VWF与ACS的相关性及不同剂量瑞舒伐他汀治疗作用的临床研究
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摘要
目的:
     目前尽管进行了再灌注和优化的药物治疗,但仍有相当一部分急性冠脉综合征(acute coronary syndrome, ACS)患者显示出异常的心肌灌注,导致梗死面积扩大、左室射血分数降低和存活率减少。内皮细胞激活和炎症因子的释放在ACS发生发展过程中扮演着重要的角色。血管性血友病因子(von Willebrand factor, VWF)是反映急性内皮损伤极为特异性的炎症因子,大量的研究表明,血浆VWF水平增高是ACS患者预后不良的独立危险因素。他汀类药物是冠心病治疗的基础药物,除了降脂外,还有稳定斑块、改善内皮功能、抗炎、抗氧化等重要作用。本研究旨在:1,观察VWF在健康人群、稳定型心绞痛和ACS患者中不同的表达程度以评价VWF与ACS的相关性;2,观察不同剂量瑞舒伐他汀对VWF的抑制作用,以寻求一种新的、具有潜在价值的治疗ACS的思路。
     方法:
     共入选110例研究对象:20例健康正常人(对照组),30例稳定型心绞痛患者(SA组)、30例ACS患者(ACS组)、30例使用高剂量瑞舒伐他汀ACS患者(H组);ACS组和H组分别于入院时和一周后共抽血两次,对照组和SA组于入院时抽血一次;应用酶联免疫吸附法(enzyme-like immunosorbent assay, ELISA)测定血浆VWF水平。
     结果:
     1.稳定型心绞痛组与对照组之间血浆VWF水平无显著差异(P>0.05);ACS组和H组之间血浆VWF水平无显著差异(P>0.05);ACS组和H组较稳定型心绞痛组和对照组血浆VWF水平显著升高(P<0.05);
     2.ACS组一周后血浆VWF水平与入院时相比无显著变化(P>0.05);H组一周后血浆VWF水平较入院时显著降低(P<0.05)。
     结论:
     1.在一般人群中,血浆VWF水平只是一个很弱的冠心病预测指标;
     2.血浆VWF水平升高是ACS发生的标志物,VWF在ACS的进程中可能扮演着重要的角色;
     3.使用高剂量瑞舒伐他汀可以降低ACS患者的血浆VWF水平,具有内皮保护作用,而且其作用独立于降脂作用之外。
The Clinical Research of The Correlation between VWF and ACS and The Therapeutical Effect of Different doses of Rosuvastatin
     Objective:
     Despite of receiving reperfusion therapy and optimal medication, abnormal myocardial perfusion can be seen in patients with acute coronary syndrome (ACS) which expands the infarction area, decreases the left ventricular ejection fraction, and reduces the livability. The activation of endothelial cell and the releasing of inflammation factors play an important role in the occurrence and process of ACS. Von Willebrand factor (VWF) is a very specific inflammation factor reflecting acute endothelial injuries. A number of studies showed that increased concentration of plasma VWF was an independent risk factor of unfavorable prognosis in patients with ACS. Statins is the base drug in the treatment of coronary heart disease. Besides of lowering cholesterol, statins stabilize plaque, improve endothelial function, anti-inflammation, anti-oxidant etc. This study aims to:1.observe various plasma concentration of VWF in health adult, patients with stable angina and ACS to evaluate the correlation between VWF and ACS; 2.observe the inhibition of VWF by different doses of Rosuvastatin to seek a new and potential valued treatment of ACS.
     Methods:
     Selected 110 subjects. They were divided into four groups:20 healthy adults (control group); 30 patients with stable angina (SA group); 30 patients presenting with ACS (ACS group); 30 patients with ACS treated by high-dose Rosuvastatin (H group). Patients in ACS group and H group had plasma samples taken at admission and one week later. The control group and UA group had plasma samples taken at admission. Plasma concentration of von Willebrand factor was measured by enzyme-like immunosorbent assay (ELISA).
     Results:
     1. There was no significant difference of the VWF plasma concentration between SA group and the control group (P>0.05)、the ACS group and the H group (P>0.05); VWF plasma concentration is significantly higher of the patients in the ACS group and the H group than that of the patients in the SA group and the control group (P<0.05).
     3. There is no significant change of VWF plasma concentration one week later in ACS group (P<0.05). But significant depression of the VWF plasma concentration was observed in the H group one week later (P<0.05).
     Conclusions:
     1. Plasma VWF concentration is a weak predictor of coronary heart disease in the general population;
     2. The increased VWF plasma concentration is a marker of the occurrence of ACS; it may play an important role in the process of ACS;
     3. High dose of Rosuvastatin can decrease VWF plasma concentration in patients with ACS, has endothelial protective effect. And this is independent of its lipid-lowering effects.
引文
[1]Henriques JP, Zijlstra F,Vant Hof AW et al.Angiographic assessment of reperfusion in acute myocardial infarction by myocardial blush grade. Circulation.2003;107:2115-2119.
    [2]刘小慧,罗太阳.内皮功能和功能异常的检测及临床意义.心脏病学实践2007.人民卫生出版社2007;55-69.
    [3]陈良龙,罗育坤.急性冠脉综合征与炎症性生物标记物.心脏病学实践2006.人民卫生出版社2006;55-67.
    [4]Siedlecki CA, Lestini BJ, Kottke-Marchant KK et al. Shear-dependent changes in the hree-dimensional structure of human von Willebrand factor. Blood.1996;88:2939-2950.
    [5]Wagner-DD. Cell biology of von Willebrand factor. Annu Rev Cell Biol,1990;6:217-46.
    [6]叶任高,陆再英. 内科学.第六版人民卫生出版社2004;663-668.
    [7]周玉杰,杨士伟.PCI术前负荷量他汀类药物显著降低术后心血管事件.心脏病学实践2009.人民卫生出版社2009;152-165.
    [8]吕树铮,陈韵岱. 冠脉介入诊治技巧及器械选择.第二版人民卫生出版社2006;15-24.
    [9]GENSINI G G. A more meaningful scoring system for determining the severity of coronary heart disease.Am J Cardiol,1983,51(3):606-609.
    [10]陈文强,张运.动脉粥样硬化不稳定斑块的研究进展.心脏病学实践2007.人民卫生出版社2007;27-36.
    [11]Vischer UM, Wagner DD. von Willebrand factor proteolytic processing and multimerization precede the formation of Weibel-Palade bodies. Blood 1994; 83:3536-44.
    [12]Reininger AJ, Heijnen HF,Schumann et al. Mechanism of platelet adhesion to von Willebrand factor and microparticle formation under high shear stress. Blood.2006; 107: 3537-3545.
    [13]Santoro SA. Adsorption of von Willebrand factor/factor VIII by the genetically distinct interstitial collagens. Thromb Res.1981;21:689-691.
    [14]Koedam JA, Meijers JC, Sixma JJ, Bouma BN. Inactivation of human factor VIII by activated protein C:cofactor activity of protein S and protective effect of von Willebrand factor. J Clin Invest.1988;82:1236-1243.
    [15]Gill JC, Endres-Brooks J,Bauer PJ et al. The effect of ABO blood group on the diagnosis of von Willebrand disease. Blood 1987 Jun; 69(6):1691-5.
    [16]Jager A, van Hinsbergh VW,Kostense PJ et al. von Willebrand factor, C-reactive protein, and 5-year mortality in diabetic and nondiabetic subjects:the Hoorn Study. Arterioscler Thromb Vasc Biol 1999 Dec; 19(12):3071-8.
    [17]Danesh J,Wheeler JG, Hirschfield GM et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. N Engl J Med 2004; 350:1387-97.
    [18]Blann AD, Herrick A, Jayson MI. Altered levels of soluble adhesion molecules in rheumatoid arthritis, vasculitis and systemic sclerosis. Br J Rheumatol 1995; 34:814-9.
    [19]Stehouwer CDA, Gall M-A,Twisk JW et al. Increased urinary albumin excretion, endothelial dysfunction, and chronic low-grade inflammation in type 2 diabetes: progressive, interrelated, and independently associated with risk of death. Diabetes 2002; 51:1157-65.
    [20]Schooten CJ, Tjernberg P,Westein E et al. Cysteine-mutations in von Willebrand factor associated with increased clearance. J Thromb Haemost 2005; 3:2228-37.
    [21]Price JF, Mowbray PI,Lee AJ et al. Relationship between smoking and cardiovascular risk factors in the development of peripheral arterial disease and coronary artery disease: Edinburgh Artery Study. Eur Heart J.1999;20:344-353.
    [22]Conway DS, Pearce LA,Chin BS et al.Prognostic value of plasma von Willebrand factor and soluble P-selectin as indices of endothelial damage and platelet activation in 994 patients with nonvalvular atrial fibrillation. Circulation.2003;107:3141-3145.
    [23]Folsom AR, Wu KK,Rosamond WD et al.Prospective study of hemostatic factors and incidence of coronary heart disease:the Atherosclerosis Risk in Communities (ARIC) Study. Circulation.1997; 96:1102-1108.
    [24]Morange PE, Simon C,Alessi MC et al.Endothelial cell markers and the risk of coronary heart disease:the Prospective Epidemiological Study of Myocardial Infarction (PRIME) study. Circulation.2004; 109:1343-1348.
    [25]Li M, Goto S,Sakai H et al. Enhanced shear-induced von Willebrand factor binding to platelets in acute myocardial infarction. Thromb Res.2000 Nov 15;100(4):251-61.
    [26]Lee KW, Blann AD, Lip GY. Effects of omega-3 polyunsaturated fatty acids on plasma indices of thrombogenesis and inflammation in patients post-myocardial infarction. Thromb Res.2006;118:305-312.
    [27]Tousoulis D, Bosinakou E, KotsopoulouM et al.Effects of early administration of atorvastatin treatment on thrombotic process in normocholesterolemic patients with unstable angina. Int J Cardiol.2006; 106:333-337.
    [28]Lee KW, Blann AD, Lip GY. Inter-relationships of indices of endothelial damage/ dysfunction [circulating endothelial cells, von Willebrand factor and flow-mediated dilatation] to tissue factor and interleukin-6 in acute coronary syndromes. Int J Cardiol. 2006; 111:302-308.
    [29]余丹,贾三庆.VWF升高预测非ST段抬高的急性冠脉综合征患者的不良预后.杭州师范学院学报医学版.2008.
    [30]邓家栋.临床血液学上海科学技术出版社2001.1190.
    [31]Design and baseline characteristics of a study of primary prevention of coronary events with pravastatin among Japanese with mildly elevated cholesterol levels. Management of Elevted Cholesterol in the Primary Prevention Group of Adult Japanese (MEGA) Study Group. Circ J.2004 Sep; 68(9):860-7.
    [32]Huskey J, Lindenfeld J,Cook T et al. Effect of simvastatin on kidney function loss in patients with cornaty heart disease:findings from the Scandinavian Simvastatin Survival Study (4S). Atherosclerosis.2009 Jul; 205(1):202-6.
    [33]Briguori C, Visconti QFocaccio A et al. Novel approaches for preventing or limiting events (Naples) II trial:impact of a single high loading dose of atorvastatin on periprocedural myocardial infarction. J Am Coll Cardiol.2009 Dec 1;54 (23):2157-63.
    [34]Pasceri V, Patti G, Nusca A et al. ARMYDA Investigators. Randomized trial of atorvastatin for reduction of myocardial damage during coronary intervention:results from the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) study. Circulation.2004 Aug 10;110(6):674-8.
    [35]Patti G, Pasceri V,Colonna G et al. Atrovastatin pretreatment improves outcomes in patients with acute Coronary syndromes undergoing early percutaneous coronary intervention: results of the ARMYDA-ACS randomized trial. J Am Coll Cardiol.2007 Mar 27;49 (12): 1272-8.
    [36]Di Sciascio G, Patti G,Pasceril V et al.Efficacy of atorvastatin reload in patients on chronic statin therapy undergoing percutaneous coronary intervention:results of the ARMYDA-RECAPTURE (Atorvastatin for Reduction of Myocardial Damage During Angioplasty) Randomized Trial. J Am Coll Cardiol.2009 Aug 4;54(6):558-65.
