Cassar Kevin, Bachoo Paul, Ford Isobel, Greaves Mike, Brittenden Julie
Department of Vascular Surgery, University of Aberdeen, Scotland, United Kingdom.
J Vasc Surg. 2005 Aug;42(2):252-8. doi: 10.1016/j.jvs.2005.04.027.
Coagulation activation markers are significantly elevated in patients with peripheral arterial disease compared with healthy controls. The more severe the disease, the higher the markers. Increased coagulation activation may contribute to the disease process and the risk of complications in patients with peripheral arterial disease, particularly after endovascular intervention. Animal studies have shown that clopidogrel significantly inhibits coagulation activation. The aim of this study was to determine whether combination of aspirin and clopidogrel affects thrombin-antithrombin III and D-dimer in patients with intermittent claudication undergoing angioplasty, compared with aspirin alone.
This was a double blind, randomized placebo-controlled trial conducted in a vascular unit in a tertiary referral center. One hundred thirty-two patients with intermittent claudication were randomized to clopidogrel and aspirin or placebo and aspirin, with a loading dose 12 hours before endovascular intervention. D-dimer and thrombin-antithrombin III (TAT) levels were measured using enzyme-linked immunosorbent assay at baseline, 1 hour before, and 1 hour, 24 hours, and 30 days after intervention in 103 patients who underwent endovascular intervention.
There was a significant rise in D-dimer levels at 1 hour and 24 hours after angioplasty in both groups (placebo group: 63.69, 141.45, 122.18 ng/mL; clopidogrel group: 103.79, 159.95, 134.69 ng/mL), but no difference between the two groups (P = .514). Similarly there was a significant rise in TAT levels at 1 hour after angioplasty in both groups (placebo group: 2.93, 6.16 microg/L; clopidogrel group: 3.39, 5.27 microg/L), with no significant difference between the two groups (P = .746).
Endovascular intervention results in a significant increase in TAT and D-dimer. The addition of clopidogrel to aspirin has no effect on TAT and D-dimer before or after endovascular intervention.
与健康对照相比,外周动脉疾病患者的凝血激活标志物显著升高。疾病越严重,标志物水平越高。凝血激活增加可能促成外周动脉疾病患者的疾病进程及并发症风险,尤其是在血管内介入治疗后。动物研究表明,氯吡格雷可显著抑制凝血激活。本研究的目的是确定与单独使用阿司匹林相比,阿司匹林和氯吡格雷联合用药对接受血管成形术的间歇性跛行患者的凝血酶 - 抗凝血酶III及D - 二聚体是否有影响。
这是一项在三级转诊中心的血管科进行的双盲、随机、安慰剂对照试验。132例间歇性跛行患者被随机分为氯吡格雷与阿司匹林组或安慰剂与阿司匹林组,在血管内介入治疗前12小时给予负荷剂量。对103例接受血管内介入治疗的患者,在基线、介入前1小时、介入后1小时、24小时及30天使用酶联免疫吸附测定法测量D - 二聚体和凝血酶 - 抗凝血酶III(TAT)水平。
两组在血管成形术后1小时和24小时D - 二聚体水平均显著升高(安慰剂组:63.69、141.45、122.18 ng/mL;氯吡格雷组:103.79、159.95、134.69 ng/mL),但两组间无差异(P = 0.514)。同样,两组在血管成形术后1小时TAT水平均显著升高(安慰剂组:2.93、6.16 μg/L;氯吡格雷组:3.39、5.27 μg/L),两组间无显著差异(P = 0.746)。
血管内介入治疗导致TAT和D - 二聚体显著增加。在阿司匹林基础上加用氯吡格雷对血管内介入治疗前后的TAT和D - 二聚体无影响。