胸痹贴Ⅰ号对不稳定型心绞痛气虚血瘀证CD40L影响的临床研究
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摘要
目的观察胸痹贴Ⅰ号对气虚血瘀型不稳定型心绞痛患者临床疗效以及CD40L的影响,分析揭示其对该病的治疗机制。
方法60例气虚血瘀型不稳定型心绞痛患者随机分成对照组(西医基础治疗)和治疗组(西药基础治疗+胸痹贴Ⅰ号),每组各30例,治疗两周,观察疗前疗后CD40L的变化、西雅图心绞痛量表评分等指标。
结果1.两组CD40L均较疗前有所降低(P<0.05)。2.与对照组相比,治疗组降低血小板CD40L更明显(P<0.05)。3.两组心绞痛量表评分均有提高(P<0.05)。4.与对照组相比,治疗组心绞痛量表评分提高更明显(P<0.05)。
结论1.胸痹贴Ⅰ号能够有效降低外周血中CD40L的含量。2.胸痹贴Ⅰ号可以提高西雅图心绞痛量表的各项评分,表明该药贴可以提高病人生活质量及改善机体功能状态。
Objective To observe the effect of the xiongbitie-I on the clinical treatment of UA and the expression of CD40L and analysis the mechanism of its treatment on UA.
Methods 60 patients with unstable angina pectoris were randomly divided into 2 groups. The treatment group and the control group both have 30 patients. There is no obvious difference in age、sex、illness course and severity degree between the two groups. Observe the change of the level of CD40L and the curative effect of unstable angina pectoris.
Results 1. The level of CD40L in both groups reduced (p< 0.05) 2. The level of CD40L in treatment group reduced more obviously than the control group 3.xiongbitie-Ⅰhas a obvious curative effect.
Conclusion 1.xiongbitie-Ⅰcould depress the level of CD40L in blood.2. xiongbitie-Ⅰcould improve the quality of life and the functional status of patients.
方法60例气虚血瘀型不稳定型心绞痛患者随机分成对照组(西医基础治疗)和治疗组(西药基础治疗+胸痹贴Ⅰ号),每组各30例,治疗两周,观察疗前疗后CD40L的变化、西雅图心绞痛量表评分等指标。
结果1.两组CD40L均较疗前有所降低(P<0.05)。2.与对照组相比,治疗组降低血小板CD40L更明显(P<0.05)。3.两组心绞痛量表评分均有提高(P<0.05)。4.与对照组相比,治疗组心绞痛量表评分提高更明显(P<0.05)。
结论1.胸痹贴Ⅰ号能够有效降低外周血中CD40L的含量。2.胸痹贴Ⅰ号可以提高西雅图心绞痛量表的各项评分,表明该药贴可以提高病人生活质量及改善机体功能状态。
Objective To observe the effect of the xiongbitie-I on the clinical treatment of UA and the expression of CD40L and analysis the mechanism of its treatment on UA.
Methods 60 patients with unstable angina pectoris were randomly divided into 2 groups. The treatment group and the control group both have 30 patients. There is no obvious difference in age、sex、illness course and severity degree between the two groups. Observe the change of the level of CD40L and the curative effect of unstable angina pectoris.
Results 1. The level of CD40L in both groups reduced (p< 0.05) 2. The level of CD40L in treatment group reduced more obviously than the control group 3.xiongbitie-Ⅰhas a obvious curative effect.
Conclusion 1.xiongbitie-Ⅰcould depress the level of CD40L in blood.2. xiongbitie-Ⅰcould improve the quality of life and the functional status of patients.
引文
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[7]张菲斐,邵建华,朱兴雷,等.不稳定型心绞痛患者活化血小板表达细胞分化抗原40配体及其与可溶性黏附分子水平的关系[J].中国循环杂志,2002,17(1)：20-22.
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[9]Jamieson GA. Patho physiology of platelet thrombin receptors[J].Thromb Haemost,1997,78:242～246.
[10]孙冰.普思复对老年冠心病血液流变学的影响[J].现代中西医结合杂志2006,14(16)：2140.
[11]高中芳,杨宝珍.老年冠心病患者血液流变学检测分析[J].中国血液流变学杂志,2006,16(1)：108、109.
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[14]Yasue H, Horio Y, Naka muira N, et al. Induction of coronary artery spasm by Aeetylcholine in Patients With variantangina:Possible role of the Parasym-athetie nervous system in the Pathogenesis of coronary artery spasm[J].Circulation,1986, 74:955—963.
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[16]Zaman AG, Helft G, Worthley SG,et al.The role of plaque rupture and thrombosis in coronary disease[J].Atherosclerosis,2000,149(2):251～256.
