Key result
Post-STEMI sST2 and MR-proADM display distinct early kinetics, peaking at ~12 and ~24 hours.
Why the study?
The optimal timing of biomarker assessment after acute STEMI remains uncertain, limiting prognostic evaluation in the early phase post-infarction.
What are the early temporal dynamics of emerging cardiovascular biomarkers (sST2, Gal-3, MR-proADM, GDF-15) in the first 96 hours after STEMI treated with primary PCI?
Observational (n=30)
No
What are the early temporal dynamics of emerging cardiovascular biomarkers (sST2, Gal-3, MR-proADM, GDF-15) in the first 96 hours after STEMI treated with primary PCI?
Following STEMI, sST2 and MR-proADM display significant temporal kinetics within the first 96 hours, potentially offering informative sampling windows for early prognostic assessment.
Answers are grounded in this paper and cite their sources.
Informs sampling timing in post-STEMI biomarker studies; leaves open clinical risk stratification utility.
Introduction: Acute ST-segment elevation myocardial infarction (STEMI) remains a major cause of cardiovascular morbidity and mortality. Despite successful primary percutaneous coronary intervention (pPCI), early myocardial injury and stress may contribute to left ventricular dysfunction. The optimal timing of biomarker assessment after STEMI remains uncertain. Objective: To characterize the early kinetics of soluble suppression of tumorigenicity-2 (sST2), galectin-3 (Gal-3), mid-regional pro-adrenomedullin (MR-proADM), and growth differentiation factor 15 (GDF-15) during the first 96 h after STEMI and identify potentially informative sampling time points for future prognostic assessment. Secondary, exploratory objectives were to evaluate differences in biomarker concentrations according to symptom duration, left ventricular ejection fraction (LVEF), and infarct-related artery. Methods: In this prospective, single-center, exploratory pilot study, patients aged 18–75 years with first STEMI treated with pPCI within 6 h of symptom onset were enrolled between September 2024 and November 2025. Blood samples were collected at admission and 12 ± 4, 24 ± 4, 48 ± 8, and 96 ± 8 h after pPCI. Biomarkers were measured by ELISA, with high-sensitivity cardiac troponin I (hs-cTnI) as a reference marker of myocardial injury. Results: Of 46 enrolled patients, 16 were excluded, mostly due to early discharge, and 30 patients with complete samples at all five time points were included in the analysis (mean age 57.9 ± 11.1 years; 66.7% male). sST2, MR-proADM, and hs-cTnI showed significant temporal variation (all p < 0.001), with the highest measured concentrations of sST2 at 12 h and of MR-proADM at 24 h. No significant change over time was found for Gal-3 and GDF-15. In exploratory analyses, sST2 and MR-proADM concentrations were higher in patients with LVEF < 40%, and sST2 concentrations were higher in patients with left anterior descending artery (LAD) infarction. Symptom duration was not associated with biomarker concentrations. Conclusions: sST2 and MR-proADM show distinct early post-STEMI kinetics, suggesting potentially informative sampling windows for future prognostic studies. Larger prospective studies are needed to confirm these kinetics and the exploratory differences according to left ventricular function and infarct location, and to evaluate the prognostic value of these sampling windows with echocardiographic and clinical follow-up.
No takes yet. Share an insight, caveat, or question.
Živković et al. (2026) conducted an observational in Acute ST-segment elevation myocardial infarction (STEMI) (n=30). Early cardiovascular biomarkers (sST2, Gal-3, MR-proADM, and GDF-15) was evaluated on Early kinetics of sST2, Gal-3, MR-proADM, and GDF-15 during the first 96 hours after STEMI (p=<0.001). Early biomarker assessment post-STEMI revealed significant temporal variation for sST2, MR-proADM, and hs-cTnI (all p<0.001), with sST2 peaking at 12 hours and MR-proADM at 24 hours.
Synapse has enriched 10 related papers. Consider them for comparative context: