Since data on the agreement between light transmission aggregometry (LTA) and multiple electrode aggregometry (MEA) in patients on the more potent P2Y₁₂ 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% (p = 0.07) by LTA and 19 AU and 20 AU (p = 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 p ≥ 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, p < 0.001), but not in those receiving ticagrelor (r = 0.09, p = 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 P2Y₁₂ inhibition.

由于关于更有效的 P2Y ₁₂患者中光透射聚集测定 (LTA) 和多电极聚集测定 (MEA) 之间一致性的数据迄今为止缺少抑制剂，我们研究了在 160 名接受阿司匹林和普拉格雷或替格瑞洛双重抗血小板治疗的急性冠状动脉综合征 (ACS) 患者（各 n = 80）中，是否可以用 MEA 代替对 LTA 治疗反应性的评估。对二磷酸腺苷 (ADP) 或花生四烯酸 (AA) 的高治疗中残余血小板反应性 (HRPR) 的临界值是根据先前的研究定义的，这些研究表明 HRPR 与不良缺血性结局的发生有关。在普拉格雷和替格瑞洛治疗的患者中，LTA 的 ADP 诱导血小板聚集分别为 33% 和 37%（p = 0.07），MEA 分别为 19 AU 和 20 AU（p = 0.38）。使用普拉格雷和替格瑞洛的患者中，LTA 的 AA 诱导性血小板聚集分别为 2% 和 3%，MEA 为 15 AU 和 16 AU（所有 p ≥ 0.3）。陆交局，HRPR ADP 和 HRPR AA 在接受普拉格雷和替格瑞洛治疗的患者中分别有 5%/5% 和 4%/13%。根据 MEA，分别在 3%/25% 和 0%/24% 的普拉格雷和替格瑞洛治疗的患者中观察到 HRPR ADP 和 HRPR AA。在普拉格雷治疗的患者中，MEA 引起的 ADP 诱导血小板反应性与 LTA ADP 显着相关（r = 0.4，p < 0.001），但在接受替格瑞洛的患者中则不然（r = 0.09，p = 0.45）。LTA 和 MEA 引起的 AA 诱导血小板聚集与普拉格雷和替格瑞洛治疗的患者无关。在普拉格雷治疗的患者中，MEA 检测 HRPR 通过 LTA 检测 HRPR 的敏感性/特异性分别为 25%/99% 和 100%/79% MEA ADP，以及 0%/100% 和 70%/83替格瑞洛治疗患者中 MEA AA 的百分比。综上所述，LTA 和 MEA 的治疗中残留的 ADP 诱导血小板反应性在普拉格雷治疗但不是替格瑞洛治疗的患者中显示出显着相关性。然而，在两组中，LTA 和 MEA 在将患者分类为 P2Y 的反应者或非反应者方面显示出异质性结果₁₂抑制。