EXPLORING ISCHEMIA-INDUCED CARDIAC FIBROSIS IN POST-MYOCARDIAL INFARCTION PATIENTS

Abstract

Ischemia-induced cardiac fibrosis is a key contributor to adverse ventricular remodeling and heart failure following myocardial infarction (MI), yet its underlying mechanisms and clinical consequences remain incompletely defined. This study aimed to comprehensively characterize the extent, drivers, and functional impact of post-MI fibrosis using a multi-modal approach involving serum biomarkers, cardiac imaging, histopathology, and functional assessment. A cohort of 150 post-MI patients was analyzed, with mean age 61.2 ± 10.4 years and high prevalence of cardiovascular comorbidities. Cardiovascular magnetic resonance imaging identified a significant amount of fibrotic tissue (ECV = 28.5 ± 5.4%) and an average scar size of 19.3 ± 6.1%.  Fibrosis assessed by imaging was consistently linked with higher levels of TGF-β (356.2 ± 89.1 pg/mL), galectin-3 (18.5 ± 4.2 ng/mL), NT-proBNP (1567 ± 604 pg/mL) and hs-CRP (4.8 ± 2.3 mg/mL).  A histological examination on 30 biopsies revealed that processes of fibroblast transition, collagen deposition and senescent cell accumulation are mechanisms underlying scar formation.  Increased galectin-3 concentrations were closely linked to higher fibrosis measurements as the patient group was stratified by ECV.  The extent of fibrosis is linked to reduced cardiopulmonary exercise capacity and low functional abilities in individuals with heart failure.  Clinical outcomes in heart failure patients may be improved by applying a combination of biomarkers, advanced imaging techniques and focused fibrotic therapies. Fibrosis is therefore identified as a key driver for both the evolution of structural changes and impairment of cardiac function.