Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Division of Pharmacology and Therapeutics, Graduate School of Medical and Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.
J Thromb Haemost. 2016 Apr;14(4):850-9. doi: 10.1111/jth.13256. Epub 2016 Feb 19.
Accurate evaluation of thrombogenicity helps to prevent thrombosis and excessive bleeding. The total thrombus-formation analysis system (T-TAS) was developed for quantitative analysis of platelet thrombus formation by the use of microchips with thrombogenic surfaces (collagen, platelet chip [PL-chip]; collagen plus tissue factor, atherome chip [AR-chip]). We examined the utility of the T-TAS in the assessment of the efficacy of antiplatelet therapy in patients with coronary artery disease (CAD).
In this cross-sectional study, 372 consecutive patients admitted to the cardiovascular department were divided into three groups: patients not receiving any antiplatelet therapy (control, n = 56), patients receiving aspirin only (n = 69), and patients receiving aspirin and clopidogrel (n = 149). Blood samples were used for the T-TAS to measure the platelet thrombus-formation area under the curve (AUC) at various shear rates (1500 s(-1) [PL18 -AUC10 ] and 2000 s(-1) [PL24 -AUC10 ] for the PL-chip; 300 s(-1) [AR10 -AUC30 ] for the AR-chip). The on-clopidogrel platelet aggregation was measured by the use of P2Y12 reaction units (PRUs) with the VerifyNow system. The mean PL24 -AUC10 levels were 358 ± 111 (± standard deviation) (95% confidence interval [CI] 328.9-387.1) in the control group, 256 ± 108 (95% CI 230.5-281.5) in the aspirin group, and 113 ± 91 (95% CI 98.4-127.6) in the aspirin/clopidogrel group. In the aspirin/clopidogrel group, the PL24 -AUC10 was higher in poor metabolizers (PMs) with cytochrome P450 2C19(CYP2C19) polymorphisms (152 ± 112, 95% CI 103.4-200.6) than in the non-PM group (87 ± 74, 95% CI 73.8-100.2).
Our findings suggest that the PL24 -AUC10 level measured by the T-TAS is a potentially suitable index for the assessment of antiplatelet therapy in CAD patients.
准确评估血栓形成有助于预防血栓形成和过度出血。总血栓形成分析系统(T-TAS)是通过使用具有血栓形成表面的微芯片(胶原、血小板芯片[PL-chip];胶原加组织因子,动脉粥样硬化芯片[AR-chip])来定量分析血小板血栓形成而开发的。我们研究了 T-TAS 在评估冠心病(CAD)患者抗血小板治疗效果中的效用。
在这项横断面研究中,将 372 名连续入院心血管科的患者分为三组:未接受任何抗血小板治疗的患者(对照组,n=56)、仅接受阿司匹林治疗的患者(n=69)和接受阿司匹林和氯吡格雷治疗的患者(n=149)。使用 T-TAS 测量不同剪切率下的血小板血栓形成曲线下面积(AUC):PL-chip 的 1500 s-1(PL18-AUC10)和 2000 s-1(PL24-AUC10);AR-chip 的 300 s-1(AR10-AUC30)。使用 VerifyNow 系统的 P2Y12 反应单位(PRUs)测量氯吡格雷诱导的血小板聚集。对照组 PL24-AUC10 水平平均值为 358±111(±标准差)(95%置信区间[CI] 328.9-387.1),阿司匹林组为 256±108(95% CI 230.5-281.5),阿司匹林/氯吡格雷组为 113±91(95% CI 98.4-127.6)。在阿司匹林/氯吡格雷组中,细胞色素 P450 2C19(CYP2C19)多态性的代谢不良者(PMs)的 PL24-AUC10 较高(152±112,95% CI 103.4-200.6),而非 PM 组的 PL24-AUC10 较低(87±74,95% CI 73.8-100.2)。
我们的研究结果表明,T-TAS 测量的 PL24-AUC10 水平可能是评估 CAD 患者抗血小板治疗的合适指标。