血清可溶性髓样细胞触发受体-1水平对冠状动脉粥样斑块进展的预测价值被引量：13

Value of serum soluble triggering receptor expressed on myeloid cells-1 level for predicting coronary plaque progression

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摘要目的：探讨冠状动脉（冠脉）粥样硬化性心脏病患者血清可溶性髓样细胞触发受体-1（sTREM-1）水平对冠脉粥样硬化斑块进展的预测价值。方法：入选82例稳定型心绞痛患者,检测首次冠脉造影前空腹血清sTREM-1水平,患者接受冠脉造影随访复查,根据冠脉病变定量分析结果将患者分为斑块进展组（n=47）和无斑块进展组（n=35）。结果：斑块进展组血清sTREM-1水平显著高于无斑块进展组[（349.57±222.89）pg/mL对（176.85±118.62）pg/mL,P〈0.001]。血清sTREM-1水平与进展斑块数（P=0.002）及累计斑块进展积分（P=0.009）显著相关。经校正传统危险因素和冠脉病变血管数后,血清sTREM-1水平增高是斑块进展的独立危险因素（OR=2.008,95%CI：1.377~2.930,P〈0.001）。sTREM-1水平预测斑块进展的ROC曲线下面积为0.754（95%CI：0.650~0.857,P〈0.001）,最适截断值为238.74 pg/mL（敏感度61.7%,特异性80.0%）。结论：血清sTREM-1水平升高可能是冠脉粥样硬化斑块进展的预测指标之一。 Objective： To investigate the possible role of serum soluble triggering receptor expressed on myeloid cells-1 （sTREM-1） level in predicting coronary plaque progression （PP） in patients with coronary atherosclerotic heart disease. Methods： 82 patients with stable angina who underwent repeat coronary angiography were enrolled and divided into patients with PP （n = 47） and without PP （n = 35） according to quantitative coronary analysis. Serum levels of sTREM-1 were measured using ELISA kits before the first operation. Results： Serum sTREM-1 was significantly higher in patients with PP than those without PP [（349. 57± 222. 89） pg/mL vs. （176. 85± 118. 62） pg/mL, P 0. 001], and correlated with the number of PP （P = 0. 002） and cumulative obstruction score （P = 0. 009）. After adjusting for conventional risk factors and number of total coronary artery lesions, serum sTREM-1 remained an independent determinant for PP （OR = ：2. 008,95% CI： 1. 377±2. 930, P 0. 001）. ROC curve showed an area under the curve of sTREM-1 was 0. 754 （95% CI：0. 650±0. 857, P〈0. 001） with an optimal cut-off point of ：238. 74 pg/mL for predicting PP biomarker （sensitivity 61.7%, specificity 80. 0%） . Conclusion： Increased serum sTREM-1 level is a potential predicting biomarker for coronary PP.

作者戴道鹏沈迎张瑞岩丁风华陆林陶蓉

机构地区上海交通大学医学院附属瑞金医院心脏科

出处《国际心血管病杂志》 2016年第5期303-306,共4页 International Journal of Cardiovascular Disease

关键词可溶性髓样细胞触发受体-1 冠状动脉粥样硬化性心脏病斑块进展 Soluble triggering receptor expressed on myeloid cells-l Coronary artery disease Plaque progression

分类号 R541.4 [医药卫生—心血管疾病]

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1Newby LK, LaPointe NM, Chen AY, et al. Long-term adherence to evidence-based secondary prevention therapies in coronary artery disease [J ]. Circulation, 2006, 113 (2) 203-212.
2Morice MC, Serruys PW, Sousa JE, et al. A randomized comparison of a sirolimus-eluting stent with a standard stent for coronary revascularization[J]. New Engl J Med, 2002, 346(23) : 1773-1780.
3Zairis MN, Ambrose JA, Manousakis SJ, et al. The impact of plasma levels of C-reactive protein, lipoprotein (a) and homocysteine on the long-term prognosis after successful coronary stentingz The Global Evaluation of New Events and Restenosis After Stent Implantation Study[J]. J Am (2011 Cardiol, 2002, 40(8): 1375-1382.
4Hansson GK. Inflammation, atherosclerosis, and coronary artery disease [J]. N Engl J Med, 2005, 352 (16): 1685-1695.
5Bouchon A, Dietrich J, Colonna M. Cutting edge: inflammatory responses can be triggered by TREM-1, a novel receptor expressed on neutrophils and monocytes [J ]. J Immunol, 2000, 164(10): 4991- 4995.
6Gingras MC, Lapillonne H, Margolin JF. TREM1, MDL-1, and DAP12 expression is associated with a mature stage of myeloid development[J]. Mol Immunol, 2002, 38 (11): 817-824.
7Veldsquez S, Matute JD, Gamez LY, et al. Characterization of nCD64 expression in neutrophils and levels of s-TREM-1 and HMGPrl in patients with suspected infection admitted in an emergency department[J]. Biomedica, 2013, 33(4): 643- 652.
8Gibot S, Kolopp-Sarda MN, Bene MC, et al. Plasma level of a triggering receptor expressed on myeloid cells-1:its diagnostic accuracy in patients with suspected sepsis[J]. Ann Interrn Med, 2004, 141(1): 9 -15.
9Boufenzer A, Lemari4 J, Simon T, et al. TREM-1 mediates inflammatory injury and cardiac remodeling following myocardial infarction [J]. Circ Res, 2015, 116 (11): 1772-1782.
10Fraker TD, Fihn SD. 2007 chronic angina focused update of the ACC/AHA 2002 guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology:American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 guidelines for the management of patients with chronic stable angina[J]. J Am Coll Cardiol, 2007, 50(23): 2264-2274.

二级参考文献52

1Koenen RR, Weber C. Chemokines: established and noveltargets in atherosclerosis [J]. EMBO Mol Med, 2011,3(12); 713-725.
2Kadi A, Meher AK* Sharma PR,et al. Identification of anovel macrophage phenotype that develops in response toatherogenic phospholipids via Nr.2 [ J Circ Res, 2010,107(6): 737-746.
3Stoger JL, Gijbels MJ,van der Velden S,et al. Distributionof macrophage polarization markers in human atherosclerosis[J]. Atherosclerosis, 2012, 225(2) : 461-468.
4Gui T, Shimokado A, Sun Y, et al. Diverse roles of macrophagesin atherosclerosis: from inflammatory biology to biomarkerdiscovery[J]. Mediators Inflamm, 2012,2012;693083.
5Woollard KJ,Geissmann F. Monocytes in atherosclerosis :subsets and functions [J]. Nat Rev Cardiol, 2010,7(2):77-86.
6Makinen PI, Lappalainen JP,Heinonen SE, et al. Silencingof either SR-A or CD36 reduces atherosclerosis inhyperlipidaemic mice and reveals reciprocal upregulation ofthese receptors[J]. Cardiovasc Res, 2010,88(3) : 530-538.
7Little PJ,Chait A, Bobik A. Cellular and cytokine-basedinflammatory processes as novel therapeutic targets for theprevention and treatment of atherosclerosis [J]. PharmacolTher, 2011,131(3) : 255-268.
8Businaro R, Tagliani A* Buttari B,et al. Cellular and molecularplayers in the atherosclerotic plaque progression^Jl. Ann NY Acad Sci, 2012,1262 : 134-141.
9Go GW, Mani A. Low-density lipoprotein receptor (LDLR)family orchestrates cholesterol homeostasis [J]. Yale J BiolMed, 2012,85(1) : 19-28.
10Moore KJ, Tabas I. Macrophages in the pathogenesis ofatherosclerosis[J]. Cell, 2011,145(3) : 341-355.