脂蛋白（a）颗粒浓度与质量浓度在冠状动脉粥样硬化性心脏病风险性评估中的应用

目的探讨脂蛋白（a）［LP（a）］颗粒（P）浓度与质量（M）浓度在冠状动脉粥样硬化性心脏病（CAHD）患者风险性评估中的临床应用价值。 方法选取2015年10月至2017年4月在北京大学人民医院确诊的657例CAHD患者为研究对象，同时收集2016年4月至8月，在北京大学人民医院体检并排除各项疾病的472名健康者作为健康对照组。同时检测CAHD患者和健康对照组患者的LP（a）-P波度和LP（a）-M浓度及肝功、肾功、血糖和血脂等生化指标。采用t检验比较2组患者年龄、血糖（GLU）、胆固醇（CHO）、三酰甘油（TG）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、载脂蛋白A1（ApoA1）、载脂蛋白B（ApoB）水平差异，采用Mann-Whitney U非参数检验比较2组患者同型半胱氨酸（HCY）、超敏C反应蛋白（hs-CRP）、小而密低密度脂蛋白（sdLDL-C）及LP（a）颗粒浓度［LP（a）-P］和LP（a）质量浓度［LP（a）-M]水平差异。以CAHD为因变量，年龄、GLU、CHO、TG、HDL-C、LDL-C、ApoA1、ApoB、HCY、hs-CRP、sdLDL-C、LP（a）-P和LP（a）-M为自变量进行logistic二元逐步回归方程分析，以P值小于0.1纳入，大于0.1剔除为模型。LP（a）-P和LP（a）-M进行直线回归，一致性分析采用Kappa检验。 结果CAHD组TG水平高于健康对照组［（1.62±1.25）nmol/L vs （1.47±0.75）nmol/L］，组间比较差异无统计学意义（t=0.361，P=0.705）；年龄、GLU、CHO、LDL-C、ApoB、HCY、hs-CRP、sdLDL-C、LP（a）-P和LP（a）-M水平高于健康对照组［（65.73±11.23）岁vs（57.62±12.28）岁；（5.80±1.43）mmol/L vs （5.44±1.23）mmol/L；（4.73±1.04）mmol/L vs （4.25±1.09）mmol/L；（3.01±0.78）mmol/L vs （2.64±0.75）mmol/L；（93.56±34.71）g/L vs （73.56±26.28）g/L；11.99（10.22）μmol/L vs 9.58（5.61）μmol/L；4.14（7.65）mg/L vs 1.05（1.45）mg/L；0.824（0.443）mmol/L vs 0.609（0.361）mmol/L；39.71（48.37）nmol/L vs 34.69（38.56）nmol/L；101.87（235.91）mg/L vs 81.75（150.65）mg/L］，差异均具有统计学意义（t=5.746，P<0.001；t=4.782，P<0.001；t=4.616，P<0.001；t=5.461，P<0.001；t=7.52，P<0.001；Z=-8.64，P<0.001；Z=-13.60，P<0.001；Z=-5.61，P<0.001；Z=-5.46，P=0.002；Z=-3.02，P<0.001）；HDL-C和ApoA1水平低于健康对照组［（1.03±0.30）mmol/L vs （1.33±0.42）mmol/L；（116.83±29.67）g/L vs （175.83±30.04）g/L］，差异具有统计学意义（t=-7.361，P<0.001；t=-8.21，P<0.001）。经过Logistics二元逐步回归方程分析得到年龄、GLU、LDL-C、sdLDL-C、LP（a）-P和LP（a）-M是CAHD的独立风险因素（OR=1.055，P<0.001；OR=1.257，P<0.001；OR=1.143，P<0.001；OR=2.041，P=0.031；OR=1.312，P<0.001；OR=1.269，P<0.001）。LP（a）-M对LP（a）-P的直线回归方程为Y=0.2039X＋18.406，R²=0.8718。一致性检验认为两种方法对个体分组不一致（Kappa值为0.594）。 结论LP（a）水平与CAHD的发生、严重程度显著相关，是CAHD严重程度的独立危险因素。

