• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

循环血小板上P选择素高表达和CD36低占有率是冠心病患者冠状动脉支架置入术后再狭窄的有力预测指标。

High P-selectin expression and low CD36 occupancy on circulating platelets are strong predictors of restenosis after coronary stenting in patients with coronary artery disease.

作者信息

Murasaki Kagari, Kawana Masatoshi, Murasaki Satoshi, Tsurumi Yukio, Tanoue Kenjiro, Hagiwara Nobuhisa, Kasanuki Hiroshi

机构信息

Department of Cardiology, The Heart Institute of Japan, Tokyo Women's Medical University, Tokyo 162-8666, Japan.

出版信息

Heart Vessels. 2007 Jul;22(4):229-36. doi: 10.1007/s00380-006-0966-5. Epub 2007 Jul 20.

DOI:10.1007/s00380-006-0966-5
PMID:17653516
Abstract

Recent studies have shown that circulating platelets play an important role in the development of restenosis early after coronary stent implantation. We investigated P-selectin expression and CD36 blockade on platelets by flow cytometry in 48 consecutive patients who underwent coronary stenting. P-selectin expression was significantly higher 1 day after stenting in patients who had restenosis (n = 15) than in those who had no restenosis (n = 28), and the odds ratio for restenosis in patients with high P-selectin levels (MFI > 6.5) was 11.67 (P < 0.001) as compared with patients who had intermediate and low P-selectin levels. CD36 blockade was assessed with the use of two anti-CD36 antibodies, OKM5 and GS95 (our new anti-CD36 antibody), the binding of which indicates total CD36 amount and free CD36 unoccupied by lipid-related ligands, respectively. Binding of OKM5 to platelets was similar before and after stenting in both groups. CD36 blockade on platelets was seen 1 day after stenting in the non-restenosis group, and the odds ratio for restenosis in patients without CD36 blockade [GS95 binding ratio >0.8 as compared with binding before stenting] on day 1 was 28.60 (P < 0.001). P-selectin expression and unoccupied CD36 on platelets shortly after stenting may be strong predictors of post-stent restenosis.

摘要

近期研究表明,循环血小板在冠状动脉支架植入术后早期再狭窄的发生过程中起重要作用。我们通过流式细胞术对48例接受冠状动脉支架置入术的连续患者的血小板上P-选择素表达及CD36阻断情况进行了研究。再狭窄患者(n = 15)支架置入术后1天的P-选择素表达显著高于无再狭窄患者(n = 28),与P-选择素水平中等和较低的患者相比,P-选择素水平高(平均荧光强度>MFI>6.5)的患者发生再狭窄的比值比为11.67(P<0.001)。使用两种抗CD36抗体OKM5和GS95(我们新的抗CD36抗体)评估CD36阻断情况,它们的结合分别表示总的CD36量和未被脂质相关配体占据的游离CD36。两组患者支架置入前后OKM5与血小板的结合情况相似。非再狭窄组在支架置入术后1天出现血小板CD36阻断,第1天无CD36阻断[GS95结合率>0.8,与支架置入前的结合情况相比]的患者发生再狭窄的比值比为28.60(P<0.001)。支架置入后不久血小板上的P-选择素表达及未被占据的CD36可能是支架后再狭窄的有力预测指标。

相似文献

1
High P-selectin expression and low CD36 occupancy on circulating platelets are strong predictors of restenosis after coronary stenting in patients with coronary artery disease.循环血小板上P选择素高表达和CD36低占有率是冠心病患者冠状动脉支架置入术后再狭窄的有力预测指标。
Heart Vessels. 2007 Jul;22(4):229-36. doi: 10.1007/s00380-006-0966-5. Epub 2007 Jul 20.
2
Cilostazol inhibits leukocyte integrin Mac-1, leading to a potential reduction in restenosis after coronary stent implantation.西洛他唑抑制白细胞整合素Mac-1,从而可能降低冠状动脉支架植入术后的再狭窄发生率。
J Am Coll Cardiol. 2004 Oct 6;44(7):1408-14. doi: 10.1016/j.jacc.2004.06.066.
3
Blood level of CD45+ platelets and development of restenosis after drug-eluting stent implantation in patients with stable coronary artery disease.稳定性冠心病患者药物洗脱支架植入术后CD45+血小板的血药浓度与再狭窄的发生
Wien Klin Wochenschr. 2016 Dec;128(23-24):898-905. doi: 10.1007/s00508-016-1074-x. Epub 2016 Sep 8.
4
Periprocedural soluble P- and E-selectin levels fail as predictors of clinical restenosis in patients treated with elective coronary stenting.在接受择期冠状动脉支架置入术的患者中,围手术期可溶性P选择素和E选择素水平不能作为临床再狭窄的预测指标。
Int J Mol Med. 2007 Jan;19(1):187-95.
5
Peripheral CD34+ cells and the risk of in-stent restenosis in patients with coronary heart disease.外周血CD34+细胞与冠心病患者支架内再狭窄风险
Am J Cardiol. 2005 Oct 15;96(8):1116-22. doi: 10.1016/j.amjcard.2005.06.042. Epub 2005 Aug 29.
6
Comparison of activation process of platelets and neutrophils after coronary stent implantation versus balloon angioplasty for stable angina pectoris.冠状动脉支架植入术与球囊血管成形术治疗稳定型心绞痛后血小板和中性粒细胞激活过程的比较
Am J Cardiol. 2000 Nov 15;86(10):1057-62. doi: 10.1016/s0002-9149(00)01159-0.
7
The amount of fibrinogen-positive platelets predicts the occurrence of in-stent restenosis.纤维蛋白原阳性血小板的数量可预测支架内再狭窄的发生。
Atherosclerosis. 2008 Mar;197(1):190-6. doi: 10.1016/j.atherosclerosis.2007.03.020. Epub 2007 May 7.
8
Novel Biomarkers for Coronary Restenosis Occurrence After Drug-Eluting Stent Implantation in Patients With Diabetes Having Stable Coronary Artery Disease.糖尿病合并稳定型冠状动脉疾病患者药物洗脱支架植入术后冠状动脉再狭窄发生的新型生物标志物
Clin Appl Thromb Hemost. 2018 Nov;24(8):1308-1314. doi: 10.1177/1076029618771752. Epub 2018 May 1.
9
Increase in soluble E-selectin level after PTCA and stent implantation: a potential marker of restenosis.
Int J Cardiol. 2004 Jan;93(1):13-8. doi: 10.1016/s0167-5273(03)00111-6.
10
Integrity(®) bare-metal coronary stent-induced platelet and endothelial cell activation results in a higher risk of restenosis compared to Xience(®) everolimus-eluting stents in stable angina patients.在稳定型心绞痛患者中,与Xience®依维莫司洗脱支架相比,Integrity(®)裸金属冠状动脉支架引起的血小板和内皮细胞活化导致再狭窄风险更高。
Platelets. 2016 Jul;27(5):410-9. doi: 10.3109/09537104.2015.1112368. Epub 2016 Jan 14.