    [37]Ridker PM, Fonseca FA, Genest J, et al; JUPITER Trial Study Group. Baseline characteristics of participants in the JUPITER trial, a randomized placebo-controlled primary prevention trial of statin therapy among individuals with low low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein. Am J Cardiol. 2007; 100:1659-1664.
    [38]Crouse JR 3rd, Raichlen JS, Riley WA, et al; METEOR Study Group.Effect of rosuvastatin on progression of carotid intima-media thickness in low-risk individuals with subclinical atherosclerosis:the METEOR Trial. JAMA.2007;297:1344-1353.
    [39]Nissen SE, Nicholls SJ, Sipahi I, et al; ASTEROID Investigators. JAMA.2006; 295: 1556-1565.
    [40]Sobel M, McNeill PM, Carlson PL et al. Heparin inhibition of von Willebrand factor-dependent platelet function in vitro and in vivo. J Clin Invest.1991;87:1787-1793
    [41]Gold HK, Gimple LW, Yasuda T et al.Pharmacodynamic study of F(ab_)2 fragments of murine monoclonal antibody 7E3 directed against human platelet glycoprotein Ⅱb/Ⅲa in patients with unstable angina pectoris. J Clin Invest.1990;86:651-659.
    [42]Girma JP, Fressinaud E, Christophe O et al.Aurin tricarboxylic acid inhibits platelet adhesion to collagen by binding to the 509-695 disulphide loop of von Willebrand factor and competing with glycoprotein Ib. Thromb Haemost.1992;68:707-713.
    [43]Wilson C, Keefe AD. Building oligonucleotide therapeutics using nonnatural chemistries. Curr Opin Chem Biol.2006;10:607-614.
    [44]Kageyama S, Yamamoto H,Yoshimoto R et al.Anti-human von Willebrand factor monoclonal antibody AJvW-2 prevents thrombus deposition and neointima formation after balloon injury in guinea pigs. Arterioscler Thromb Vasc Biol.2000;20:2303-230.
    [45]Staelens S, Hadders MA, Vauterin S et al. Paratope determination of the antithrombotic antibody 82D6A3 based on the crystal structure of its complex with the von Willebrand factor A3-domain. J Biol Chem 2006; 281:2225-2231.
    [1]Hollestelle MJ, Thinnes T, Crain K et al. Tissue distribution of factor Ⅷgene expression in vivo:a closer look. Thromb Haemost.2001;86:855-861.
    [2]叶任高,陆再英.内科学.第六版.人民卫生出版社2004;663-668.
    [3]Pernerstorfer T, Stohlawetz P, Kapiotis S et al. Partial inhibition of nitric oxide synthase primes the stimulated pathway of VWF-secretion in man. Atherosclerosis.2000; 148:43-47.
    [4]Brinkhous KM, Sandberg H, Garris JB et al. Purified human factor VIII procoagulant protein:comparative hemostatic response after infusions into hemophilic and von Willebrand disease dogs. Proc Natl Acad Sci U S A.1985;82:8752-8756.
    [5]刘小慧,罗太阳.内皮功能和功能异常的检测及临床意义.心脏病学实践2007.人民卫生出版社2007;55-69.
    [6]陈良龙,罗育坤.急性冠脉综合征与炎症性生物标记物.心脏病学实践2006.人民卫生出版社2006;55-67.
    [7]Siedlecki CA, Lestini BJ, Kottke-Marchant KK et al. Shear-dependent changes in the hree-dimensional structure of human von Willebrand factor. Blood.1996;88:2939-2950.
    [8]Mannucci PM. Platelet von Willebrand factor in inherited and acquired bleeding disorders. Proc Natl Acad Sci U S A.1995;92:2428-2432.
    [9]Pinsky DJ, Naka Y, Liao H et al. Hypoxia-induced exocytosis of endothelial cell Weibel-Palade bodies:a mechanism for rapid neutrophil recruitment after cardiac preservation. J Clin Invest.1996;97:493-500.
