中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2010年
5期
462-464
,共3页
刘文卫%魏敏%江华%刘永胜%朱锐%李彬%关思虞%赵玉琴%叶剑文
劉文衛%魏敏%江華%劉永勝%硃銳%李彬%關思虞%趙玉琴%葉劍文
류문위%위민%강화%류영성%주예%리빈%관사우%조옥금%협검문
冠状动脉介入术%氟伐他汀%白细胞介素-18%肿瘤坏死因子-α%白细胞介素-6
冠狀動脈介入術%氟伐他汀%白細胞介素-18%腫瘤壞死因子-α%白細胞介素-6
관상동맥개입술%불벌타정%백세포개소-18%종류배사인자-α%백세포개소-6
Percutaneous transluminal coronary intervention%Fluvastatin%IL-18%TNF-α%IL-6
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.
目的 探討冠狀動脈介入術(PCI)後心血管事件髮生及氟伐他汀改善預後的作用.方法 選擇2005年6月至2008年2月在我院經過選擇性冠狀動脈造影證實冠狀動脈狹窄≥70%併行PCI術的187例患者,入院後隨機分為2組,常規治療組91例,給予常規藥物治療;氟伐他汀榦預組96例,在常規藥物治療基礎上加用氟伐他汀40 mg/d;分彆于入院後藥物治療前、藥物治療後(PCI術前)及PCI術後12、24 h和術後2週空腹採集肘部靜脈血,採用酶聯免疫吸附試驗檢測各組血清白細胞介素(IL)-18、腫瘤壞死因子(TNF)-α、IL-6濃度.結果 2組患者藥物治療前血清IL-18、TNF-α、IL-6濃度差異均無統計學意義(P均＞0.05),常規治療組與氟伐他汀榦預組藥物治療後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]明顯降低(P＜0.05或＜0.01),且氟伐他汀榦預組較常規治療組更為明顯(P均＜0.01).常規治療組術後12 h IL-18、TNF-α、IL-6濃度增高,分彆為(423.5±298.7)、(316.1±72.6)、(42.3±10.1)ng/L(P均＜0.05),在術後24 h達高峰併且明顯高于藥物治療前(P均＜0.01),而氟伐他汀榦預組在術後12 h與術後24 h僅略高于PCI術前,差異均無統計學意義(P均＞0.05).同期比較氟伐他汀榦預組術後12 h IL-18、TNF-α、IL-6濃度分彆為(276.5±189.4)、(175.3±51.9)、(10.1±8.1)ng/L,較常規治療組低(P均＜0.01).術後2週氟伐他汀榦預組IL-18為(137.0±34.2)ng/L,TNF-α為(35.1±21.6)ng/L,IL-6為(8.7±3.2)ng/L,較入院時明顯降低(P均＜0.01).結論 PCI術可能在短期內觸髮併加重瞭冠狀動脈炎性反應,應用他汀類藥物可以減弱炎癥反應.IL-18、TNF-α、IL-6是反映PCI後早期炎性反應的敏感指標,其變化程度對不良心血管事件的髮生可能具有預測價值,可以成為一級預防中他汀類藥物治療的靶目標,可以用于評價PCI、他汀類藥物以及二者聯閤的效果.
목적 탐토관상동맥개입술(PCI)후심혈관사건발생급불벌타정개선예후적작용.방법 선택2005년6월지2008년2월재아원경과선택성관상동맥조영증실관상동맥협착≥70%병행PCI술적187례환자,입원후수궤분위2조,상규치료조91례,급여상규약물치료;불벌타정간예조96례,재상규약물치료기출상가용불벌타정40 mg/d;분별우입원후약물치료전、약물치료후(PCI술전)급PCI술후12、24 h화술후2주공복채집주부정맥혈,채용매련면역흡부시험검측각조혈청백세포개소(IL)-18、종류배사인자(TNF)-α、IL-6농도.결과 2조환자약물치료전혈청IL-18、TNF-α、IL-6농도차이균무통계학의의(P균＞0.05),상규치료조여불벌타정간예조약물치료후IL-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]명현강저(P＜0.05혹＜0.01),차불벌타정간예조교상규치료조경위명현(P균＜0.01).상규치료조술후12 h IL-18、TNF-α、IL-6농도증고,분별위(423.5±298.7)、(316.1±72.6)、(42.3±10.1)ng/L(P균＜0.05),재술후24 h체고봉병차명현고우약물치료전(P균＜0.01),이불벌타정간예조재술후12 h여술후24 h부략고우PCI술전,차이균무통계학의의(P균＞0.05).동기비교불벌타정간예조술후12 h IL-18、TNF-α、IL-6농도분별위(276.5±189.4)、(175.3±51.9)、(10.1±8.1)ng/L,교상규치료조저(P균＜0.01).술후2주불벌타정간예조IL-18위(137.0±34.2)ng/L,TNF-α위(35.1±21.6)ng/L,IL-6위(8.7±3.2)ng/L,교입원시명현강저(P균＜0.01).결론 PCI술가능재단기내촉발병가중료관상동맥염성반응,응용타정류약물가이감약염증반응.IL-18、TNF-α、IL-6시반영PCI후조기염성반응적민감지표,기변화정도대불양심혈관사건적발생가능구유예측개치,가이성위일급예방중타정류약물치료적파목표,가이용우평개PCI、타정류약물이급이자연합적효과.
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.
