Siller-Matula Jolanta M, Specht Simon, Kubica Jacek, Alexopoulos Dimitrios, De Caterina Raffaele, Hobl Eva-Luise, Jilma Bernd, Christ Günter, Lang Irene M
Department of Cardiology, Medical University of Vienna, Vienna, Austria.
Department of Cardiology and Internal Medicine, Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz, Poland.
Br J Clin Pharmacol. 2016 Nov;82(5):1343-1350. doi: 10.1111/bcp.13053. Epub 2016 Jul 24.
The present study investigated whether the glycoprotein (GP)IIb/IIIa receptor blocker abciximab might be a successful bridging strategy to achieve adequate levels of platelet inhibition rapidly in cases where prasugrel is used in morphine-pretreated ST-elevation myocardial infarction (STEMI) patients.
In a prospective observational cohort study, 32 patients presenting with STEMI were given prasugrel at a loading dose of 60 mg. Patients were stratified into four groups, according to morphine and/or abciximab use. Adenosine diphosphate (ADP)-induced platelet aggregation was measured at four time points: at baseline, and at 2 h, 1 day and 2 days after prasugrel loading.
Morphine use was associated with a three-fold higher level of ADP-induced platelet aggregation 2 h after prasugrel loading compared with no morphine/no abciximab (P = 0.019). However, when abciximab was infused in the catheterization laboratory, the effect of morphine on ADP-induced platelet aggregation disappeared (P = 0.884). This interaction was also seen in the presence of high on-treatment platelet reactivity (HTPR) at 2 h; while HTPR was seen in 88% of morphine users/no abciximab users, it was found in only 17-20% in the three other groups (P = 0.003). The effect of morphine disappeared by day 1 - 2.
The infusion of the GPIIb/IIIa receptor blocker abciximab allows immediate and efficient platelet inhibition in STEMI patients concomitantly receiving the oral ADP receptor blocker prasugrel and morphine.
本研究调查了在吗啡预处理的ST段抬高型心肌梗死（STEMI）患者中使用普拉格雷时，糖蛋白（GP）IIb/IIIa受体阻滞剂阿昔单抗是否可能是一种成功的桥接策略，以迅速达到足够的血小板抑制水平。
在一项前瞻性观察队列研究中，32例STEMI患者接受了60mg负荷剂量的普拉格雷。根据吗啡和/或阿昔单抗的使用情况，将患者分为四组。在四个时间点测量二磷酸腺苷（ADP）诱导的血小板聚集：基线时，以及普拉格雷负荷后2小时、1天和2天。
与未使用吗啡/未使用阿昔单抗相比，使用吗啡与普拉格雷负荷后2小时ADP诱导的血小板聚集水平高三倍相关（P = 0.019）。然而，当在导管实验室输注阿昔单抗时，吗啡对ADP诱导的血小板聚集的影响消失（P = 0.884）。在2小时时存在高治疗期血小板反应性（HTPR）的情况下也观察到这种相互作用；虽然88%的吗啡使用者/未使用阿昔单抗使用者出现HTPR，但在其他三组中仅发现17%-20%（P = 0.003）。吗啡的影响在第1-2天消失。
在同时接受口服ADP受体阻滞剂普拉格雷和吗啡的STEMI患者中，输注GPIIb/IIIa受体阻滞剂阿昔单抗可立即有效地抑制血小板。
