Department of Internal Medicine II, 27271Medical University of Vienna, Vienna, Austria.
Department of Blood Group Serology and Transfusion Medicine, 27271Medical University of Vienna, Vienna, Austria.
J Cardiovasc Pharmacol Ther. 2021 May;26(3):260-268. doi: 10.1177/1074248420968706. Epub 2020 Oct 27.
Since data on the agreement between light transmission aggregometry (LTA) and multiple electrode aggregometry (MEA) in patients on the more potent P2Y inhibitors are missing so far, we investigated if the evaluation of the responsiveness to therapy by LTA can be replaced by MEA in 160 acute coronary syndrome (ACS) patients on dual antiplatelet therapy with aspirin and prasugrel or ticagrelor (n = 80 each). Cut-off values for high on-treatment residual platelet reactivity (HRPR) in response to adenosine diphosphate (ADP) or arachidonic acid (AA) were defined according to previous studies showing an association of HRPR with the occurrence of adverse ischemic outcomes. ADP- inducible platelet aggregation was 33% and 37% ( = 0.07) by LTA and 19 AU and 20 AU ( = 0.38) by MEA in prasugrel- and ticagrelor-treated patients, respectively. AA- inducible platelet aggregation was 2% and 3% by LTA and 15 AU and 16 AU by MEA, (all ≥ 0.3) in patients on prasugrel and ticagrelor, respectively. By LTA, HRPR ADP and HRPR AA were seen in 5%/5% and in 4%/ 13% of patients receiving prasugrel- and ticagrelor, respectively. By MEA, HRPR ADP and HRPR AA were seen in 3%/ 25% and 0%/24% of prasugrel- and ticagrelor-treated patients, respectively. ADP-inducible platelet reactivity by MEA correlated significantly with LTA ADP in prasugrel-treated patients (r = 0.4, < 0.001), but not in those receiving ticagrelor (r = 0.09, = 0.45). AA-inducible platelet aggregation by LTA and MEA did not correlate in prasugrel- and ticagrelor-treated patients. Sensitivity/specificity of HRPR by MEA to detect HRPR by LTA were 25%/99% for MEA ADP and 100%/79% for MEA AA in prasugrel-treated patients, and 0%/100% for MEA ADP and 70%/83% for MEA AA in ticagrelor-treated patients. In conclusion, on-treatment residual ADP-inducible platelet reactivity by LTA and MEA shows a significant correlation in prasugrel- but not ticagrelor-treated patients. However, in both groups LTA and MEA revealed heterogeneous results regarding the classification of patients as responders or non-responders to P2Y inhibition.
由于目前缺乏关于在使用更有效的 P2Y 抑制剂的患者中,光透射聚集测定(LTA)和多重电极聚集测定(MEA)之间的一致性的数据,因此我们在 160 名接受双重抗血小板治疗的急性冠脉综合征(ACS)患者中研究了 LTA 评估治疗反应的能力是否可以被 MEA 替代,这些患者分别接受阿司匹林和普拉格雷或替格瑞洛治疗(每组 80 例)。根据先前的研究结果,高ADP 诱导的血小板反应性(HRPR)与不良缺血结局的发生相关,因此根据这些研究结果,确定了针对 ADP 和花生四烯酸(AA)的高 HRPR 的截断值。普拉格雷和替格瑞洛治疗患者中,LTA 诱导的 ADP 诱导的血小板聚集分别为 33%和 37%(= 0.07),MEA 分别为 19 AU 和 20 AU(= 0.38)。LTA 诱导的 AA 诱导的血小板聚集分别为 2%和 3%,MEA 诱导的 AA 诱导的血小板聚集分别为 15 AU 和 16 AU,(所有均≥0.3)在接受普拉格雷和替格瑞洛治疗的患者中。LTA 显示,接受普拉格雷和替格瑞洛治疗的患者中,ADP 诱导的 HRPR 和 AA 诱导的 HRPR 分别为 5%/5%和 4%/13%。MEA 显示,接受普拉格雷和替格瑞洛治疗的患者中,ADP 诱导的 HRPR 和 AA 诱导的 HRPR 分别为 3%/25%和 0%/24%。在接受普拉格雷治疗的患者中,MEA 诱导的 ADP 诱导的血小板反应性与 LTA ADP 呈显著相关(r = 0.4, < 0.001),但在接受替格瑞洛治疗的患者中无相关性(r = 0.09, = 0.45)。在接受普拉格雷和替格瑞洛治疗的患者中,LTA 和 MEA 诱导的 AA 诱导的血小板聚集没有相关性。在接受普拉格雷治疗的患者中,MEA 检测到的 HRPR 的 MEA 的敏感性/特异性分别为 MEA ADP 的 25%/99%和 MEA AA 的 100%/79%,而在接受替格瑞洛治疗的患者中,MEA ADP 的敏感性/特异性为 0%/100%,MEA AA 的敏感性/特异性为 70%/83%。总之,LTA 和 MEA 检测到的治疗后残留 ADP 诱导的血小板反应性在接受普拉格雷治疗的患者中具有显著相关性,但在接受替格瑞洛治疗的患者中则无相关性。然而,在两组患者中,LTA 和 MEA 对于将患者分类为对 P2Y 抑制的反应者或非反应者,均显示出不一致的结果。