Association of soluble ST2 and infarct location within 12–24 h in STEMI: A cross-sectional study

Abstract

BackgroundST-Segment Elevation Myocardial Infarction (STEMI) causes the release of soluble ST2 biomarkers at high level on acute phase. However, sST2 has never been used as adjunct biomarker in ESC/AHA guideline for STEMI. Furthermore, the specific onset that sST2 may have role in acute phase of STEMI related with infarct location has not been established. This study aimed to prove the association between serum ST2 levels and infarct location in STEMI. Material and methodsThis study was cross-sectional. STEMI patients with onset of anginal pain 12–24 h were included in study. The exclusion criterias were patients with AMI aside from STEMI and other potential confounders affecting the sST2 level. Serum sST2 was collected on first medical contact when admitted to emergency unit. The patients were grouped into anterior STEMI and non-anterior STEMI. sST2 levels were compared with demographics data, clinical and laboratory variables using Student's t-test. Correlation of sST2 levels was analyzed using Spearman's correlation coefficient. Results19 subjects were included in the anterior STEMI and 20 subjects were included in the non-anterior STEMI. We found no difference in sST2 levels between anterior STEMI and non-anterior STEMI (mean ± SD; 729.97 pg/mL ± 147.78 pg/mL vs 606.87 pg/mL ± 147.78 pg/mL, p = 0.119). Onset was correlated with serum sST2 levels in male subjects (r = −0.459, p = 0.012). We found significant difference of mean sST2 between 2 onset groups divided at median (12–18 h vs 19–24 h, Δ mean = 107.75 pg/mL, p-value = 0.021). ConclusionsST2 was not associated with infarct location within 12–24 h onset of STEMI. This results suggest that infarct location might not responsible for the elevation of serum sST2 levels in acute phase of STEMI.