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在接受经皮冠状动脉介入治疗的患者中测量阿司匹林抵抗、氯吡格雷反应性和心肌坏死的术后标志物。

Measuring aspirin resistance, clopidogrel responsiveness, and postprocedural markers of myonecrosis in patients undergoing percutaneous coronary intervention.

作者信息

Buch Ashesh N, Singh Suman, Roy Probal, Javaid Aamir, Smith Kimberly A, George Christopher E, Pichard Augusto D, Satler Lowell F, Kent Kenneth M, Suddath William O, Waksman Ron

机构信息

Department of Medicine, Division of Cardiology, Washington Hospital Center, Washington, DC, USA.

出版信息

Am J Cardiol. 2007 Jun 1;99(11):1518-22. doi: 10.1016/j.amjcard.2007.01.023. Epub 2007 Apr 13.

Abstract

Aspirin and clopidogrel are proven to prevent thromboembolic events during percutaneous coronary intervention (PCI). Enzyme release of creatine kinase-MB (CK-MB) enzyme during PCI has been associated with an increased risk of future adverse cardiac events. This study examined the correlation between measurements of aspirin resistance and the level of inhibition of the thienopyridine-specific P2Y12 platelet receptor and CK-MB release after PCI. We prospectively studied 330 patients with elective PCI treated with drug-eluting stents. Patients were pretreated with aspirin and clopidogrel. Patients with positive CK-MB or acute coronary syndrome and those on glycoprotein IIb/IIIa inhibitors were excluded. Serum assays of aspirin resistance (Ultegra Rapid Platelet Function Assay-ASA, Accumetrics) and clopidogrel resistance (Rapid Platelet Function Assay P2Y12, Accumetrics) were performed before PCI. Serum troponinI and CK-MB levels were measured at 8, 16, and 24 hours after PCI. Aspirin resistance unit (ARU) measurement > or =550 was detected in 12 patients (3.7%). Mean platelet reactivity unit (PRU; measurement of inhibition of P2Y12 activity) was 192.2 +/- 95.4 (lower PRU, more inhibition of P2Y12 receptor). There was no correlation between level of ARU or PRU and troponin I or CK-MB release after PCI at any time point. Only multivessel coronary disease was found to be a predictor of any increase in CK-MB in a multivariate analysis (odds ratio 2.2, 95% confidence interval 1.4 to 3.3, p = 0.0003). A positive correlation was found between levels of ARU and PRU. Target vessel revascularization/major adverse cardiac event rate at 6 months was 8.2% with no correlation between ARU or PRU and release of cardiac enzymes or occurrence of adverse cardiac events. In conclusion, this study does not support routine measurements of aspirin and clopidogrel resistance in stable patients undergoing PCI.

摘要

阿司匹林和氯吡格雷已被证实可预防经皮冠状动脉介入治疗(PCI)期间的血栓栓塞事件。PCI期间肌酸激酶同工酶MB(CK-MB)的酶释放与未来发生不良心脏事件的风险增加有关。本研究检测了阿司匹林抵抗测量值与噻吩并吡啶特异性P2Y12血小板受体抑制水平以及PCI后CK-MB释放之间的相关性。我们前瞻性地研究了330例接受药物洗脱支架治疗的择期PCI患者。患者接受了阿司匹林和氯吡格雷预处理。排除CK-MB阳性或急性冠状动脉综合征患者以及使用糖蛋白IIb/IIIa抑制剂的患者。在PCI前进行血清阿司匹林抵抗检测(Ultegra快速血小板功能检测-ASA,Accumetrics公司)和氯吡格雷抵抗检测(快速血小板功能检测P2Y12,Accumetrics公司)。在PCI后8、16和24小时测量血清肌钙蛋白I和CK-MB水平。12例患者(3.7%)检测到阿司匹林抵抗单位(ARU)测量值≥550。平均血小板反应性单位(PRU;P2Y12活性抑制测量值)为192.2±95.4(PRU越低,P2Y12受体抑制越明显)。在任何时间点,PCI后ARU或PRU水平与肌钙蛋白I或CK-MB释放之间均无相关性。在多变量分析中,仅发现多支冠状动脉疾病是CK-MB升高的预测因素(比值比2.2,95%置信区间1.4至3.3,p = 0.0003)。ARU和PRU水平之间存在正相关。6个月时的靶血管重建/主要不良心脏事件发生率为8.2%,ARU或PRU与心脏酶释放或不良心脏事件的发生之间无相关性。总之,本研究不支持对接受PCI的稳定患者常规检测阿司匹林和氯吡格雷抵抗。

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