    [10]Chignard M, Balloy V, Renesto P. Leucocyte elastase-mediated release of von Willebrand factor from cultured endothelial cells. Eur Respir J.1993;6:791-796.
    [11]Mannucci PM, Ruggeri ZM, Pareti FI et al.1-Deamino-8-darginine vasopressin:a new pharmacological approach to the management of haemophilia and von Willebrands' diseases. Lancet.1977;1:869-872.
    [12]Salder JE.Biochemistry and genetics of von Willebrand factor.Annu Rev Biochem,1998, 67:395-424.
    [13]de Lange M, Snieder H, Ariens RAS et al. The genetics of haemostasis:a twin study. Lancet 2001; 357:101-05.
    [14]Gallinaro L, Cattini MG, Sztukowska M et al. A shorter von Willebrand factor survival in 0 blood group subjects explains how ABO determinants influence plasma von Willebrand factor. Blood 2008; 111:3540-3545.
    [15]Gill JC, Endres-Brooks J, Bauer PJ et al.The effect of ABO blood group on the diagnosis of von Willebrand disease. Blood 1987; 69:1691-95.
    [16]Jager A, van Hinsbergh VW, Kostense PJ et al.Von Willebrand factor, C-reactive protein, and 5-year mortality in diabetic and nondiabetic subjects:the Hoorn Study. Arterioscler Thromb Vasc Biol 1999; 19:3071-8.
    [17]Danesh J,Wheeler JG, HirschfieldGM et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. N Engl J Med 2004; 350:1387-97.
    [18]Blann AD, Herrick A, Jayson MI. Altered levels of soluble adhesion molecules in rheumatoid arthritis, vasculitis and systemic sclerosis. Br J Rheumatol 1995; 34:814-9.
    [19]Meigs JB, Mittleman MA, Nathan DM et al.Hyperinsulinemia, hyperglycemia, and impaired hemostasis:the Framingham offspring study. JAMA 2000; 283:221-28.
    [20]Schooten CJ, Tjernberg P,Terraube V et al. Cysteine-mutations in von Willebrand factor associated with increased clearance. J Thromb Haemost 2005; 3:2228-37.
    [21]Terrell DR, Williams LA, Vesely SK et al. The incidence of thrombotic thrombocytopenic purpura-hemolytic uremic syndrome:all patients,idiopathic patients, and patients with severe ADAMTS-13 deficiency. J Thromb Haemost 2005; 3:1432-1436.
    [22]Reininger AJ, Heijnen HF, Schumann H et al.Mechanism of platelet adhesion to von Willebrand factor and microparticle formation under high shear stress. Blood.2006; 107:3537-3545.
    [23]Ruggeri ZM, Orje JN, Habermann R et al. Activation-independent platelet adhesion and aggregation under elevated shear stress. Blood 2006;108:1903-1910.
    [24]Santoro SA. Adsorption of von Willebrand factor/factor VIII by the genetically distinct interstitial collagens. Thromb Res.1981;21:689-691.
    [25]Koedam JA, Meijers JC, Sixma JJ et al. Inactivation of human factor VIII by activated protein C:cofactor activity of protein S and protective effect of von Willebrand factor. J Clin Invest.1988;82:1236-1243.
    [26]Dong JF, Moake JL, Nolasco L et al. ADAMTS-13 rapidly cleaves newly secreted ultralarge von Willebrand factor multimers on the endothelial surface under flowing conditions. Blood.2002;100:4033-4039.
    [27]Price JF, Mowbray PI, Lee AJ et al.Relationship between smoking and cardiovascular risk factors in the development of peripheral arterial disease and coronary artery disease:Edinburgh Artery Study. Eur Heart J.1999;20:344-353.
    [28]Conway DS, Pearce LA, Chin BS et al. Prognostic value of plasma von Willebrand factor and soluble P-selectin as indices of endothelial damage and platelet activation in 994 patients with nonvalvular atrial fibrillation. Circulation.2003; 107:3141-3145.
    [29]廖荣宏,刘作金.血管内皮细胞损害与急性冠脉综合征患者凝血纤溶状态改变的关系第三军医大学学报2006.
