Institute of Cardiology, University of Ferrara, Ferrara, Italy.
J Thromb Haemost. 2010 Sep;8(9):1903-11. doi: 10.1111/j.1538-7836.2010.03972.x.
On top of aspirin, an abciximab bolus-only regimen results in a 30% drop in platelet inhibition at 6 h as compared with the on-label regimen. The concomitant administration of high loading dose clopidogrel, by bridging with abciximab bolus, may sustain suppression of platelet activity over time.
To investigate the non-inferiority of abciximab bolus-only and concomitant high loading dose clopidogrel vs. abciximab bolus + infusion with respect to the inhibition of platelet aggregation (IPA) as determined by light transmission aggregometry.
PATIENTS/METHODS: Seventy-three patients with non-ST segment elevation acute coronary syndromes underwent double-blind randomization to abciximab bolus followed by a 12-h placebo infusion and concomitant 600-mg clopidogrel vs. abciximab bolus + a 12-h infusion and 300 mg of clopidogrel. IPA was determined by light transmission aggregometry throughout 24 h. Clopidogrel poor responsiveness was defined as ≥ 50% 5 μmol L⁻¹ ADP-induced maximum platelet aggregation.
In clopidogrel responders (n = 68), IPA after 20 μmol L⁻¹ ADP at 4 h was 89% ± 13% in the bolus-only arm vs. 92% ± 14% in the bolus + infusion arm (P = 0.011 for non-inferiority). IPA after 5 or 20 μmol L⁻¹ ADP and 5 or 15 μmol L⁻¹ TRAP and the proportion of patients showing ≥ 80% IPA did not differ at any time point, irrespective of clopidogrel responsiveness status. Thirty-day outcomes were similar, whereas hemoglobin (0.91 ± 0.8 vs. 0.5 ± 0.7 g dL⁻¹ ; P = 0.01) and platelet count mean drop (41.7 ± 57 vs. 18.6 ± 34 10⁹ L⁻¹; P = 0.042) were significantly reduced in the bolus-only arm.
Withholding abciximab post-bolus infusion in patients receiving high loading dose clopidogrel does not impair platelet inhibition throughout 24 h, and has the potential to improve the safety profile of the drug at reduced costs.
与标签治疗方案相比,在阿司匹林的基础上加用阿昔单抗单次推注可使血小板抑制率在 6 小时时降低 30%。通过阿昔单抗单次推注桥接高负荷剂量氯吡格雷,可以持续抑制血小板活性。
通过透光比浊法测定血小板聚集抑制(IPA),研究阿昔单抗单次推注与同时给予高负荷剂量氯吡格雷与阿昔单抗单次推注+输注相比,在抑制血小板聚集方面的非劣效性。
患者/方法:73 例非 ST 段抬高型急性冠状动脉综合征患者行双盲随机分组,分别接受阿昔单抗单次推注+12 小时安慰剂输注和同时给予 600mg 氯吡格雷(n=36),或阿昔单抗单次推注+12 小时输注和 300mg 氯吡格雷(n=37)。在 24 小时内通过透光比浊法测定 IPA。氯吡格雷反应不佳定义为 5μmol L⁻¹ ADP 诱导的最大血小板聚集率≥50%。
在氯吡格雷反应良好的患者(n=68)中,20μmol L⁻¹ ADP 作用 4 小时后的 IPA 在单次推注组为 89%±13%,在单次推注+输注组为 92%±14%(非劣效性 P=0.011)。在任何时间点,5 或 20μmol L⁻¹ ADP、5 或 15μmol L⁻¹ TRAP 后的 IPA 以及达到 80%IPA 的患者比例均无差异,无论氯吡格雷反应状态如何。30 天结局相似,但单次推注组血红蛋白(0.91±0.8 vs. 0.5±0.7 g dL⁻¹;P=0.01)和血小板计数平均下降量(41.7±57 vs. 18.6±34×10⁹ L⁻¹;P=0.042)显著降低。
在接受高负荷剂量氯吡格雷治疗的患者中,不给予阿昔单抗推注后输注并不会损害 24 小时内的血小板抑制,并且有可能降低药物成本的同时改善其安全性。