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首页> 外文期刊>Circulation journal >Endothelial Progenitor Cell Mobilization and Platelet Microparticle Release Are Influenced by Clopidogrel Plasma Levels in Stable Coronary Artery Disease
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Endothelial Progenitor Cell Mobilization and Platelet Microparticle Release Are Influenced by Clopidogrel Plasma Levels in Stable Coronary Artery Disease

机译：稳定冠状动脉疾病中氯吡格雷血浆水平影响内皮祖细胞动员和血小板微粒释放。

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Background: Increased numbers of endothelial (EMP) and platelet (PMP) microparticles have been related to cardiovascular risk factors and coronary artery disease. Little is known about the early effects of statins and clopidogrel on these new biomarkers of vascular homeostasis. The aim of the present study was to evaluate pharmacokinetic interactions between atorvastatin and clopidogrel and their effects, alone or combined, on EMP, PMP, and endothelial progenitor cells (EPC). Methods and Results: A prospective open-label study enrolled subjects with stable coronary disease (n=26). Drugs were given daily for 3 weeks (atorvastatin 80mg, visits 1-3; clopidogrel 75mg, visits 2-4). Counts of EPC (CD34+/CD133+/KDR+), EMP (CD51+) and PMP (CD42+/CD31+), and pharmacokinetic parameters over 24h were assessed at each visit. Atorvastatin plasma concentrations were increased by concomitant therapy with clopidogrel (maximum serum concentration [Cmax], P=0.002; area under the clopidogrel or atorvastatin plasma concentration vs. time curve from 0 to the last detectable concentration [AUClast], P=0.03). After atorvastatin withdrawal there was an increase in clopidogrel plasma concentrations (Cmax, P=0.009; AUClast, P=0.039). PMP were inversely correlated with clopidogrel Cmax on visit 3 (rho=-0.57, P=0.006) and on visit 4 (rho=-0.54, P=0.01), and with clopidogrel AUClast on visit 3 (rho=-0.44, P=0.04), and on visit 4 (rho=-0.57, P=0.005). In addition, clopidogrel Cmax was correlated with EPC (CD133+/KDR+) on visit 4 (rho=0.48, P=0.025). No correlations of atorvastatin and MP or EPC were found. Conclusions: The balance between platelet MP release and EPC mobilization seems influenced by clopidogrel plasma levels, suggesting a protective mechanism on coronary artery disease. ( Circ J 2012; 76: 729-736)
机译：背景：内皮（EMP）和血小板（PMP）微粒的数量增加与心血管危险因素和冠状动脉疾病有关。他汀类药物和氯吡格雷对血管稳态的这些新生物标志物的早期作用知之甚少。本研究的目的是评估阿托伐他汀和氯吡格雷之间的药代动力学相互作用以及它们单独或联合对EMP，PMP和内皮祖细胞（EPC）的作用。方法和结果：前瞻性开放性研究招募了稳定冠心病患者（n = 26）。每天服药3周（阿托伐他汀80mg，第1-3次;氯吡格雷75mg，第2-4次）。每次访视时，评估24小时内EPC（CD34 + / CD133 + / KDR +），EMP（CD51 +）和PMP（CD42 + / CD31 +）的计数以及药代动力学参数。并用氯吡格雷治疗可增加阿托伐他汀血浆浓度（最大血清浓度[C max ]，P = 0.002;氯吡格雷或阿托伐他汀下血浆面积与时间的关系，从0到最后可测出的浓度[ AUC last ]，P = 0.03）。阿托伐他汀撤药后，氯吡格雷血浆浓度增加（C max ，P = 0.009; AUC last ，P = 0.039）。 PMP与氯吡格雷C max 在第3次就诊（rho = -0.57，P = 0.006）和第4次就诊（rho = -0.54，P = 0.01）以及氯吡格雷AUC 呈负相关最后访问3（rho = -0.44，P = 0.04）和访问4（rho = -0.57，P = 0.005）。此外，氯吡格雷C max 在第4次就诊时与EPC（CD133 + / KDR +）相关（rho = 0.48，P = 0.025）。没有发现阿托伐他汀与MP或EPC的相关性。结论：氯吡格雷血浆水平影响血小板MP释放和EPC动员之间的平衡，表明对冠状动脉疾病具有保护作用。 （Circ J 2012; 76：729-736）

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