Saw Jacqueline, Densem Cameron, Walsh Simon, Jokhi Percy, Starovoytov Andrew, Fox Rebecca, Wong Graham, Buller Christopher, Ricci Donald, Mancini G B John, Fung Anthony
Division of Cardiology, Vancouver General Hospital, University of British Columbia, Vancouver, British Columbia, Canada.
JACC Cardiovasc Interv. 2008 Dec;1(6):654-9. doi: 10.1016/j.jcin.2008.08.017.
The purpose of this study was to evaluate the effects of aspirin and clopidogrel response on myonecrosis after percutaneous coronary intervention (PCI) with glycoprotein (GP) IIb/IIIa blockade.
Aspirin and clopidogrel resistance is increasingly recognized, but its effects on PCI outcomes with GP IIb/IIIa blockade are unknown.
This was a prospective, pre-specified substudy of the BRIEF-PCI (Brief Infusion of Intravenous Eptifibatide Following Successful Percutaneous Coronary Intervention) trial, which randomized 624 patients to 18-h or <2-h eptifibatide infusion after uncomplicated PCI. To be eligible, patients must have been pre-treated with aspirin (>or=5 days) and clopidogrel (75 mg/day >or=5 days, 300 mg loading >or=6 h, or 600 mg loading >or=2 h) and must not have received GP IIb/IIIa inhibitors within 48 h. Verify-Now Aspirin and Clopidogrel (P2Y(12)) assays were performed at baseline before PCI. Patients with aspirin reaction unit (ARU) >or=550 were labeled as aspirin resistant. Clopidogrel low-responders were defined as those in the lowest quartile of platelet inhibition. The primary end point was the prevalence of myonecrosis within 24 h after PCI.
We enrolled 209 patients into our substudy, of which 185 had aspirin response assessed, 198 had clopidogrel response assessed, and 174 had both assessed. There were 4.9% who were aspirin resistant. Clopidogrel low-responders were defined as those in the lowest quartile with platelet inhibition <19%. Only 1.1% had both aspirin resistance and low clopidogrel response. There was no difference in myonecrosis prevalence among aspirin-resistant compared with aspirin-sensitive patients (11.1% vs. 27.8%, p = 0.259) or among clopidogrel low-responders compared with clopidogrel responders (23.5% vs. 29.3%, p = 0.433).
Aspirin and clopidogrel response did not affect myonecrosis prevalence amongst patients who received eptifibatide for PCI.
本研究旨在评估阿司匹林和氯吡格雷反应对经皮冠状动脉介入治疗(PCI)联合糖蛋白(GP)IIb/IIIa受体阻滞剂时心肌坏死的影响。
阿司匹林和氯吡格雷抵抗日益受到关注,但其对PCI联合GP IIb/IIIa受体阻滞剂治疗结果的影响尚不清楚。
这是BRIEF-PCI(经皮冠状动脉介入治疗成功后静脉注射依替巴肽短期输注)试验的一项前瞻性、预先指定的子研究,该试验将624例患者随机分为PCI成功后接受18小时或<2小时依替巴肽输注两组。符合条件的患者必须已预先接受阿司匹林治疗(≥5天)和氯吡格雷治疗(75毫克/天≥5天,负荷剂量300毫克≥6小时,或负荷剂量600毫克≥2小时),且在48小时内未接受GP IIb/IIIa抑制剂治疗。在PCI前基线时进行Verify-Now阿司匹林和氯吡格雷(P2Y(12))检测。阿司匹林反应单位(ARU)≥550的患者被标记为阿司匹林抵抗。氯吡格雷低反应者定义为血小板抑制处于最低四分位数的患者。主要终点是PCI后24小时内心肌坏死的发生率。
我们将209例患者纳入子研究,其中185例评估了阿司匹林反应,198例评估了氯吡格雷反应,174例两者均进行了评估。阿司匹林抵抗者占4.9%。氯吡格雷低反应者定义为血小板抑制<19%的最低四分位数患者。只有1.1%的患者同时存在阿司匹林抵抗和氯吡格雷低反应。阿司匹林抵抗患者与阿司匹林敏感患者的心肌坏死发生率无差异(11.1%对27.8%,p = 0.259),氯吡格雷低反应者与氯吡格雷反应者的心肌坏死发生率也无差异(23.5%对29.3%,p = 0.433)。
在接受依替巴肽进行PCI的患者中,阿司匹林和氯吡格雷反应不影响心肌坏死发生率。