[17]Liao J K.Endothelium and acute coronary syndromes[J].Clin Chem,1998, 44(8):1799～1808.
[18]MACH F,SCHONBECK LL,BONNEFOY JY, et al.Activation of monocyte/macrophage functions related to acute atheroma complication by ligation of CD40:induction of collagenase,stromelysin,and tissue factor[J].Circulation.
[19]SchonbeckU,Mach F, Libby P. CD154(CD401igand) [J]. Int J Biochem cell Bio.l 2000,32(7):687-693.
[20]AndreP, Nannizzi-Alaimo L, Prasad SK, et al. Platelet-derived CD40L:the switch-hitting player of cardiovascular disease[J]. Circulation,2002,106(8):896-899.
[21]LangerF,IngersollSB,AmirkhosraviA,etal.The role of CD40 in CD40L and antibody-mediated plateletactivation[J].ThrombHaemost,2005,93(6):1137-1146.
[22]Andre P, Prasad KS, Denis CV, et al. CD40L stabilizes arterial thrombi by a beta-3 intgrin-dependent mechanism [J]. Nat Med,2002,8(3):247-252.
[23]BruemmerD,RiggersU,Holzmeiste J, et al.Expression of CD40 in vascular smooth muscle cells and macrophages is associated with early development of human atherosclerotic lesions[J].Am J Cardio,12001,87(1):21-27.
[24]Hakonarson H, Kim C,Whelan R, et al. Bi-directional activation between human airway smooth muscle cells and T lymphocytes:role in induction of altered airway responsiveness[J]. J Immuno,l 2001,166(1):293-303.
[25]CybulskyMI, IilyamaK,LiH, et al. A major role forVCAM-1, but not ICAM-1, in early atherosclerosis[J]. J Clin Invest,2001,107 (10):1255-1262.
[26]Collins RG,VeljiR,GuevaraNV,etal.P-selection or intercellular adhesion molecule(ICAM)-1 deficiency substantially protects against atherosclerosis in apolipoprotein E-deficientmice[J].J Exp Med,2000,191(1):189-194.
[27]ShibuyaH, Nagai T, Ishii A, et al. Differential regulation of Th1 responses and CD154 expression in human CD4+T cells by IFN-al-pha [J].Clin Exp Immuno,l 2003, 132(2):216-224.
[28]籍振国,刘坤申.从循证医学看目前冠心病的药物治疗.医学与哲学,2005,26.
[29]Antithrombotic Trialists collaboration.Collaborative meta-analysis of randomized trial of anti platelet therapy for prevention of death, myocardial infarction,and stroke in high risk patients[J].Br Med J,2002,324(7329):71～86.
[30]Watson R DS, Chin B SP,Lip G YH.ABC of antithrombotic therapy. Antithrombotic therapy in acute coronary syndromes [J].Br Med J,2002.325(7376):1348～1351.
[31]Zusman RM, Chesebro JH,Comerota A, et al.Antiplatelet therapy in the prevention of ischemic vascular events:literature review and evidence-based guidelines for drug selection[J].Clin Cardiol,1999,22(9):559～573.
[32]Talleson TR, O'Shea JC,Bittl JA,et al.Relationship between heparin anticoagution and clinical outcomes in coronary stent intervention:observation from e the ESPRIT trial[J].J Am Coll Cardiol,2003,41 (3):386～393.
[33]Van Es RF,Jonker JJ,Verheugt FW, et al.Aspirin and coumadin after acute coronary syndrome(the ASPECT-2Study):a randomised controlled trial[J].lancet,2002, 360(9350):2078.
[34]Lip G YH,Chin B SP, Presad N.ABC of antithrombotic therapy.Antithrombotic therapy in myocardial infarction and stable angina [J].Br Med J.2002,325(7375):1287～1289.
[35]Schwartz GG,Olsson AG,Ezekowitz M, et al.Effects of atorvastatin on early recurrent ischemic events in acute coronary syndrome es:the MIRACL study:a randomized controlled trial[J].JAMA,2001,285(13):1711～1718.
[36]Dujowe CA, Harris WS,Altman R, et al. Effect of atorvastatin on hemorheologic-hemostatin parameters and serum fibrinogen levels in hyperlipidemic patients[J].Am J Cardiol,2000,85(3):350～353.
[37]Undas A,Bmmrael KE, Musial J,et al.Simvostatin depresses blood clotting by inhibiting activation of prothrombin, factor V, and factor Ⅻ and by enhancing factor Vainactivation [J].Circulation,2001,103(18):2248～2253.
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