急性脑梗死患者血清sdLDL-C与PTX-3水平与颈动脉粥样硬化斑块性质的关系

The relationship between serum levels of sdLDL-C and PTX-3 and the occurrence of acute cerebral infarction and the stability of carotid atherosclerotic plaque

目的通过联合测定血清小而密低密度脂蛋白胆固醇(sdLDL-C)、正五聚蛋白3(PTX3)水平探讨与急性脑梗死发生及颈动脉粥样硬化斑块性质的关系。方法纳入急性脑梗死患者150例为观察组,根据颈动脉粥样硬化斑块稳定性分为稳定型斑块组64例、易损斑块组86例,另取体检健康者102例为对照组。采用(ELISA)法检测血清sdLDL-C、PTX3水平。应用非条件多因素Logistic回归分析sdLDL-C、PTX3与急性脑梗死患者颈动脉粥样硬化斑块性质的关系。结果观察组血清sdLDL-C及PTX3水平明显高于对照组(P <0. 01);易损斑块组TG、LDL-C、sdLDL-C、PTX3均高于稳定斑块组(P <0. 01),但HDL-C水平低于稳定斑块组(P <0. 05);非条件多因素Logistic回归分析显示LDL-C、sdLDL-C、PTX3为急性脑梗死患者颈动脉粥样斑块稳定性的独立危险因素(P <0. 05)。结论血清sdLDL-C和PTX-3水平升高是急性脑梗死发生及不稳定颈动脉粥样硬化斑块形成的危险因素。

Objective To investigate the relationship between serum levels of small dense low density lipoprotein cholesterol( sd LDL-C) and pentamer 3( PTX3) and the occurrence of acute cerebral infarction and the nature of carotid atherosclerotic plaques. Methods According to the stability of carotid atherosclerosis plaque,150 patients with acute cerebral infarction were divided into stable plaque group( 64 cases),vulnerable plaque group( 86 cases),and 102 healthy people were selected as control group. Serum levels of sdLDL-C and PTX3 were detected by ELISA. The relationship between sdLDL-C,PTX3 and carotid atherosclerotic plaque in patients with acute cerebral infarction was analyzed by unconditional multivariate logistic regression. Results The levels of serum SdLDL-C and PTX3 in the observation group were significantly higher than those in the control group( P < 0. 05);the levels of TG,LDL-C,SdLDL-C and PTX3 in vulnerable plaque group were higher than those in stable plaque group( P < 0. 05),but the levels of HDL-C were lower than those in stable plaque group( P < 0. 05);unconditional logistic regression analysis showed that LDL-C,sdLDL-C and PTX3 are independent risk factors for carotid atherosclerotic plaque stability in patients with acute cerebral infarction( P < 0. 05). Conclusion Elevated serum levels of sdLDL-C and PTX-3 are risk factors for acute cerebral infarction and unstable carotid atherosclerotic plaque formation.