每天至少吸烟 10 支会增加 ST 段抬高型心肌梗死患者氯吡格雷的血小板抑制作用。

Smoking at least 10 cigarettes per day increases platelet inhibition by clopidogrel in patients with ST-segment-elevation myocardial infarction.

机构信息

Division of Cardiology, Department of Internal Medicine, Gyeongsang National University Hospital, 90 Chiram-dong, Jinju, 660-702, Gyeongsangnam-do, South Korea.

出版信息

Thromb Res. 2010 Oct;126(4):e334-8. doi: 10.1016/j.thromres.2010.03.020. Epub 2010 May 6.

DOI:10.1016/j.thromres.2010.03.020

PMID:20451242

Abstract

BACKGROUND

Recent data suggest that cigarette smoking (CS) might decrease the risk of cardiovascular events in patients with ST-segment-elevation myocardial infarction (STEMI) or established cardiovascular disease. Although it may be related to the effect of CS on the metabolism of clopidogrel, the association between the extent of CS and clopidogrel-induced platelet inhibition has not been well defined.

PATIENTS AND METHODS

We tested the association between smoking status and inhibition of platelet aggregation (IPA) in response to a clopidogrel loading of 600-mg in 20 healthy subjects. We then enrolled 138 consecutive STEMI patients treated with primary coronary stenting. On-clopidogrel platelet reactivity (PR) was assessed with conventional aggregometry and the VerifyNow P2Y(12) assay, according to smoking status.

RESULTS

After 6 hours post-loading in healthy subjects, CS patients on ≥10 cigarettes/day showed a significantly higher value of 5 μmol/L ADP-stimulated IPA (P=0.006), and had a trend toward a greater value of 20 μmol/L ADP-stimulated IPA (P=0.093) compared with non-smokers. In STEMI patients, there was no difference in PR between non-smokers (n=66) and CS patients<10 cigarettes/day (n=16). CS patients on ≥10 cigarettes/day (n=56) demonstrated lower PR with 5 and 20 μmol/L ADP (40.9±16.1% versus 46.6±11.7%, P=0.028, and 53.8±16.6% versus 59.2±12.2%, P=0.040, respectively) and lower P2Y(12) reaction units (204±85 versus 270±69, P<0.001) than non-smokers. On multivariate analyses, CS≥10 cigarettes/day was the only predictor of low on-clopidogrel PR (≤33%; the lowest quartile of 5 μmol/L ADP-induced PR; odds ratio 4.651, 95% confidence interval 1.181-18.519, P=0.028).

CONCLUSION

CS seems to increase antiplatelet response to clopidogrel in healthy volunteers and STEMI patients. Smoking 10 or more cigarettes/day can significantly decrease on-clopidogrel platelet reactivity in these populations.

摘要

背景

最近的数据表明，吸烟（CS）可能会降低 ST 段抬高型心肌梗死（STEMI）或已存在心血管疾病患者发生心血管事件的风险。虽然这可能与 CS 对氯吡格雷代谢的影响有关，但 CS 的程度与氯吡格雷诱导的血小板抑制之间的关系尚未明确。

患者和方法

我们在 20 名健康受试者中检测了吸烟状况与氯吡格雷负荷 600mg 后血小板聚集抑制（IPA）之间的关系。然后，我们纳入了 138 例连续的 STEMI 患者，这些患者接受了直接经皮冠状动脉介入治疗。根据吸烟状况，采用常规聚集仪和 VerifyNow P2Y(12)检测试剂盒评估氯吡格雷治疗后的血小板反应性（PR）。

结果

在健康受试者中，负荷后 6 小时，每天吸烟≥10 支的 CS 患者显示出更高的 5μmol/L ADP 刺激 IPA 值（P=0.006），并且 20μmol/L ADP 刺激 IPA 值也呈现出更大的趋势（P=0.093）。在 STEMI 患者中，非吸烟者（n=66）和每天吸烟<10 支的 CS 患者（n=16）之间的 PR 没有差异。每天吸烟≥10 支的 CS 患者（n=56）表现出较低的 PR，使用 5μmol/L 和 20μmol/L ADP 时分别为 40.9±16.1%和 53.8±16.6%，与非吸烟者相比，差异有统计学意义（P=0.028 和 P=0.040）。并且 P2Y(12)反应单位较低（204±85 与 270±69，P<0.001）。多变量分析显示，CS≥10 支/天是低氯吡格雷 PR（≤33%；5μmol/L ADP 诱导的 PR 的最低四分位数）的唯一预测因子（优势比 4.651，95%置信区间 1.181-18.519，P=0.028）。