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吸烟可促进双联抗血小板治疗患者中氯吡格雷介导的血小板抑制。

Smoking promotes clopidogrel-mediated platelet inhibition in patients receiving dual antiplatelet therapy.

机构信息

Division of Angiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.

出版信息

Thromb Res. 2009 Nov;124(5):588-91. doi: 10.1016/j.thromres.2009.06.012. Epub 2009 Jul 23.

DOI:10.1016/j.thromres.2009.06.012
PMID:19631365
Abstract

BACKGROUND

High on-treatment residual platelet reactivity is associated with an increased risk of adverse events after coronary stenting. Recent data suggest that cigarette smoking might enhance clopidogrel-mediated platelet inhibition. We therefore sought to investigate the influence of cigarette smoking on clopidogrel- and aspirin-mediated platelet inhibition after percutaneous intervention with stent implantation.

PATIENTS AND METHODS

Platelet aggregation was assessed by the VerifyNow P2Y12 and aspirin assays in 102 patients on dual antiplatelet therapy 24 hours after peripheral, coronary or carotid artery stenting. Among these, there were 33 nonsmokers, 29 former smokers and 40 current smokers. Patients in the fourth quartile of the VerifyNow assays were considered as patients with high on-treatment platelet reactivity.

RESULTS

Current smokers had significantly lower P2Y12 Reaction Units compared with nonsmokers (p = 0.028). Former smokers also had lower adenosine diphosphate (ADP)-inducible platelet aggregation than nonsmokers, but the difference was not significant (p = 0.52). A high on-treatment residual ADP-inducible platelet aggregation was more common among nonsmokers than among current smokers (14 vs 5; p = 0.004). In a multivariate regression analysis smoking was an independent influencing variable for post-treatment ADP-inducible platelet reactivity (p = 0.026). Aspirin-mediated platelet inhibition showed no significant differences between nonsmokers and former smokers or current smokers (p>0.3).

CONCLUSION

By in vitro testing, cigarette smoking is associated with enhanced clopidogrel- but not aspirin-mediated platelet inhibition. The clinical implications have to be evaluated in large prospective trials.

摘要

背景

治疗后血小板高反应性与冠状动脉支架置入术后不良事件风险增加相关。最近的数据表明,吸烟可能增强氯吡格雷介导的血小板抑制作用。因此,我们试图研究吸烟对经皮介入治疗后支架植入术双联抗血小板治疗患者的氯吡格雷和阿司匹林介导的血小板抑制作用的影响。

方法

102 例外周、冠状动脉或颈动脉支架置入术后接受双联抗血小板治疗 24 小时的患者,采用 VerifyNow P2Y12 和阿司匹林检测试剂盒检测血小板聚集。其中,33 例为非吸烟者,29 例为曾经吸烟者,40 例为现吸烟者。VerifyNow 检测试剂盒第四四分位的患者被认为是治疗后血小板高反应性的患者。

结果

与非吸烟者相比,现吸烟者的 P2Y12 反应单位显著降低(p = 0.028)。与非吸烟者相比,曾经吸烟者的二磷酸腺苷(ADP)诱导的血小板聚集也较低,但差异无统计学意义(p = 0.52)。与现吸烟者相比,非吸烟者的治疗后残留 ADP 诱导的血小板聚集更为常见(14 比 5;p = 0.004)。在多变量回归分析中,吸烟是治疗后 ADP 诱导的血小板反应性的独立影响因素(p = 0.026)。非吸烟者、曾经吸烟者和现吸烟者之间,阿司匹林介导的血小板抑制无显著差异(p>0.3)。

结论

通过体外检测,吸烟与氯吡格雷介导的血小板抑制作用增强有关,而与阿司匹林介导的血小板抑制作用无关。这一临床意义需要在大型前瞻性试验中进行评估。

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