引用本文的文献

1
Temporal changes in circulating P-selectin, plasminogen activator inhibitor-1, magnesium, and creatine kinase after percutaneous coronary intervention.经皮冠状动脉介入治疗后循环中 P-选择素、纤溶酶原激活物抑制剂-1、镁和肌酸激酶的时间变化。
J Zhejiang Univ Sci B. 2010 Aug;11(8):575-82. doi: 10.1631/jzus.B1001006.
2
Acute myocardial infarction as a systemic prothrombotic condition evidenced by increased von Willebrand factor protein over ADAMTS13 activity in coronary and systemic circulation.急性心肌梗死作为一种全身性血栓形成前状态,表现为在冠状动脉和体循环中血管性血友病因子蛋白水平升高超过ADAMTS13活性。
Heart Vessels. 2008 Sep;23(5):301-7. doi: 10.1007/s00380-008-1053-x. Epub 2008 Sep 20.

本文引用的文献

1
Detection of In Vivo Activated Platelets in Experimental Cerebral Thrombosis: Studies Using a New Monoclonal Antibody 2T60, Specific for Activated Human and Rabbit Platelets.体内活化血小板在实验性脑血栓形成中的检测:使用新的单克隆抗体 2T60(特异性识别人及兔活化血小板)的研究。
Platelets. 1993;4(1):31-9. doi: 10.3109/09537109309013193.
2
Physiological and pathological roles of a multi-ligand receptor CD36 in atherogenesis; insights from CD36-deficient patients.多配体受体CD36在动脉粥样硬化发生中的生理和病理作用;来自CD36缺陷患者的见解。
Mol Cell Biochem. 2007 May;299(1-2):19-22. doi: 10.1007/s11010-005-9031-4.
3
Takotsubo-shaped cardiomyopathy with type I CD36 deficiency.
Heart Vessels. 2005 May;20(3):123-5. doi: 10.1007/s00380-004-0787-3.
4
A novel role for CD36 in VLDL-enhanced platelet activation.CD36在极低密度脂蛋白增强血小板活化中的新作用。
Diabetes. 2003 May;52(5):1248-55. doi: 10.2337/diabetes.52.5.1248.
5
Comparison of activation process of platelets and neutrophils after coronary stent implantation versus balloon angioplasty for stable angina pectoris.冠状动脉支架植入术与球囊血管成形术治疗稳定型心绞痛后血小板和中性粒细胞激活过程的比较
Am J Cardiol. 2000 Nov 15;86(10):1057-62. doi: 10.1016/s0002-9149(00)01159-0.
6
PS-liposome and ox-LDL bind to different sites of the immunodominant domain (#155-183) of CD36: a study with GS95, a new anti-CD36 monoclonal antibody.PS脂质体和氧化型低密度脂蛋白(ox-LDL)与CD36免疫显性结构域(#155-183)的不同位点结合:一项使用新型抗CD36单克隆抗体GS95的研究。
Thromb Res. 2000 Mar 1;97(5):317-26. doi: 10.1016/s0049-3848(99)00179-6.
7
Circulating platelets show increased activation in patients with acute cerebral ischemia.急性脑缺血患者循环血小板的活化增加。
Thromb Haemost. 1999 Mar;81(3):373-7.
8
New intracoronary stent designs: form follows function versus function follows form.
Curr Opin Cardiol. 1998 Jul;13(4):232-9. doi: 10.1097/00001573-199807000-00003.
9
A clinical trial comparing three antithrombotic-drug regimens after coronary-artery stenting. Stent Anticoagulation Restenosis Study Investigators.一项比较冠状动脉支架置入术后三种抗血栓药物治疗方案的临床试验。支架抗凝再狭窄研究组。
N Engl J Med. 1998 Dec 3;339(23):1665-71. doi: 10.1056/NEJM199812033392303.
10
The stent decade: 1987 to 1997. Stanford Stent Summit faculty.
Am Heart J. 1998 Oct;136(4 Pt 1):578-99. doi: 10.1016/s0002-8703(98)70004-3.