MODULATION OF THE WNT/BETA-CATENIN PATHWAY IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION (BETA-MI STUDY)

Background: Cardiac fibrosis is central to post-infarction remodeling and heart failure development. The Wnt/β-catenin pathway is involved in fibrosis and myocardial repair, but its clinical significance remains unclear. This study aims to investigates β-catenin and its inhibitor DKK1 after a myocardial infarction and explores their modulation by P2Y12 inhibitors. Methods: A single-center observational cohort study included 50 patients undergoing PCI: 40 with STEMI and 10 with CCS. β-catenin and DKK1 levels were measured by ELISA method and qPCR at multiple timepoints. Echocardiographic indices were assessed alongside clinical outcomes. Patients treated with ticagrelor or prasugrel were compared. Results: β-catenin and DKK1 levels were higher in STEMI patients than CCS at all timepoints (p<0.001), though stable over time (β-catenin ELISA p=0.8; DKK1 ELISA p=0.9). Baseline β-catenin levels (ELISA) correlated positively with LVEF at follow-up (p=0.028). In multivariate analysis, β-catenin remained an independent predictor (p=0.047). No differences in biomarker levels were found between ticagrelor and prasugrel groups. FMD improved significantly with ticagrelor over time (p=0.048), and was higher than in the prasugrel group (p=0.015). Conclusion: Sustained activation of Wnt/β-catenin signaling occurs after STEMI and may support myocardial recovery. β-catenin appears to be a promising prognostic marker, while the role of DKK1 remains uncertain. Larger studies are needed to validate these findings.