Key result
Progressive border zone remodeling drives post-infarct VT, challenging the view of purely passive fibrotic channels.
Why the study?
The structural concept of surviving myocardial bundles within fibrotic scar alone does not fully account for the complex electrophysiological behaviours observed in post-myocardial infarction ventricular tachycardia.
This review reconceptualizes post-MI VT circuits as dynamic, multicellular environments rather than passive fibrotic channels, with implications for electroanatomical mapping and ablation.
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Challenges fibrosis-centric model of post-MI VT; extends mechanistic focus to multicellular interactions in re-entry.
Obeidat et al. (2026) 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.
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