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瑞舒伐他汀联合氯吡格雷对脑梗死急性期患者血小板活化及聚集状态的影响 被引量:12

Effects of Atorvastatin combined with Clopidogrel on platelet activation and aggregation state in patients with acute cerebral infarction
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摘要 目的探讨瑞舒伐他汀联合氯吡格雷对脑梗死急性期患者血小板活化及聚集状态的影响。方法脑梗死急性期患者76例,随机分为2组。对照组给予氯吡格雷治疗,观察组给予瑞舒伐他汀联合氯吡格雷治疗。结果治疗后,观察组神经功能缺损评分及疗效优于对照组,差异具有统计学意义(P<0.05)。治疗后,观察组CD63表达水平(0.2±0.1)%,CD62P表达水平(1.4±0.8)%均优于对照组(0.4±0.2)%、(2.6±1.0)%,差异有统计学意义(P<0.05)%。治疗后,观察组AA水平(83.8±21.2)%及ADP途径诱导的血小板抑制率(50.0±18.1)%高于对照组的(65.5±21.9)%、(37.2±10.4)%,差异有统计学意义(P<0.05)。结论瑞舒伐他汀联合氯吡格雷可有效抑制脑梗死急性期患者血小板活化及聚集,促进神经功能损伤恢复。 Objective To explore the effects of Atorvastatin combined with Clopidogrel on platelet activation and aggrega tion state in patients with acute cerebral infarction. Methods Totally 76 patients with acute cerebral infarction were randomly di- vided into two groups. Patients in the control group were given Clopidogrel and others in the observation group received Atorvasta tin combined with Clopidogrel. Results The neurological deficit scores and clinical efficacy in the observation group were shown to be better than those in the control group, where the differences were statistically significant(P 〈0.05). After treatment, the ex- pression levels of CD63 and CD62P in the observation group were 0.2±0. 1 and 1.4±0.8,respectively,better than 0.4±0.2 and 2.6± 1.0 in the control group,and all the differences were statistically significant(P〈0.05). After treatment,the AA level in the observation group was 83.8±21.2 and platelet inhibition rate via ADP transduction pathway was 50.0 ± 18. 1, respectively, which were higher than 65.5±21.9 and 37.2± 10.4 in the control group with statistically significant differences(P〈0.05). Conclusion Atorvastatin combined with Clopidogrel can effectively inhibit the platelet activation and aggregation state in patients with acute cerebral infarction and boost the recovery of neurological deficits.
作者 赵晓玲
出处 《中国实用神经疾病杂志》 2017年第8期28-31,共4页 Chinese Journal of Practical Nervous Diseases
关键词 瑞舒伐他汀 氯吡格雷 脑梗死急性期 血小板活化 血小板聚集 Rosuvastatin Clopidogrel Acute cerebral infarction Platelet activation Platelet aggregation
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