摘要
目的观察阿托伐他汀对体外循环冠状动脉旁路移植术(CABG)患者围手术期心肌损伤和血清炎性因子的影响。方法 50例择期行CABG患者,随机分为阿托伐他汀组(n=25)和对照组(n=25)。分别于转流前、术毕、术后6、24和48h监测心肌肌钙蛋白(IcTnI)和肌酸激酶同工酶(CKMB)的水平;并测定血清肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)的浓度。结果两组患者血清cTnI和CKMB水平从术后6h开始升高(P<0.05),在术后24h达到峰值;阿托伐他汀组术后6、24和48h血清cTnI和CKMB水平较对照组明显降低(P<0.01)。两组麻醉诱导前血清TNF-α和IL-6水平差异无显著性,术毕均明显升高,但阿托伐他汀组血清TNF-α在术毕和术后6h均低于对照组(P<0.05);IL-6在术毕、术后6h、24h和48h均低于对照组(P<0.05)。结论术前使用阿托伐他汀可降低CABG患者围手术期心肌损伤和炎症反应。
[Objective]To investigate the effects of atorvastatin treatment on perioperative myocardial damage and serum inflammatory mediators in patients undergoing coronary artery bypass grafting surgery under on-pump. [Methods]Fifty subjects undergoing elective coronary artery bypass grafting were randomized to atorvastatin group （n =25） and control group （n =25） before surgery. Serum levels of troponin I （cTnI）, creatine phosphokinase（CK）-MB, tumour necrosis factor-alpha （TNF-alpha） and interleukin （IL）-6 were measured before induction, and postoperative 0 h, 6 h, 24 h and 48 h, respectively[.Results]The serum cTnI and CKMB level of two groups increased at postoperative 6 h （P 0.05）, reached peak at postoperative 24 h. Compared to control group, the serum concentration of cTnI and CKMB in atorvastatin group were significantly lower at postoperative 6 h, 24 h and 48 h （P 0.05）. There were no difference on the serum concentration of TNF-α and IL-6 of two groups at the time point before induction, but increased at postoperative 0 h （P 0.05）. Atorvastatin group had significantly lower levels of TNF-α than control group at postoperative 0 h and 6 h （P 0.05）; as well as significantly lower IL-6 levels than control group at postoperative 0 h, 6 h, 24 h and 48 h （P 0.05）.[Conclusion]Preoperative treatment with atorvastatin in patients undergoing elective CABG might reduce the perioperative cardiac injury and inflammatory response.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2010年第11期1684-1687,共4页
China Journal of Modern Medicine
基金
湖南省科技厅基金项目(No:2009SK2010)
关键词
冠状动脉旁路移植
阿托伐他汀
心肌保护
炎性因子
coronary artery bypass grafting
atorvastatin
myocardial protection
inflammatory mediators
