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目的观察瑞舒伐他汀和阿托伐他汀对氯吡格雷抗血小板活性的影响。方法选择60例冠心病患者接受阿司匹林100mg/d、氯吡格雷75 mg/d及低分子肝素5000 U/12 h治疗,5 d后随机分为阿托伐他汀20mg/d(阿托伐他汀组,30例)和瑞舒伐他汀10 mg/d(瑞舒伐他汀组,30例)。在服用氯吡格雷之前(基线值)、加用他汀类药物之前及服用他汀类药物3d后,用全血阻抗法分别测定不同浓度二磷酸腺苷(5、10、20μmol/L)诱导的血小板聚集率。结果与基线值比较,服用氯吡格雷5 d后和加服他汀类药物治疗3 d后,2组患者血小板聚集率明显降低,差异有统计学意义(P<0.05);与治疗前比较,阿托伐他汀组患者血小板聚集率有所升高,而瑞舒伐他汀组患者血小板聚集率有所下降,但差异无统计学意义(P>0.05)。结论经细胞色素3A4途径代谢的阿托伐他汀及不经细胞色素3A4代谢的瑞舒伐他汀,短期内对氯吡格雷抗血小板活性无影响。
Objective To observe the effect of rosuvastatin and atorvastatin on the antiplatelet activity of clopidogrel. Methods Sixty patients with coronary heart disease were treated with aspirin 100 mg / d, clopidogrel 75 mg / d and low molecular weight heparin 5000 U / 12 h, and were randomly divided into atorvastatin 20 mg / d (atorvastatin group , 30 cases) and rosuvastatin 10 mg / d (rosuvastatin group, 30 cases). Before taking clopidogrel (baseline), before adding statins and after taking statins for 3d, the platelets induced by different concentrations of adenosine diphosphate (5, 10, 20 μmol / L) were determined by whole blood impedance method Aggregation rate. Results Compared with the baseline, after 5 days of clopidogrel and statin therapy for 3 days, the platelet aggregation rate was significantly decreased in both groups (P <0.05). Compared with the baseline, The platelet aggregation rate was increased in patients in the atorvastatin group, while the platelet aggregation rate was decreased in the rosuvastatin group, but the difference was not statistically significant (P> 0.05). Conclusion Atorvastatin metabolized by cytochrome 3A4 pathway and rosuvastatin metabolized by cytochrome 3A4 have no effect on antiplatelet activity of clopidogrel in a short term.