Reed Grant W, Cannon Christopher P, Waalen Jill, Teirstein Paul S, Tanguay Jean-Francois, Berger Peter B, Angiolillo Dominick J, Price Matthew J
Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio.
Cardiovascular Division, Brigham and Women's Hospital, Boston, Massachusetts.
Catheter Cardiovasc Interv. 2017 Feb 1;89(2):190-198. doi: 10.1002/ccd.26428. Epub 2016 Feb 23.
To examine the influence of smoking on the antiplatelet effect of clopidogrel following percutaneous coronary intervention (PCI).
Certain studies suggest smokers may have enhanced clopidogrel-induced platelet inhibition compared to non-smokers after PCI. Whether this is affected by clopidogrel dose is unknown.
In this study, we conducted an analysis of 5,429 patients in the Gauging Responsiveness With A VerifyNow P2Y12 Assay: Impact on Thrombosis and Safety (GRAVITAS) trial. Platelet reactivity was assessed 12-24 hr after PCI (baseline). Patients with high on-treatment platelet reactivity (OTR) (P2Y12 reaction units [PRU] ≥ 230) were randomized to clopidogrel 75 mg or 150 mg daily. Reactivity was subsequently assessed at 30-days, and 6-months. Patients were stratified by smoking status.
Smoking was independently associated with lower PRU (P = 0.001), and smokers were less likely to have high OTR (odds ratio 0.80, 95% confidence interval 0.68-0.94; P = 0.006) at baseline. Among patients assigned to clopidogrel 75 mg, smokers had lower PRU and were less likely to still have high OTR at 30-days (P < 0.001) and 6-months (P < 0.001). However, in patients assigned clopidogrel 150 mg, PRU and high OTR did not differ by smoking status at any time. Tests demonstrated an interaction between smoking and dose at 30 days (P = 0.007), and a trend at 6-months (P = 0.098).
Smokers treated with clopidogrel exhibit reduced platelet reactivity and are less likely to have persistent high OTR than non-smokers. This difference is mitigated by clopidogrel 150 mg, indicating non-smokers may require double-dose therapy to achieve a similar antiplatelet effect after PCI. © 2016 Wiley Periodicals, Inc.
探讨吸烟对经皮冠状动脉介入治疗（PCI）后氯吡格雷抗血小板作用的影响。
某些研究表明，与非吸烟者相比，吸烟者在PCI后可能对氯吡格雷诱导的血小板抑制作用增强。这是否受氯吡格雷剂量的影响尚不清楚。
在本研究中，我们对“使用VerifyNow P2Y12检测评估反应性：对血栓形成和安全性的影响（GRAVITAS）”试验中的5429例患者进行了分析。在PCI后12 - 24小时（基线）评估血小板反应性。高治疗期血小板反应性（OTR）（P2Y12反应单位[PRU]≥230）的患者被随机分为每日服用氯吡格雷75毫克或150毫克。随后在30天和6个月时评估反应性。患者按吸烟状态分层。
吸烟与较低的PRU独立相关（P = 0.001），吸烟者在基线时发生高OTR的可能性较小（比值比为0.80，95%置信区间为0.68 - 0.94；P = 0.006）。在服用氯吡格雷75毫克的患者中，吸烟者的PRU较低，在30天时（P < 0.001）和6个月时（P < 0.001）仍发生高OTR的可能性较小。然而，在服用氯吡格雷150毫克的患者中，PRU和高OTR在任何时候都不因吸烟状态而异。检验显示在30天时吸烟与剂量之间存在相互作用（P = 0.007），在6个月时有这种趋势（P = 0.098）。
接受氯吡格雷治疗的吸烟者血小板反应性降低，与非吸烟者相比，持续高OTR的可能性较小。氯吡格雷150毫克可减轻这种差异，表明非吸烟者可能需要双倍剂量治疗才能在PCI后获得类似的抗血小板效果。© 2016威利期刊公司
