sST2 for Predicting Major Adverse Cardiovascular Events in STEMI Patients: A Prospective Cohort Study

Background Soluble suppression of tumorigenicity 2 (sST2) has emerged as a promising prognostic biomarker for cardiovascular conditions. Nevertheless, the prognostic value of sST2 following percutaneous coronary intervention (PCI) in patients with ST‐segment elevation myocardial infarction (STEMI) has been insufficiently studied. This study aimed to explore the association between sST2 levels and the incidence of major adverse cardiovascular events (MACE) in STEMI patients post‐PCI. Methods This prospective, single‐center study enrolled 289 STEMI patients, who were randomly divided into training ( n = 202) and validation ( n = 87) cohorts at a 7:3 ratio. The primary endpoint was the occurrence of MACE within 6 months post‐STEMI. The relationships between sST2 concentrations and MACE were analyzed using Kaplan–Meier survival analysis, Cox proportional hazards regression models, and restricted cubic spline (RCS) plots. The predictive accuracy of sST2, NT‐proBNP, and their combined model was assessed using receiver operating characteristic (ROC) curves, concordance indices (C‐index), calibration plots, decision curve analysis (DCA), and net reclassification improvement (NRI). Subgroup analyses were conducted by stratifying patients based on age, gender, body mass index (BMI), and culprit vessel characteristics. Results A total of 289 patients were included in the analysis. Kaplan–Meier survival curves in the training cohort demonstrated a higher cumulative incidence of MACE among patients with elevated sST2 levels. Multivariate Cox regression analysis confirmed sST2 as an independent predictor of MACE (HR = 1.012, 95% CI 1.006–1.018, p < 0.001). When compared to the traditional biomarker NT‐proBNP, sST2 displayed a comparable discriminative capability, with each biomarker offering unique strengths regarding accuracy and clinical usefulness. In the validation cohort, sST2 similarly exhibited acceptable predictive performance for MACE. Adding sST2 to the NT‐proBNP baseline model did not significantly improve the predictive performance for MACE in STEMI patients. Subgroup analyses did not reveal any significant interactions with sST2. Conclusion In this study, sST2 was independently associated with MACE within 6 months post‐PCI in patients with STEMI and showed some discriminative ability when used alone. However, adding it to NT‐proBNP did not significantly improve risk prediction, and its incremental prognostic value and clinical utility remain limited and uncertain.