抗血小板治疗反应独立于内源性凝血酶生成潜能。
Response to antiplatelet therapy is independent of endogenous thrombin generation potential.
机构信息
Division of Angiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
出版信息
Thromb Res. 2013 Jul;132(1):e24-30. doi: 10.1016/j.thromres.2013.04.008. Epub 2013 Apr 25.
BACKGROUND
Thrombin is the most potent platelet activator, and achieves rapid platelet activation even in the presence of antiplatelet therapy. Since activated platelets respond stronger to additional stimuli, the extent of endogenous thrombin generation may in part be responsible for the reported response variability to aspirin and clopidogrel therapy.
PATIENTS AND METHODS
Thrombin generation potential was measured with a commercially available assay, and platelet reactivity was assessed with the vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay, light transmission aggregometry (LTA), the VerifyNow aspirin and P2Y12 assays, and multiple electrode aggregometry (MEA) in 316 patients on dual antiplatelet therapy undergoing angioplasty and stenting.
RESULTS
Peak thrombin, the lag phase and the area under the curve of thrombin generation correlated poorly with on-treatment platelet reactivity by all test systems. High on-treatment residual platelet reactivity (HRPR) in response to arachidonic acid was seen in 33 (10.5%), 41 (13%), and 79 (25.7%) patients by LTA, the VerifyNow aspirin assay, and MEA, respectively. HRPR in response to adenosine diphosphate was seen in 150 (48.1%), 48 (15.3%), 106 (33.7%), and 118 (38.3%) patients by the VASP assay, LTA, the VerifyNow P2Y12 assay, and MEA, respectively. Peak thrombin generation did not differ between patients without and with HRPR by the VASP assay, LTA, the VerifyNow P2Y12 assay and MEA. In the VerifyNow aspirin assay, patients without HRPR had higher peak thrombin generation than patients with HRPR (p=0.01). Finally, patients without and with high peak thrombin generation exhibited similar on-treatment platelet reactivity by all test systems, and high peak thrombin generation occurred to a similar extent in patients without and with HRPR.
CONCLUSION
Response to antiplatelet therapy with aspirin and clopidogrel is not associated with thrombin generation potential.
背景
凝血酶是最强的血小板激活剂，即使在抗血小板治疗存在的情况下，也能迅速激活血小板。由于激活的血小板对额外的刺激反应更强，因此内源性凝血酶生成的程度可能部分解释了阿司匹林和氯吡格雷治疗反应的可变性。
患者和方法
使用商业上可获得的测定法测量凝血酶生成潜能，并使用血管扩张刺激磷酸蛋白（VASP）磷酸化测定法、光传输聚集测定法（LTA）、VerifyNow 阿司匹林和 P2Y12 测定法以及多电极聚集测定法（MEA）评估 316 名接受经皮冠状动脉介入治疗和支架置入术的双联抗血小板治疗患者的血小板反应性。
结果
最大凝血酶、滞后期和凝血酶生成曲线下面积与所有测试系统的治疗后血小板反应性相关性差。LTA、VerifyNow 阿司匹林测定法和 MEA 分别在 33（10.5%）、41（13%）和 79（25.7%）患者中观察到花生四烯酸反应性高治疗后残留血小板反应性（HRPR）。VASP 测定法、LTA、VerifyNow P2Y12 测定法和 MEA 分别在 150（48.1%）、48（15.3%）、106（33.7%）和 118（38.3%）患者中观察到二磷酸腺苷反应性 HRPR。在 VASP 测定法、LTA、VerifyNow P2Y12 测定法和 MEA 中，无 HRPR 的患者与有 HRPR 的患者的最大凝血酶生成无差异。在 VerifyNow 阿司匹林测定法中，无 HRPR 的患者的最大凝血酶生成高于有 HRPR 的患者（p=0.01）。最后，所有测试系统中，无高最大凝血酶生成的患者与有高最大凝血酶生成的患者的治疗后血小板反应性相似，且无 HRPR 的患者与有 HRPR 的患者的高最大凝血酶生成发生程度相似。
结论
阿司匹林和氯吡格雷抗血小板治疗的反应与凝血酶生成潜能无关。
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