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[摘要]
目的 探讨颈动脉重度狭窄患者支架成形术后氯吡格雷对其血小板功能及炎症因子的影响。方法 选取120例经颈动脉支架成形术治疗的颈动脉重度狭窄患者,随机分为两组,对照组应用阿司匹林联合阿托伐他汀,观察组应用氯呲格雷联合阿托伐他汀,术前使用3~5 d,术后均连续服用3个月。观察用药后血清D-二聚体(DD)水平、纤维蛋白原(FIB)水平、炎症因子P-选择素水平以及再狭窄事件的发生率。结果 术前,两组DD及FIB水平无显著差异;术后24 h,对照组及观察组DD及FIB水平均明显升高(P<0.05)。术后1个月,两组DD及FIB水平均明显下降,但仍明显高于术前(P<0.05)。术后3个月,DD及FIB水平和术前相比,无显著差异,DD及FIB水平均在正常范围内。术后24 h、1个月、3个月,观察组DD及FIB水平均明显低于对照组,差异有统计学意义(P<0.05)。术前,两组的P-选择素对比无统计学意义,术后均明显下降,且观察组低于对照组(P<0.05);观察组的再狭窄事件的发生率均低于对照组(P<0.05)。结论 氯吡格雷联合阿托伐他汀可抑制重度颈动脉狭窄患者术后血小板聚集预防血栓形成,降低再狭窄事件的发生率,同时可抑制炎症因子P-选择素的表达预防动脉粥样硬化。
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[Abstract]
Objective To investigate the effect of clopidogrel on platelet function and inflammation factor in treatment of severe carotid artery stenosis after stent-assisted angioplasty.Methods Patients (120 cases) with severe carotid artery stenosis after stent-assisted angobservation group were given atorvastatin combined with chlorine. The serum coagulants DD level, FIB level, inflammation factor P-chosen element level and restenosis event incidence of two groups were observed.Results D-double polymer of two groups had no significant difference; After surgery, the D-double polymer and FIB level of two groups were all higher (P<0.05). After surgery for 24 h, the D-double polymer and FIB level of observation group were higher, after 3 months of surgery, the D-double polymer and FIB level had no significant differences compared with before surgery, which were all in normal level. After 24 h, 1 month, 3 months of surgery, the D-double polymer and FIB level of observation group were all lower than control group (P<0.05). Before treatment, the P-chosen selectin of two groups had no significant differences, which were all decreased after surgery, and the observation group was lower than control group (P<0.05); The restenosis event of observation group was lower than control group (P<0.05).Conclusion Clopidogrel could control the platelet aggregation of severe carotid stenosis after surgery to prevent the thrombogenesis and decrease the restriction incidence, while control the inflammation factor expression to prevent the atherosclerosis.
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