急性冠脉综合征患者冠脉斑块易损性与sCD40配体等血管因子的定量关系

目的研究急性冠脉综合征(ACS)患者易损斑块[通过血管内超声(IVUS)判定]和可溶性黏附分子CD40配体(sCD40L)及其他血管因子的定量关系以及临床意义。方法42例ACS患者,发病时取血,应用液相蛋白芯片结合流式细胞分析方法测定sCD40L及相应的炎性因子水平;常规冠状动脉造影并通过IVUS检测42个靶病变处动脉粥样斑块形态学及性质特征。并对各指标间的相关性进行分析。结果sCD40L浓度在易损斑块破裂组高于非破裂组[(474±126)pg/mlvs(238±35)pg/ml],差异有统计学意义(P<0.05),且单核细胞趋化蛋白-1(MCP-1)和P选择素(sPE)在易损斑块破裂组高于非破裂组,差异有统计学意义(P<0.05,P<0.01),但白介素-8(IL-8)和IL-6差异无统计意义(均P>0.05)。sCD40L与sPE、MCP-1呈高度正相关(依次为r=0.93,P<0.01;r=0.57,P<0.01),而与IL-8和IL-6未见相关性。sCD40L在ACS中合并高血压组(279.8pg/ml±95.7pg/ml)较非合并高血压组(99.2pg/ml±56.4pg/ml)升高(P<0.05)。结论sCD40L、MCP-1和sPE可能是冠脉易损斑块发生急性破裂的血清学标志。

Quantitative study between vulnerable atherosclerotic plaque and the expression of soluble CD40 ligand in acute coronary syndrome

Objective To investigate the quantitative relationship between coronary vulnerable atheresclerotic plaque using intravascular ultrasound （IVUS） and plasma levels of vascular factors including soluble CD40 ligand （sCD4OL） in patients with acute coronary syndrome（ACS）. Methods Forty two patients with ACS who underwent IVUS and coronary angiography. Plasma levels of sCD4OL, sPE and MCP- 1 were detected by liquid protein chip measured through cytometer, and 42 target atherosclerotic plaque morphology were assessed with IVUS. Results The plasma sCD4OL, sPE and MCP-1 showed significantly higher level in patients with vulnerable plaque rupture than without rupture[ （474 ± 126 vs 238 ± 35）pg/ml, （ P 〈 0.05） ]. There were significant difference in levels of MCP-1 and sPE （ P 〈 0.05, P 〈 0.01 ）, but no significant difference was found in IL-8 and IL-6 between the groups with and without plaque rupture （ P 〉 0.05）. It showed that the level of sCD40L had positive correlation with sPE and MCP- 1 （ r = 0.93, P 〈 0.01 ; r = 0.57, P 〈 0.01 ）, and no correlation with IL-8 and IL-6. Patients with hypertension （279.8 pg/ml ± 95.7 pg/ml） were significantly increased in plasma sCD40L than patients without hypertension [（99.2 pg/ml±56.4 pg/ml）, P 〈 0.05].Conclusion High plasma concentrations of sED4OL, MEP-1 and sPE may be novel makers of plaque rupture in ACS patients, and inflammation influences unstable plaque and active platelets.