Relationship between particle or mass concentration of lipoprotein (a) and coronary atherosclerotic heart disease

ObjectiveTo investigate the clinical value of serum particle or mass concentration of lipoprotein(a) LP(a)-P and LP(a)-M] in coronary atherosclerotic heart disease (CAHD). MethodsSix hundred and fifty-seven patients who were diagnosed with CAHD at the Peking University People's Hospital from October 2015 to April 2017 were included. Besides, 472 healthy persons were included as a control group. The LP(a)-P and LP(a)-M, liver function, renal function, blood glucose (GLU) and blood lipid in the CAHD group and healthy control group were detected. Data including age, GLU, cholesterol (CHO), triglyceride, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), apolipoprotein A1 (ApoA1) and apolipoprotein B (ApoB) were compared by the independent t-test between the two groups. The Mann-Whitney U nonparametric test was used for comparing homocysteine (HCY), hypersensitive C-reactive protein (hs-CRP), small-dense low density lipoprotein cholesterol (sdLDL-C) and lipoprotein(a). The risk for CAHD was analyzed by logistic regression, the relationship between LP(a)-P and LP(a)-M was assessed by linear regression analysis, and the concordance was analyzed using the Kappa test. ResultsThe level of TG in the CAHD group was similar to that in the healthy control group (1.62±1.25) nmol/L vs (1.47±0.75) nmol/L, t=0.361, P=0.705]. Age, GLU, CHO, LDL-C, ApoB, HCY, hs-CRP, sdLDL-C, LP(a)-P and LP(a)-M in the CAHD group were significantly higher than those in the healthy control group (65.73±11.23) years vs (57.62±12.28) years, t=5.746, P<0.001; (5.80±1.43) mmol/L vs (5.44±1.23) mmol/L, t=4.782, P<0.001; (4.73±1.04) mmol/L vs (4.25±1.09) mmol/L, t=4.616, P<0.001; (3.01±0.78) mmol/L vs (2.64±0.75) mmol/L, t=5.461, P<0.001; (93.56±34.71) g/L vs (73.56±26.28) g/L, t=7.52, P<0.001; 11.99 (10.22) μmol/L vs 9.58 (5.61) μmol/L, Z=-8.64, P<0.001; 4.14 (7.65) mg/L vs 1.05 (1.45) mg/L, Z=-13.60, P<0.001; 0.824 (0.443) mmol/L vs 0.609 (0.361) mmol/L, Z=-5.61, P<0.001; 39.71 (48.37) nmol/L vs 34.69 (38.56) nmol/L, Z=-5.46, P=0.002; 101.87 (235.91) mg/L vs 81.75 (150.65) mg/L, Z=-3.02, P<0.001), while the levels of HDL-C and ApoA1 in the CAHD group were significantly lower than those in the healthy control group (1.03±0.30) mmol/L vs (1.33±0.42) mmol/L, t=-7.361, P<0.001; (116.83±29.67) g/L vs (175.83±30.04) g/L, t=-8.21, P<0.001]. Binary stepwise regression analysis demonstrated that age, GLU, LDL-C, sdLDL-C, LP(a)-P and LP(a)-M were independently associated with the severity of CAHD (OR=1.055, P<0.001; OR=1.257, P<0.001; OR=1.143, P<0.001; OR=2.041, P=0.031; OR=1.312, P<0.001; OR=1.269, P<0.001). The linear regression equation of LP(a)-M and LP(a)-P is Y=0.2039X+ 18.406, R²=0.8718. Consistency test indicated that the two parameters were not consistent when used for distinguishing the two groups (Kappa=0.594). ConclusionsLP(a) plays an important role in the occurrence and progression of CAHD and is an independent important risk factor for the severity of this disease.