To 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).

Six 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.

The 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).

LP(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.