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Infarcted and peri-infarct myocardium refers to the anatomical regions of the heart muscle affected by a myocardial infarction (MI). The infarcted zone consists of necrotic tissue where cardiomyocytes have died due to prolonged ischemia, eventually being replaced by a non-contractile collagen scar [1]. The peri-infarct myocardium, or border zone, is the surrounding area of viable but stressed tissue that undergoes significant pathological changes, including inflammation, oxidative stress, and structural remodeling [2]. This region is a critical focus for therapeutic intervention, as salvageable myocytes in the peri-infarct zone can be protected to limit total infarct size and prevent the progression to chronic heart failure [3]. While not a single molecular target, this tissue environment is the site of action for various pharmacological agents, such as ACE inhibitors and beta-blockers, as well as emerging regenerative therapies like stem cell transplantation and gene therapy [4]. Understanding the molecular landscape of these zones is essential for developing precision medicines that target specific pathways like fibrosis or angiogenesis within the damaged heart [5].
Drugs targeting this region typically aim to reduce myocardial oxygen demand, inhibit adverse ventricular remodeling, suppress inflammatory cascades, or promote angiogenesis and cellular repair within the salvageable border zone.
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