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替格瑞洛治疗的非 ST 段抬高型心肌梗死患者停用阿司匹林。

Aspirin withdrawal in patients treated with ticagrelor presenting with non-ST elevation myocardial infarction.

机构信息

Cardiovascular Division, Intensive Cardiac Care Unit, Sheba Medical Center, Tel Aviv, Israel.

The Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel.

出版信息

J Thromb Haemost. 2018 Apr;16(4):663-669. doi: 10.1111/jth.13977. Epub 2018 Mar 15.

Abstract

UNLABELLED

Essentials Strong P2Y blockade may cause platelet inhibition that is only minimally enhanced by aspirin. We evaluated aspirin withdrawal on platelet reactivity in ticagrelor treated patients. Aspirin withdrawal resulted in increased platelet reactivity to arachidonic acid. Aspirin withdrawal caused little difference in adenosine diphosphate-induced platelet aggregation.

SUMMARY

Background Recent studies have shown that the thromboxane A -dependent pathway is dependent on the ADP-P2Y pathway, and that strong P2Y receptor blockade alone causes inhibition of platelet aggregation that is minimally enhanced by aspirin. Data from the PLATO trial suggested that, among ticagrelor-treated patients, high-dose versus low-dose (< 100 mg day ) aspirin is associated with an increased risk fof ischemic events. Objectives To evaluate the impact of aspirin withdrawal on platelet reactivity in acute coronary syndrome (ACS) patients treated with a potent P2Y blocker. Patients/Methods This was a current prospective, randomized, placebo-controlled, double-blind, cross-over study. The study population comprised 22 consecutive ACS patients who underwent percutaneous coronary intervention and were treated with aspirin (100 mg day ) and ticagrelor. Thirty days post-ACS, open-label aspirin was stopped, and patients were randomized to either blinded aspirin or placebo for 2 weeks, with each patient crossing over to the other arm for an additional 2 weeks. Platelet reactivity to arachidonic acid and ADP determined with light-transmission aggregometry (LTA) and VerifyNow was evaluated at baseline, and 2 weeks and 4 weeks later. Results Aspirin withdrawal resulted in an increase in arachidonic-acid induced platelet reactivity as determined with both LTA (77.0% ± 11.3% versus 20.8% ± 4.4%) and VerifyNow (607.7 ± 10.6 aspirin reaction units [ARU] versus 408.5 ± 14.4 ARU). Platelet response to ADP, as determined with both LTA and VerifyNow, did not differ with either aspirin or placebo (32.9% ± 2.6% versus 35.8% ± 3.6%, and 33.5 ± 6.4 P2Y reaction units (PRU) versus 29.6 ± 5.7 PRU, respectively). Conclusions Aspirin withdrawal early post-ACS results in increased platelet reactivity in response to arachidonic acid, despite concomitant treatment with the potent P2Y blocker ticagrelor.

摘要

未标记

研究背景:强效 P2Y 受体阻断剂可能引起血小板抑制,而小剂量阿司匹林几乎不会增强这种抑制作用。我们评估了替格瑞洛治疗患者中停用阿司匹林对血小板反应性的影响。停用阿司匹林导致花生四烯酸诱导的血小板反应性增加。ADP 诱导的血小板聚集,停用阿司匹林后差异较小。

摘要

背景:最近的研究表明,血栓素 A 依赖性途径依赖于 ADP-P2Y 途径,单独使用强效 P2Y 受体阻滞剂即可引起血小板聚集抑制,而小剂量阿司匹林几乎不会增强这种抑制作用。PLATO 试验的数据表明,在接受替格瑞洛治疗的患者中,高剂量(<100mg/天)与低剂量(<100mg/天)阿司匹林相比,缺血事件风险增加。目的:评估急性冠状动脉综合征(ACS)患者接受强效 P2Y 阻滞剂治疗时停用阿司匹林对血小板反应性的影响。

患者/方法:这是一项当前的前瞻性、随机、安慰剂对照、双盲、交叉研究。研究人群包括 22 例连续接受经皮冠状动脉介入治疗的 ACS 患者,这些患者接受阿司匹林(100mg/天)和替格瑞洛治疗。ACS 后 30 天,停用阿司匹林,然后将患者随机分为接受阿司匹林或安慰剂治疗 2 周,每位患者交叉至另一臂治疗 2 周。使用光传输聚集测定法(LTA)和 VerifyNow 测定血小板对花生四烯酸和 ADP 的反应性,在基线时以及 2 周和 4 周后进行评估。

结果

停用阿司匹林后,通过 LTA(77.0%±11.3%比 20.8%±4.4%)和 VerifyNow(607.7±10.6 阿司匹林反应单位[ARU]比 408.5±14.4 ARU)检测到花生四烯酸诱导的血小板反应性增加。通过 LTA 和 VerifyNow 测定,ADP 诱导的血小板反应性无差异,无论使用阿司匹林还是安慰剂(32.9%±2.6%比 35.8%±3.6%,33.5±6.4 P2Y 反应单位[PRU]比 29.6±5.7 PRU)。

结论

ACS 后早期停用阿司匹林会导致花生四烯酸反应性的血小板反应性增加,尽管同时使用了强效 P2Y 阻滞剂替格瑞洛。

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