a Division of Cardiology , Fondazione IRCCS Policlinico San Matteo , Pavia , Italy.
b Coronary Care Unit and Laboratory of Clinical and Experimental Cardiology, Fondazione IRCCS Policlinico San Matteo , Pavia , Italy.
Platelets. 2018 May;29(3):309-311. doi: 10.1080/09537104.2017.1394452. Epub 2017 Dec 5.
Smokers receiving clopidogrel show a lower residual platelet reactivity than non-smokers, a phenomenon generally ascribed to smoking-induced increased production of clopidogrel active metabolite, but also associated with the high hemoglobin levels of smokers, which decreases platelet reactivity in tests that measure platelet function in whole blood. We evaluated the impact of cigarette smoking and of hemoglobin levels on platelet reactivity index (PRI) measured by the vasodilator-stimulated phosphoprotein phosphorylation (VASP-P) assay in whole blood samples from patients with non-ST elevation acute coronary syndrome (NSTE-ACS) undergoing percutaneous coronary interventions, both before and after clopidogrel administration. PRI was measured in 718 clopidogrel-naïve NSTE-ACS patients, both before and 1 month after treatment with clopidogrel (75 mg daily). Smokers (n = 347, 48%) had significantly lower mean PRI levels at both baseline (57.7 ± 24.1 vs. 64.8 ± 19.8, p < 0.001) and 1 month (43.4 ± 20.3% vs. 46.8 ± 18.0%, p = 0.017) than non-smokers. After adjusting for potential confounders (age, sex, diabetes, chronic kidney disease, Syntax score>15), the β coefficient of smoke on PRI was -8.51 [-11.90 to -5.11, p < 0.001] at baseline and -3.41 [-6.30 to -0.51, p = 0.02] after 1 month. Hemoglobin was higher in smokers (13.8 ± 1.5 g/dL) than non-smokers (13.1 ± 1.7 g/dL, p < 0.001), but was not significantly correlated with PRI both at baseline (Rho = 0.02, p = 0.60) and at 1 month (Rho = 0.01, p = 0.80). Our analysis confirms that clopidogrel-treated smokers have lower platelet reactivity, measured by the VASP-P assay, compared to clopidogrel-treated non-smokers. However, smokers had lower platelet reactivity already before receiving clopidogrel treatment, suggesting that smoke affects platelet reactivity independently of its potential effect on the pharmacokinetics of clopidogrel. Our data also indicate that such an effect is not mediated by increased hemoglobin levels.
吸烟者服用氯吡格雷后表现出比不吸烟者更低的血小板反应性，这种现象通常归因于吸烟诱导的氯吡格雷活性代谢物产生增加，但也与吸烟者的高血红蛋白水平有关，血红蛋白水平降低会导致血小板功能检测中血小板反应性降低，这些检测是在全血中测量血小板功能的。我们评估了吸烟和血红蛋白水平对接受经皮冠状动脉介入治疗的非 ST 段抬高急性冠状动脉综合征（NSTE-ACS）患者全血样本中使用血管扩张刺激磷蛋白磷酸化（VASP-P）测定法测量的血小板反应性指数（PRI）的影响，这是在氯吡格雷给药前和给药后 1 个月进行的。在 718 例氯吡格雷初治 NSTE-ACS 患者中测量了 PRI，这些患者在接受氯吡格雷（每日 75mg）治疗前后均进行了测量。吸烟者（n=347，48%）在基线时（57.7±24.1%比 64.8±19.8%，p<0.001）和 1 个月时（43.4±20.3%比 46.8±18.0%，p=0.017）的平均 PRI 水平显著更低。在校正潜在混杂因素（年龄、性别、糖尿病、慢性肾脏病、Syntax 评分>15）后，吸烟对 PRI 的β系数为-8.51[-11.90 至-5.11，p<0.001]，在基线时为-3.41[-6.30 至-0.51，p=0.02]，在 1 个月时为-3.41[-6.30 至-0.51，p=0.02]。吸烟者的血红蛋白水平高于不吸烟者（13.8±1.5g/dL 比 13.1±1.7g/dL，p<0.001），但在基线时（Rho=0.02，p=0.60）和 1 个月时（Rho=0.01，p=0.80）与 PRI 无明显相关性。我们的分析证实，与氯吡格雷治疗的不吸烟者相比，氯吡格雷治疗的吸烟者的血小板反应性更低，通过 VASP-P 测定法测量。然而，吸烟者在接受氯吡格雷治疗之前就已经表现出较低的血小板反应性，这表明吸烟对血小板反应性的影响独立于其对氯吡格雷药代动力学的潜在影响。我们的数据还表明，这种影响不是由血红蛋白水平升高介导的。
Zotero 插件