Paarup Dridi Nadia, Johansson Pär I, Lønborg Jacob T, Clemmensen Peter, Radu Maria D, Qayyum Abbas, Pedersen Frants, Kollslid Rudi, Helqvist Steffen, Saunamäki Kari, Kelbæk Henning, Jørgensen Erik, Engstrøm Thomas, Holmvang Lene
Department of Cardiology, The Heart Centre , Rigshosptalet , Denmark .
Platelets. 2015;26(6):521-9. doi: 10.3109/09537104.2014.948837. Epub 2014 Aug 28.
To investigate whether an intensified antiplatelet regimen could improve prognosis in stable or non-ST elevation in acute coronary syndrome (ACS) patients exhibiting high on-treatment platelet reactivity (HTPR) on clopidogrel and treated with percutaneous coronary intervention (PCI). There is a wide variability in the platelet reactivity to clopidogrel and HTPR has been associated with a poor prognosis.
In this observational study, 923 consecutive patients without ST-elevation myocardial infarction (STEMI) and adequately pre-treated with clopidogrel were screened for HTPR with multiple electrode aggregometry after assessment of the coronary anatomy. Patients were grouped based on their response to clopidogrel and the assigned antiplatelet strategy. The primary endpoint was a composite of cardiovascular death, myocardial infarction, stroke, or stent thrombosis.
HTPR was demonstrated in 237 patients (25.7%). Of these, 114 continued on conventional clopidogrel therapy, while the remaining 123 received intensified antiplatelet therapy with either double-dose clopidogrel (150 mg daily, n = 55) or the newer P2Y12-inhibitors, prasugrel or ticagrelor (n = 68) for at least 30 days after the index procedure. The median follow-up was 571 days (interquartile range, 373-746). Intensifying antiplatelet therapy reduced the rate of the composite endpoint (p < 0.001). After adjustment for potential confounders, HTPR in combination with conventional clopidogrel therapy remained independently associated with an increased risk of cardiovascular events (hazard ratio (HR), 2.92; 95% CI, 1.90-4.48), whereas intensified treatment reduced the risk to a level equivalent to that of patients exhibiting normal platelet reactivity (HR, 1.08; 95% CI, 0.59-1.99).
Tailored antiplatelet therapy significantly reduced the event rate in patients exhibiting HTPR prior to PCI.
探讨强化抗血小板治疗方案能否改善接受经皮冠状动脉介入治疗（PCI）且在使用氯吡格雷时表现出高治疗期血小板反应性（HTPR）的急性冠状动脉综合征（ACS）稳定型或非ST段抬高型患者的预后。氯吡格雷的血小板反应性存在很大差异，且HTPR与预后不良相关。
在这项观察性研究中，923例连续的无ST段抬高型心肌梗死（STEMI）且已接受氯吡格雷充分预处理的患者在评估冠状动脉解剖结构后，采用多电极聚集法筛查HTPR。患者根据其对氯吡格雷的反应和指定的抗血小板策略进行分组。主要终点是心血管死亡、心肌梗死、中风或支架血栓形成的复合终点。
237例患者（25.7%）表现出HTPR。其中，114例继续接受常规氯吡格雷治疗，其余123例在索引手术后至少30天接受强化抗血小板治疗，采用双倍剂量氯吡格雷（每日150 mg，n = 55）或新型P2Y12抑制剂普拉格雷或替格瑞洛（n = 68）。中位随访时间为571天（四分位间距，373 - 746天）。强化抗血小板治疗降低了复合终点的发生率（p < 0.001）。在对潜在混杂因素进行调整后，HTPR联合常规氯吡格雷治疗仍与心血管事件风险增加独立相关（风险比（HR），2.92；95%置信区间，1.90 - 4.48），而强化治疗将风险降低至与血小板反应性正常的患者相当的水平（HR，1.08；95%置信区间，0.59 - 1.99）。
量身定制的抗血小板治疗显著降低了PCI术前表现出HTPR的患者的事件发生率。
