarct remodelling that includes inflammatory, fibrogenic and chronic maturation phases transforms the border zone into a heterogeneous, multicellular environment, wherein surviving cardiomyocytes coexist with (myo)fibroblasts, immune cells, adipocytes and neural elements. The interactions among these cellular populations influence impulse propagation through modifications in electrotonic coupling, paracrine signalling and membrane excitability modulation. Within these constrained myocardial strands, minor alterations in intercellular coupling or ionic currents can substantially affect conduction velocity and propagation safety, leading to delayed activation while preserving the conditions necessary for re‐entry. Furthermore, we discuss how these changes contribute to the three‐dimensional architecture of re‐entrant circuits and the implications for identifying the arrhythmogenic substrate during electroanatomical mapping, as well as the interaction between ablation energy and heterogeneous infarct tissue. Collectively, these observations challenge the traditional conception of VT corridors as passive fibrotic channels. Instead, scar‐related ventricular tachycardia represents an evolving electrophysiological phenomenon resulting from progressive multicellular remodelling of the infarct border zone. image
Obeidat et al. (Sat,) conducted a review in Post-myocardial infarction ventricular tachycardia. Post-infarct ventricular tachycardia is driven by progressive multicellular remodeling of the infarct border zone, challenging the view of VT corridors as purely passive fibrotic channels.