Wnt/β-catenin pathway in patients with acute myocardial infarction: a prospective cohort study (BETA-MI STUDY)

Myocardial infarction (MI) triggers fibrotic remodeling, impairing cardiac function and increasing the risk of heart failure. Although the Wnt/β-catenin signaling pathway modulates infarct healing and fibrosis in animal models, its role in human post-MI remodeling remains unexplored. This study investigates Wnt/β-catenin activation in acute MI and its association with clinical and laboratory markers of remodeling.

Fifty patients were prospectively enrolled: 40 with ST-elevation MI (STEMI) and 10 matched controls with chronic coronary syndrome (CCS). Blood samples were collected at five time points: pre-percutaneous coronary intervention (PCI), post-PCI, day 3, discharge, and 45-day follow-up. Protein and transcript levels of β-catenin and DKK1 (encoded by CTNNB1 and DKK1) were measured. Echocardiographic, laboratory, and clinical outcomes were also assessed.

The mean patient age was 62 ± 8 years; 82% were men. STEMI patients had significantly higher β-catenin and DKK1 levels than CCS controls at all time points. In STEMI, β-catenin remained stable, while DKK1 showed a slight increase. Pre-PCI β-catenin protein levels independently predicted improved left-ventricular ejection fraction (LVEF) at follow-up.

β-catenin is elevated in STEMI patients and correlates with better post-MI LVEF, suggesting a potential role in myocardial repair. These findings support further investigation of the Wnt/β-catenin pathway as a prognostic biomarker or therapeutic target in postinfarction cardiac recovery.