急性心肌梗死4天时血清可溶性生长刺激表达基因2蛋白水平与6个月内心原性死亡关系的研究
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摘要
目的:探讨急性心肌梗死患者症状出现第4天时血清可溶性生长刺激表达基因2蛋白(sST2)水平与6个月内心原性死亡的关系。方法:入选2017年6月至2018年5月入住我院冠心病重症监护室(CCU)的424例急性心肌梗死患者,用酶联免疫吸附法测定患者从症状开始出现至第4天时(如缺乏,以之后第一次数据代替)血清sST2的表达水平,并收集患者住院期间和出院后随访6个月的临床资料,对心原性死亡患者(心原性死亡组,n=45)和生存患者(生存组,n=379)进行比较分析。结果:(1)心原性死亡组症状出现第4天时血清sST2水平明显高于生存组[242.71(84.38～340.25)ng/ml vs 42.97(29.67～81.96)ng/ml,P<0.001];(2)二元Logistic回归分析显示,症状出现第4天时血清sST2水平与6个月内心原性死亡独立相关(P<0.001),在纳入N末端B型利钠肽原(NT-proBNP)后,对心原性死亡仍有独立预测价值(P<0.001);即使在校正相关危险因素后,这种预测价值仍然存在(P<0.001)。结论:急性心肌梗死患者症状发生4天时血清sST2水平可以预测心肌梗死患者短期不良预后。
Objectives: To investigate the relationship between serum sST2 level measured within 4 days after symptom onset and6-month cardiac death in patients with acute myocardial infarction(AMI).Methods: A total of 424 patients with AMI in our CCU ward from June 2017 to May 2018 were enrolled. Serum sST2 was tested by enzyme-linked immunosorbent assay within 4 days(sST2-day4) after admission. Patients received 6 months clinical follow-up after discharge. The primary endpoint was cardiac death at 6 months after discharge. The AMI patients were divided into cardiac death group(n=45) and survival group(n=379).Results:(1) Serum sST2-day4 level was significantly higher in the cardiac death group than those in the survival group(242.71 [84.38-340.25] ng/ml vs 42.97 [29.67-81.96] ng/ml, P<0.001);(2) Binary logistic regression analysis showed that sST2-day4 was independently associated with cardiac death at 6 months(P<0.001) in AMI patients, even with the addition of NT-proBNP. sST2-day4 level remained as the independent predictor for 6-month cardiac death after adjustment for conventional cardiovascular risk factors in this patient cohort(P<0.001).Conclusions: Serum sST2 level could be used as an independent predictor for 6-month cardiac death in patients with AMI.
Objectives: To investigate the relationship between serum sST2 level measured within 4 days after symptom onset and6-month cardiac death in patients with acute myocardial infarction(AMI).Methods: A total of 424 patients with AMI in our CCU ward from June 2017 to May 2018 were enrolled. Serum sST2 was tested by enzyme-linked immunosorbent assay within 4 days(sST2-day4) after admission. Patients received 6 months clinical follow-up after discharge. The primary endpoint was cardiac death at 6 months after discharge. The AMI patients were divided into cardiac death group(n=45) and survival group(n=379).Results:(1) Serum sST2-day4 level was significantly higher in the cardiac death group than those in the survival group(242.71 [84.38-340.25] ng/ml vs 42.97 [29.67-81.96] ng/ml, P<0.001);(2) Binary logistic regression analysis showed that sST2-day4 was independently associated with cardiac death at 6 months(P<0.001) in AMI patients, even with the addition of NT-proBNP. sST2-day4 level remained as the independent predictor for 6-month cardiac death after adjustment for conventional cardiovascular risk factors in this patient cohort(P<0.001).Conclusions: Serum sST2 level could be used as an independent predictor for 6-month cardiac death in patients with AMI.
