Effects of epigallocatechin-3-gallate on left ventricular remodeling and functional recovery following aortic coarctation surgery

To investigate the effects of Epigallocatechin-3-gallate (EGCG) on left ventricular remodeling and functional recovery in mice subjected to pressure overload and subsequent unloading. A mouse model of left ventricular hypertrophy was established via transverse aortic constriction (TAC). A subset of these animals underwent a second surgery to release aorta coarctation, simulating left ventricular pressure unloading. Mice in both pressure overload and unloading conditions received an intraperitoneal injection of EGCG (40 mg/kg per day) for 4 weeks. EGCG treatment significantly improved cardiac function, as indicated by increased ractional shortening (FS) and ejection fraction (EF), and reduced heart weight to body weight (HW/BW) and heart weight to tibia length (HW/TL) ratios, as well as LVIDd, LVIDs, LVEDV, and LVESV (P < 0.05) at 8 weeks post-TAC surgery. EGCG treatment combined with pressure unloading had a cardioprotective effect on ventricular remodeling in mice with pressure overload, as evidenced by improvements in FS and EF and reductions in LVIDd, LVIDs, LVEDV, LVESV, HW/BW ratio, and HW/TL ratio (P < 0.05). Following EGCG treatment, echocardiography further confirmed a notable thinning of the left ventricle wall in mice subjected to pressure unloading. In addition, transmission electron microscopy demonstrated improved sarcomere organization and increased mitochondrial density, while wheat germ agglutinin staining showed a marked reduction in cardiomyocyte surface area (P < 0.05) in mice with left ventricular pressure overload or unloading. These findings suggest that EGCG exerts protective effects against pressure overload-induced myocardial remodeling and augments cardiac recovery following pressure unloading. Unlike previous studies, our model uniquely evaluates EGCG’s role across both disease progression and recovery phases, highlighting its novel therapeutic potential in post-repair cardiac remodeling.