Timothy Sem David, Hartopo Anggoro Budi, Anggraeni Vita Yanti, Makrufardi Firdian
Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada/Dr. Sardjito Hospital, Yogyakarta, Indonesia.
Ann Med Surg (Lond). 2021 Sep 9;70:102844. doi: 10.1016/j.amsu.2021.102844. eCollection 2021 Oct.
ST-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.
This 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.
19 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).
sST2 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.
ST段抬高型心肌梗死(STEMI)在急性期会导致可溶性ST2生物标志物高水平释放。然而,sST2从未在ESC/AHA的STEMI指南中用作辅助生物标志物。此外,sST2在与梗死部位相关的STEMI急性期可能发挥作用的具体发病时间尚未确定。本研究旨在证实STEMI患者血清ST2水平与梗死部位之间的关联。
本研究为横断面研究。纳入心绞痛发作12 - 24小时的STEMI患者。排除标准为除STEMI外的急性心肌梗死患者以及其他影响sST2水平的潜在混杂因素。患者入院至急诊科首次医疗接触时采集血清sST2。患者被分为前壁STEMI组和非前壁STEMI组。使用Student's t检验比较sST2水平与人口统计学数据、临床和实验室变量。使用Spearman相关系数分析sST2水平的相关性。
前壁STEMI组纳入19例受试者,非前壁STEMI组纳入20例受试者。我们发现前壁STEMI组和非前壁STEMI组的sST2水平无差异(均值±标准差;729.97 pg/mL±147.78 pg/mL vs 606.87 pg/mL±147.78 pg/mL,p = 0.119)。男性受试者的发病时间与血清sST2水平相关(r = -0.459,p = 0.012)。我们发现以中位数划分的两个发病时间组之间的平均sST2存在显著差异(12 - 18小时vs 19 - 24小时,平均差值 = 107.75 pg/mL,p值 = 0.021)。
STEMI发病12 - 24小时内,sST2与梗死部位无关。该结果表明梗死部位可能不是STEMI急性期血清sST2水平升高的原因。