引文
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[15]Dhillon OS,Narayan HK,Quinn PA,et al.Interleukin 33 and ST2in non-ST-elevation myocardial infarction:comparison with Global Registry of Acute Coronary Events Risk Scoring and NT-proBNP[J].Am Heart J,2011,161(6):1163-1170.DOI:10.1016/j.ahj.2011.03.025.
[2]Weinberg EO.ST2 protein in heart disease:from discovery to mechanisms and prognostic value[J].Biomark Med,2009,3(5):495-511.DOI:10.2217/bmm.09.56.
[3]Weinberg EO,Shimpo M,De Keulenaer GW,et al.Expression and regulation of ST2,an interleukin-1 receptor family member,in cardiomyocytes and myocardial infarction[J].Circulation,2002,106(23):2961-2966.DOI:10.1161/01.cir.0000038705.69871.d9.
[4]Weir RA,Miller AM,Murphy GE,et al.Serum soluble ST2:a potential novel mediator in left ventricular and infarct remodeling after acute myocardial infarction[J].J Am Coll Cardiol,2010,55(3):243-250.DOI:10.1016/j.jacc.2009.08.047.
[5]Eggers KM,Armstrong PW,Califf RM,et al.ST2 and mortality in non-ST-segment elevation acute coronary syndrome[J].Am Heart J,2010,159(5):788-794.DOI:10.1016/j.ahj.2010.02.022.
[6]何蕾,彭剑,郑璇,等.血清可溶性致癌抑制因子2水平与急性ST段抬高型心肌梗死患者近期临床预后的相关性研究[J].中国循环杂志,2017,32(1):41-45.DOI:10.3969/j.jssn.1000-3614.2017.01.010.
[7]Barbarash O,Gruzdeva O,Uchasova E,et al.Prognostic value of soluble ST2 during hospitalization for ST-segment elevation myocardial infarction[J].Ann Lab Med,2016,36(4):313-319.DOI:10.3343/alm.2016.36.4.313.
[8]Thygesen K,Alpert JS,Jaffe AS,et al.Fourth universal definition of myocardial infarction(2018)[J].Circulation,2018,138(20):e618-e651.DOI:10.1161/CIR.0000000000000617.
[9]Miller AM.Role of IL-33 in inflammation and disease[J].J Inflamm(Lond),2011,8(1):22.DOI:10.1186/1476-9255-8-22.
[10]Ciccone MM,Cortese F,Gesualdo M,et al.A novel cardiac biomarker:ST2:a review[J].Molecules,2013,18(12):15314-15328.DOI:10.3390/molecules181215314.
[11]Shimpo M,Morrow DA,Weinberg EO,et al.Serum levels of the interleukin-1 receptor family member ST2 predict mortality and clinical outcome in acute myocardial infarction[J].Circulation,2004,109(12):2186-2190.
[12]Sanada S,Hakuno D,Higgins LJ,et al.IL-33 and ST2 comprise a critical biomechanically induced and cardioprotective signaling system[J].J Clin Invest,2007,117(6):1538-1549.DOI:10.1172/JCI30634.
[13]Januzzi JL,Mebazaa A,Di Somma S.ST2 and prognosis in acutely decompensated heart failure:the international ST2 consensus Panel[J].Am J Cardiol,2015,115(7 Suppl):26B-31B.DOI:10.1016/j.amjcard.2015.01.037.
[14]Sabatine MS,Morrow DA,Higgins TJ,et al.Complementary roles for biomarkers of biomechanical strain ST2 and N-terminal prohormone B-type natriuretic peptide in patients with ST-elevation myocardial infarction[J].Circulation,2008,117(15):1936-1944.DOI:10.1161/CIRCULATIONAHA.107.728022.
[15]Dhillon OS,Narayan HK,Quinn PA,et al.Interleukin 33 and ST2in non-ST-elevation myocardial infarction:comparison with Global Registry of Acute Coronary Events Risk Scoring and NT-proBNP[J].Am Heart J,2011,161(6):1163-1170.DOI:10.1016/j.ahj.2011.03.025.