    [30]Folsom AR, Wu KK, Rosamond WD et al. Prospective study of hemostatic factors and incidence of coronary heart disease:the therosclerosis Risk in Communities (ARIC) Study. Circulation.1997;96:1102-1108.
    [31]Morange PE, Simon C, Alessi MC et al. Endothelial cell markers and the risk of coronary heart disease:the Prospective Epidemiological Study of Myocardial Infarction (PRIME) study. Circulation.2004;109:1343-1348.
    [32]Whincup PH, Danesh J, Walker M et al. von Willebrand factor and coronary heart disease:prospective study and meta-analysis. Eur Heart J.2002;23:1764-1770.
    [33]Danesh J, Wheeler JG, Hirschfield GM et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. N Engl J Med 2004; 350:1387-97.
    [34]Goto S, Sakai H, Goto M et al.Enhanced shear-induced platelet aggregation in acute myocardial infarction. Circulation.1999;99:608-613.
    [35]Tousoulis D, Bosinakou E, Kotsopoulou M et al. Effects of early administration of atorvastatin treatment on thrombotic process in normocholest-erolemic patients with unstable angina. Int J Cardiol.2006; 106:333-337.
    [36]Lee KW, Blann AD, Lip GY. Effects of omega-3 polyunsaturated fatty acids on plasma indices of thrombogenesis and inflammation in patients post-myocardial infarction. Thromb Res.2006;118:305-312.
    [37]Lee KW, Blann AD, Lip GY. Inter-relationships of indices of endothelial damage/ dysfunction [circulating endothelial cells, von Willebrand factor and flow-mediated dilatation] to tissue factor and interleukin-6 in acute coronary syndromes. Int J Cardiol. 2006; 111:302-308.
    [38]Thompson SG, Kienast J, Pyke SD et al. Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris:European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. N Engl J Med. 1995;332:635-641.
    [39]Wiman B,Andersson T,Hallqvist J et al.Plasma levels of tissue plasminogen activator/ plasminogen activator inhibitor-1 complex and von Willebrand factor are significant risk markers for recurrent myocardial infarction in the Stockholm Heart Epidemiology Program (SHEEP) study. Arterioscler Thromb Vasc Biol.2000;20:2019-2023.
    [40]魏玉杰,刘惠亮.血清sVCAM-1和vWF的水平与冠脉病变程度的相关性.心血管康复医学杂志.2006:452-455.
    [41]余丹,贾三庆.VWF升高预测非ST段抬高的急性冠脉综合征患者的不良预后.杭州师范学院学报.医学版.2008.
    [42]Chion CK, Doggen CJ, Crawley JT et al. ADAMTS13 and von Willebrand factor and the risk of myocardial infarction in men. Blood.2007;109:1998-2000.
    [43]Sakai H, Goto S,Kim JY et al.Plasma concentration of von Willebrand factor in acute myocardial infarction. Thromb Haemost.2000;84:204-209.
    [44]Frossard M, Fuchs I, Leitner JM et al. Platelet function predicts myocardial damage in patients with acute myocardial infarction.Circulation.2004; 110:1392-1397.
    [45]Ray KK, Morrow DA, Gibson CM et al.Predictors of the rise in VWF after ST elevation myocardial infarction:implications for treatment strategies and clinical outcome:an ENTIRE-TIMI 23 substudy. Eur Heart J.2005;26:440-446.
    [46]Montalescot G, Philippe F, Ankri A et al.. Early increase of von Willebrand factor predicts adverse outcome in unstable coronary artery disease:beneficial effects of enoxaparin:French Investigators of the ESSENCE Trial. Circulation.1998;98:294-299.
    [47]Hodl R, Huber K, Kraxner W et al. Comparison of effects of dalteparin and enoxaparin on hemostatic parameters and von Willebrand factor in patients with unstable angina pectoris or non-ST-segment elevation acute myocardial infarction. Am J Cardiol. 2002;89:589-592.
    [48]Campo G, Valgimigli M, Gemmati D et al. Value of platelet reactivity in predicting response to treatment and clinical outcome in patients undergoing primary coronary intervention:insights into the STRATEGY Study. J Am Coll Cardiol.2006;48:2178-2185.
