Assessing the Role of Soluble Suppression of Tumorigenicity‐2 (sST2) in Patients With Pulmonary Embolism

Background Pulmonary embolism (PE) is a serious cardiovascular condition associated with a wide range of clinical outcomes, from mild symptoms to severe hemodynamic compromise. Existing biomarkers like D‐dimer and proBNP have limitations in specificity and do not fully capture the inflammatory and hemodynamic aspects of the disease. Soluble suppression of tumorigenicity‐2 (sST2), a marker of myocardial strain and inflammation, has shown prognostic value in cardiovascular diseases, suggesting its potential as an adjunctive biomarker in PE. Methods This prospective study enrolled 60 PE patients and 62 age‐ and sex‐matched controls between April 2023 and June 2024. Results sST2 levels were significantly higher in the PE group than in controls ( p < 0.001), with an AUC of 0.731 for distinguishing PE from controls. The optimal sST2 cutoff value of 91.5 ng/mL yielded a sensitivity of 70% and specificity of 66%. sST2 showed significant correlations with WBC, right ventricular functions, and systolic pulmonary artery pressure (sPAP) but no association with conventional PE severity scores or other biomarkers like proBNP, D‐dimer, and HS‐troponin T. Conclusion Elevated sST2 levels in PE patients reflect inflammatory and hemodynamic stress, underscoring its potential as a complementary biomarker in assessing PE severity and RV strain.