脑梗死患者血清ox-LDL IL-18 Lp-PLA2水平与颈动脉硬化斑块的相关性分析

Analysis on Correlation between Serum ox-LDL IL-18 and Lp-PLA2 Levels and Carotid Atherosclerotic Plaques in Patients with Cerebral Infarction

目的:分析脑梗死患者血清氧化低密度脂蛋白(oxidized low density lipoprotein,ox-LDL)、白细胞介素-18(IL-18)以及脂蛋白相关磷酯酶A2(lipoprotein-associated phosphatase A2,Lp-PLA2)水平与颈动脉硬化斑块的相关性。方法:选取2018年3月至2019年3月本院收治的120例脑梗死患者(研究组)和同期35例健康志愿者(对照组)为对象,收集两组一般资料,比较两组血清ox-LDL、IL-18、Lp-PLA2水平,测量两组颈动脉内膜中层厚度(Carotid intima-media thickness,CIMT)、斑块最大面积,比较两组颈动脉斑块Crouse积分,分析血清ox-LDL、IL-18、Lp-PLA2水平与颈动脉硬化斑块的相关性。结果:研究组血清ox-LDL、IL-18、Lp-PLA2水平、CIMT、斑块最大面积、颈动脉斑块Crouse积分较对照组明显高(P<0.05),相关性分析提示CIMT、斑块最大面积、Crouse积分均与血清ox-LDL、IL-18、Lp-PLA2水平呈正相关(P<0.05)。结论:血清ox-LDL、IL-18、Lp-PLA2水平变化或可作为脑梗死患者颈动脉硬化斑块形成的有效预测因子。

Objective: To analyze the correlation between serum oxidized low density lipoprotein(oxidized low density lipoprotein, ox-LDL), interleukin-18(IL-18), lipoprotein-associated phosphatase A2(Lp-PLA2) and carotid atherosclerotic plaque in patients with cerebral infarction. Methods: 120 patients with cerebral infarction(study group) and 35 healthy volunteers(control group) who were admitted to the hospital from March 2018 to March 2019 were enrolled in the study. General data of both groups were collected. Serum ox-LDL, IL-18 and Lp-PLA2 levels were compared between the two groups. Carotid intima-media thickness(CIMT) and the maximum area of plaques were measured. Crouse score of carotid plaques was calculated. The correlation between serum ox-LDL, IL-18 and Lp-PLA2 levels and carotid atherosclerotic plaques was analyzed. Results: Serum ox-LDL, IL-18 and Lp-PLA2 levels, CIMT, the maximum area of plaques, Crouse score of carotid plaques in the study group were significantly higher than those of the control group(P<0.05). Correlation analysis showed that CIMT, the maximum area of plaques and Crouse score were positively correlated with serum ox-LDL, IL-18 and Lp-PLA2 levels(P<0.05). Conclusion: The changes of serum ox-LDL, IL-18 and Lp-PLA2 levels may be effective predictors of carotid atherosclerotic plaque formation in patients with cerebral infarction.