Malek Lukasz A, Grabowski Marcin, Spiewak Mateusz, Filipiak Krzysztof J, Szpotanska Monika, Imiela Tomasz, Huczek Zenon, Bobilewicz Dagna, Opolski Grzegorz
1st Department of Cardiology, Medical University of Warsaw, 1a Banacha Str, Warsaw 02-097, Poland.
J Thromb Thrombolysis. 2007 Dec;24(3):301-5. doi: 10.1007/s11239-007-0026-8. Epub 2007 Apr 3.
The study was designed to determine whether impaired antiplatelet response to clopidogrel but not to aspirin may be responsible for loss of pleiotropic effects of the drug.
Study included 34 consecutive patients with STEMI undergoing primary percutaneous coronary intervention (PCI) with stent implantation treated with aspirin (loading dose 300 mg followed by 75 mg/day) and clopidogrel (loading dose 600 mg followed by 75 mg/day). On the basis of Platelet Function Analyzer (PFA)-100 test which measured closure times (CT) in test with collagen/epinephrine (CEPI-CT) or collagen/adenosine diphosphate (CADP-CT) patients were stratified after 7 days from admission as full aspirin or clopidogrel responders (CEPI-CT or CADP-CT = 300 sec., respectively) and non-full aspirin or clopidogrel responders (CEPI-CT or CADP-CT < 300 sec., respectively). High sensitivity C-reactive protein (hs-CRP) was measured at baseline and after 7 days of treatment.
All patients received comparable statin treatment. Median and interquartile ranges (IQR) of hs-CRP increased significantly from 2.5 mg/L (0.4-44.8) at baseline to 8.05 mg/L (1.4-33.9) at day 7 (P = .002) in non-full clopidogrel responders subgroup and only slightly in the full clopidogrel responders subgroup (2.45 mg/L, IQR 0.4-48.3 vs. 4.2 mg/L, IQR 1.9-17.5) (P = .3) remaining within reference intervals. On the contrary median and IQR of hs-CRP increased significantly in both non-full aspirin responders (2.4 mg/L, IQR 1.3-3.3 vs. 5.8 mg/L, IQR 3.2-14.8, P = .01) and full aspirin responders (2.9 mg/L, IQR 2.0-3.7 vs. 5.6 mg/L, IQR 4.3-12.9, P = .04).
Impaired antiplatelet response to clopidogrel but not to aspirin may contribute to smaller anti-inflammatory response in patients with ST-elevation myocardial infarction.
本研究旨在确定对氯吡格雷而非阿司匹林的抗血小板反应受损是否可能导致该药物多效性作用的丧失。
研究纳入了34例连续接受直接经皮冠状动脉介入治疗（PCI）并植入支架的ST段抬高型心肌梗死（STEMI）患者，这些患者接受阿司匹林（负荷剂量300mg，随后75mg/天）和氯吡格雷（负荷剂量600mg，随后75mg/天）治疗。根据血小板功能分析仪（PFA）-100检测，该检测测量胶原/肾上腺素（CEPI-CT）或胶原/二磷酸腺苷（CADP-CT）检测中的封闭时间（CT），入院7天后，患者被分层为阿司匹林或氯吡格雷完全反应者（CEPI-CT或CADP-CT分别 = 300秒）和阿司匹林或氯吡格雷非完全反应者（CEPI-CT或CADP-CT分别 < 300秒）。在基线和治疗7天后测量高敏C反应蛋白（hs-CRP）。
所有患者接受了相当的他汀类药物治疗。在氯吡格雷非完全反应者亚组中，hs-CRP的中位数和四分位数间距（IQR）从基线时的2.5mg/L（0.4 - 44.8）显著增加至第7天的8.05mg/L（1.4 - 33.9）（P = .002），而在氯吡格雷完全反应者亚组中仅略有增加（2.45mg/L，IQR 0.4 - 48.3对4.2mg/L，IQR 1.9 - 17.5）（P = .3），仍在参考区间内。相反，在阿司匹林非完全反应者（2.4mg/L，IQR 1.3 - 3.3对5.8mg/L，IQR 3.2 - 14.8，P = .01）和阿司匹林完全反应者（2.9mg/L，IQR 2.0 - 3.7对5.6mg/L，IQR 4.3 - 12.9，P = .04）中，hs-CRP的中位数和IQR均显著增加。
对氯吡格雷而非阿司匹林的抗血小板反应受损可能导致ST段抬高型心肌梗死患者的抗炎反应较小。
