首页> 外文期刊>Journal of thrombosis and thrombolysis >Effects of cigarette smoking on platelet reactivity during P2Y12 inhibition in patients with myocardial infarction undergoing drug-eluting stent implantation: results from the prospective cigarette smoking on platelet reactivity (COPTER) study
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Effects of cigarette smoking on platelet reactivity during P2Y12 inhibition in patients with myocardial infarction undergoing drug-eluting stent implantation: results from the prospective cigarette smoking on platelet reactivity (COPTER) study

机译:吸烟对接受药物洗脱支架植入的心肌梗死患者抑制P2Y12期间血小板反应性的影响:前瞻性吸烟对血小板反应性的研究(COPTER)

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Interaction between cigarette smoking and efficacy of oral antiplatelet drugs is not definitely elucidated. We evaluated the effects of cigarette smoking on platelet reactivity in patients receiving different oral P2Y12 antagonists after myocardial infarction (MI) and drug-eluting stent (DES) implantation. Two-hundred-five consecutive current smokers receiving DES implantation after ST-segment elevation MI were enrolled. All patients were aspirin-treated and were on chronic therapy with clopidogrel (N = 59), prasugrel (N = 71) or ticagrelor (N = 75); by protocol, all patients at baseline had no high on-treatment platelet reactivity by the VerifyNow P2Y12 assay. Platelet reactivity, expressed by P2Y12 reaction units (PRU), was measured in all patients at baseline (T0), after a 15-day period of smoking cessation (T1) and after further 15 days of smoking resumption (T2). In the overall population there was a modest, albeit significant, reduction of PRU values from T0 to T1 (from 173 +/- A 14 to 165 +/- A 17, P < 0.0001); resumption of cigarette smoking was associated with re-increase of platelet reactivity (from 165 +/- A 17 at T1 to 170 +/- A 17 at T2, P = 0.0002). These variations were consistent in the subgroups receiving clopidogrel, prasugrel or ticagrelor and were irrespective of the number of cigarettes smoked. In conclusion, cigarette smoking weakly influences antiplatelet effects of oral P2Y12 inhibition and this was irrespective of the type of antiplatelet agent; thus, interaction between cigarette smoking and efficacy of oral antiplatelet drugs is modest and unlikely translates into clinical effects (ClinicalTrials.gov Identifier: NCT02026713).
机译:吸烟与口服抗血小板药物疗效之间的相互作用尚未明确阐明。我们评估了在心肌梗塞(MI)和药物洗脱支架(DES)植入后接受不同口服P2Y12拮抗剂的患者中吸烟对血小板反应性的影响。 ST段抬高MI后接受DES植入的255名连续吸烟者入选。所有患者均接受阿司匹林治疗,并接受氯吡格雷(N = 59),普拉格雷(N = 71)或替卡格雷(N = 75)的慢性治疗;按照协议,通过VerifyNow P2Y12分析,所有处于基线状态的患者都没有较高的治疗中血小板反应性。在戒烟15天后(T1)和戒烟15天后(T2),在基线(T0)的所有患者中测量以P2Y12反应单位(PRU)表示的血小板反应性。在总体人群中,PRU值从T0到T1有所降低(从173 +/- A 14降低到165 +/- A 17,P <0.0001),尽管有显着水平。吸烟的恢复与血小板反应性的重新升高有关(从T1时的165 +/- A 17到T2时的170 +/- A 17,P = 0.0002)。这些差异在接受氯吡格雷,普拉格雷或替卡格雷的亚组中是一致的,并且与吸烟的数量无关。总之,吸烟与口服P2Y12抑制的抗血小板作用无关,这与抗血小板剂的类型无关。因此,吸烟与口服抗血小板药疗效之间的相互作用是适度的,不太可能转化为临床效果(ClinicalTrials.gov标识符:NCT02026713)。

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