氟伐他汀对冠状动脉介入患者炎性因子及预后的影响

目的 探讨冠状动脉介入术(PCI)后心血管事件发生及氟伐他汀改善预后的作用.方法 选择2005年6月至2008年2月在我院经过选择性冠状动脉造影证实冠状动脉狭窄≥70%并行PCI术的187例患者,入院后随机分为2组,常规治疗组91例,给予常规药物治疗;氟伐他汀干预组96例,在常规药物治疗基础上加用氟伐他汀40 mg/d;分别于入院后药物治疗前、药物治疗后(PCI术前)及PCI术后12、24 h和术后2周空腹采集肘部静脉血,采用酶联免疫吸附试验检测各组血清白细胞介素(IL)-18、肿瘤坏死因子(TNF)-α、IL-6浓度.结果 2组患者药物治疗前血清IL-18、TNF-α、IL-6浓度差异均无统计学意义(P均＞0.05),常规治疗组与氟伐他汀干预组药物治疗后IL-18[(316.5±274.2)、(261.8±195.6)ng/L]、TNF-α[(201.7±56.9)、(166.4±42.5)ng/L]、IL-6[(13.4±6.2)、(9.6±7.5)ng/L]明显降低(P＜0.05或＜0.01),且氟伐他汀干预组较常规治疗组更为明显(P均＜0.01).常规治疗组术后12 h IL-18、TNF-α、IL-6浓度增高,分别为(423.5±298.7)、(316.1±72.6)、(42.3±10.1)ng/L(P均＜0.05),在术后24 h达高峰并且明显高于药物治疗前(P均＜0.01),而氟伐他汀干预组在术后12 h与术后24 h仅略高于PCI术前,差异均无统计学意义(P均＞0.05).同期比较氟伐他汀干预组术后12 h IL-18、TNF-α、IL-6浓度分别为(276.5±189.4)、(175.3±51.9)、(10.1±8.1)ng/L,较常规治疗组低(P均＜0.01).术后2周氟伐他汀干预组IL-18为(137.0±34.2)ng/L,TNF-α为(35.1±21.6)ng/L,IL-6为(8.7±3.2)ng/L,较入院时明显降低(P均＜0.01).结论 PCI术可能在短期内触发并加重了冠状动脉炎性反应,应用他汀类药物可以减弱炎症反应.IL-18、TNF-α、IL-6是反映PCI后早期炎性反应的敏感指标,其变化程度对不良心血管事件的发生可能具有预测价值,可以成为一级预防中他汀类药物治疗的靶目标,可以用于评价PCI、他汀类药物以及二者联合的效果.

Influence of fluvastatin on inflammation factors and prognosis of patients underwent percutaneous transluminal coronary intervention

Objective To assess the cardiovascular events after percutaneous transluminal coronary intervention (PCI) and the influence of fluvastatin on inflammation factors and prognosis of PCI patients.Methods One hundred and eighty-seven patients whose coronary stenosis ≥ 70% diagnosed through coronarography and underwent PCI from Jun.2005 to Feb.2008 were recruited in the current study.These patients were divided into two groups,the control group (n =91) was treated regularly and the treat group (n =96) was treated with additionally fluvastatin(40 mg/d).Fasting venous blood was obtained before and after medicine treatment,12,24 hours and two weeks after PCI.IL-18,IL-6 and TNF-α were measured through ELISA.Results Before medicine treatment,there were no difference of IL-18 ,IL-6 and TNF-α between the two groups( P ＞ 0.05 ).After medicine treatment,IL-18,TNF-α and IL-6 decreased significantly compared to those before treatment in both groups ( P ＜ 0.05 ),and these measurements decreased more in the treatment group ( P ＜ 0.01 ).At the 12th hours after PCI,IL-18,TNF-αand IL-6 in the control group increased to (423.5 ± 298.7 ),( 316.1 ± 72.6 ) and (42.3 ± 10.1 ) ng/L,respectively,and arrived the peak at the 24th hour,which were significantly higher than those before medicine treatment( P ＜ 0.01 ).In the treatment group,these measurements at the 12th and 24th hour after PCI were slightly higher than those before medicine treatment without significant difference ( P ＞ 0.05 ).After 12 hours ofPCI,IL- 18,TNF -αand IL-6were (276.5 ± 189.4 ),( 175.3 ± 51.9) and ( 10.1 ± 8.1 ) ng/L,which were significantly lower than those in the control group(P ＜ 0.01 ).Two weeks after PCI,IL-18,TNF-α and IL-6 in the treatment group were (137.0 ±34.2),(35.1 ± 21.6) and ( 8.7 ± 3.2 ) ng/L,which were significantly lower than before medicine treatment ( P ＜0.01 ).Conclusions PCI may aggravate the inflammation response of coronary artery.Statins may alleviate the inflammation response.IL-18,TNF-α and IL-6 are sensitive indices of early inflammation response after PCI,their changes might have prediction value for adverse cardiovascular events.Therefore these indices might be used as a target in the statins treatment in the primary prevention,as well as the evaluation of the effectiveness of PCI,statins and joint PCI and statins.