依那普利对冠心病患者血清CXCL16及高敏C反应蛋白浓度的影响

Effect of enalapril on serum concentrations of CXCL16 and high-sensitive C-reactive protein in patients with coronary heart disease

目的探讨依那普利治疗对冠状动脉粥样硬化性心脏病(冠心病)患者血清CXCL16及高敏C反应蛋白(high-sensitivity C-reactive protein,hs-CRP)浓度的影响。方法取98例冠心病患者血清,分为稳定型心绞痛组和急性冠脉综合征组,并给予常规治疗及联合依那普利治疗3周,比较其血清CXCL16及hs-CRP浓度与正常人的差异,进行组内及组间比较分析。结果冠心病患者血清CXCL16及hs-CRP浓度显著升高,急性冠脉综合征组较稳定型心绞痛组更高,差异有统计学意义(P<0.05)。联合依那普利治疗后急性冠脉综合征组及稳定型心绞痛组血清CXCL16及hs-CRP浓度较治疗前均显著降低,差异有统计学意义[CXCL16:(1.44±0.67)ng·mL-1 vs.(3.45±0.62)ng·mL-1,P<0.05;(1.86±0.76)ng·mL-1vs.(2.65±0.95)ng·mL-1,P<0.05。hs-CRP:(1.21±0.46)mg·L-1vs.(3.32±1.08)mg·L-1,P<0.05;(1.62±0.76)mg·L-1vs.(2.25±1.02)mg·L-1,P<0.05];其疗效优于常规治疗组,且在急性冠脉综合征组效果更优,以降低血清CXCL16浓度效应更明显。结论依那普利可能通过抑制炎症因子的释放及降低血清CXCL16浓度从而发挥对冠心病的治疗作用。

Objectives To explore the effect of enalapril treatment on serum concentrations of CXCL16 and high-sensitive C-reactive protein （hs-CRP） in patients with coronary heart disease. Methods Totally 98 patients with coronary heart disease,including stable angina peetoris （SAP） and acute coronary syndrome （ACS） groups, were signed into conventional therapy group and combined with enalapril therapy group. Their serum concentrations of CXCL16 and hs-CRP were compared and analyzed. Results Compared with healthy individuals, serum concentrations of CXCL16 and hs-CRP significantly increased in both SAP and ACS groups, especially higher in ACS group （P〈O.05）. After treatment combined with enalapril for 3 weeks, serum concentrations of CXCL16 and hs-CRP significantly decreased in both groups related to untreated [CXCL16： （1.44±0.67） ng.mL-1 vs. （3.45±0.62） ng.mL-1, P〈0.05; （1.86±0.76） ng.mL-1 vs. （2.65± 0.95） ng.mL-1,P〈0.05, hs-CRP： （1.21±0.46） mg.L-1 vs. （3.32±1.08） mg-L-1,P〈0.05; （1.62±0.76） mg-L-1vs. （2.25 ±1.02）mg .L-1,P〈0.05]. The reduction effect was more obviously when combined with enalapril therapy, specifically in ACS group. Conclusions Enalapril treatment may inhibit the release of inflammatory eytokines and decrease serum concentrations of CXCL16, thus play a critical role in the therapy of coronary heart disease.