    [49]Andreotti F, Roncaglioni MC, Antman EM et al.Early coronary reperfusion blunts the procoagulant response of plasminogen activator inhibitor-1 and von Willebrand factor in acute myocardial infarction. J Am Coll Cardiol.1990;16:1553-1560.
    [50]Lip GY, Lydakis C,Nuttall SL et al.A pilot study of streptokinase-induced endothelial injury, and platelet activation following acute myocardial infarction. J Intern Med. 2000;248:316-318.
    [51]Henriques JP, Zijlstra F, van't Hof AW et al.Angiographic assessment of reperfusion in acute myocardial infarction by myocardial blush grade. Circulation.2003; 107:2115-2119.
    [52]Heper G, Murat SN, Durmaz T et al.Prospective evaluation of von Willebrand factor release after multiple and single stenting. Angiology.2004;55:177-186.
    [53]Kefer JM, Galanti LM, Desmet S et al.Time course of release of inflammatory markers after coronary stenting:comparison between bare metal stent and sirolimus-eluting stent. Coron Artery Dis.2005;16:505-509.
    [54]Yamashita A, Sumi T, Goto S et al. Detection of von Willebrand factor and tissue factor in platelets-fibrin rich coronary thrombi in acute myocardial infarction. Am J Cardiol. 2006; 97:26-28.
    [55]Goto S, Sakai H, Goto M et al. Enhanced shear-induced platelet aggregation in acute myocardial infarction. Circulation.1999;99:608-613.
    [56]Kageyama S, Yamamoto H, Nakazawa H et al.Pharmacokinetics and pharmacodynamics of AJW200, a humanized monoclonal antibody to von Willebrand factor, in monkeys. Arterioscler Thromb Vasc Biol.2002;22:187-192.
    [57]Hawkins BM, Abu-Fadel M, Vesely SK et al. Clinical cardiac involvement in thrombotic thrombocytopenic purpura:a systematic review. Transfusion.2008;48:382-392.
    [58]McLeod BC. Myocardial infarction in a blood donor after administration of desmopressin. Lancet.1990;336:1137-1138.
    [59]Sobel M, McNeill PM, Carlson PL et al. Heparin inhibition of von Willebrand factor-dependent platelet function in vitro and in vivo. J Clin Invest.1991;87:1787-1793
    [60]Jordan R, Berger H, Collen D et al. Pharmacodynamic study of F(ab_)2 fragments of murine monoclonal antibody 7E3 directed against human platelet glycoprotein Ⅱb/Ⅲa in patients with unstable angina pectoris. J Clin Invest.1990;86:651-659.
    [61]Wilson C, Keefe AD. Building oligonucleotide therapeutics using nonnatural chemistries. Curr Opin Chem Biol.2006;10:607-614.
    [62]Lee JF, Stovall GM, Ellington AD. Aptamer therapeutics advance. Curr Opin Chem Biol. 2006; 10:282-289.
    [63]Kageyama S, Yamamoto H, Yoshimoto R. Anti-human von Willebrand factor monoclonal antibody AJvW-2 prevents thrombus deposition and neointima formation after balloon injury in guinea pigs. Arterioscler Thromb Vasc Biol.2000;20:2303-2308.
    [64]Staelens S, Hadders MA, Vauterin S et al. Paratope determination of the antithrombotic antibody 82D6A3 based on the crystal structure of its complex with the von Willebrand factor A3-domain. J Biol Chem 2006; 281:2225-2231.
    [65]彭侃夫,吴宗贵.血浆VWF、CEC与动脉粥样硬化不稳定斑块相关性及苯那普利治疗作用的实验和临床研究2001.
    [66]Richard J. FISH, Hong YANG, et al. Fluvastatin inhibits regulated secretion of endothelial cell von Willebrand factor in response to diverse secretagogues. Biochem. J. (2007) 405,597-604.
    [67]Ordulu E, Erdogan O. Early effects of low versus high dose atorvastatin treatment on coagulation and inflammation parameters in patients with acute coronary syndromes. Int J Cardiol.2008 Aug 18;128(2):282-4.

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