The Association of Lipoprotein(a), Apolipoprotein(a) Phenotypes and Autoantibodies to Lipoprotein(a) With Lower Extremity Artery Disease

Aim . Lipoprotein(a) [Lp(a)] and low molecular weight (LMW) apolipoprotein(a) [apo(a)] phenotype are risk factors of сoronary heart disease and stroke. Data about the role of Lp(a) and phenotypes apo(a) in the development of lower extremity artery disease (LEAD) is scarce. The aim of our study was to assess the association of Lp(a), apo(a) phenotypes and autoantibodies to apolipoprotein B100 (apoB100) lipoproteins with LEAD. Materials and methods . The study included 622 patients (386 male and 236 female, average age 61±12 years), examined in the Department of Atherosclerosis of National Medical Research Center of Cardiology. Patients were divided into 2 groups: the main group included 284 patients with LEAD, 338 patients without significant atherosclerosis of coronary, carotid and lower limbs arteries formed the control group. LEAD was diagnosed as atherosclerotic lesions with at least one stenosis of low limb artery ≥50 % and ankle­brachial index ≤0.9. The concentration of Lp(a), lipids was measured in blood serum of all the patients, level of autoantibodies to apoB100 lipoproteins was measured in 247 patients, and apo(a) phenotypes were determined in 389 patients. Results. Patients with LEAD were older, were more frequently male, and had a greater prevalence of risk factors including hypertension, type 2 diabetes, smoking than the control group patients (p<0.001 in all the cases). The level of Lp(a) was significantly higher in the main group compared to control group: 35 [14; 67] mg / dl vs. 14 [5; 32] mg / dl, p<0,001. ROC analysis demonstrated that the level of Lp(a) ≥26 mg / dl was associated with LEAD (sensitivity 61 %, specificity 70 %). The prevalence of Lp(a) ≥26 mg / dl and LMW apo(a) phenotype were higher in the main group in comparison with the control group: 61 % vs. 30 % and 48 % vs. 26 % respectively (p<0.001 in the both cases). The odds ratio of LEAD in the presence of Lp(a) ≥26 mg / dl was 3.7 (95 % confidence interval (CI), 2.6–5.1, p<0.001) and in the presence of LMW apo(a) phenotype was 2.6 (95 % CI, 1.7–4.0, p<0.001). In logistic regression analysis adjusted for age, sex, hypertension, smoking, diabetes, both Lp(a) and LMW apo(a) phenotype were independent predictors of LEAD when included separately. The level of IgM autoantibodies to Lp(a) was significantly higher in the control group compared to the patients with LEAD (p=0.01). Concentration of IgG autoantobodies to Lp(a) and LDL in the plasma did not differ essentially in the both groups. Conclusion. The level of Lp(a) ≥26 mg / dl and LMW apo(a) phenotype are independent predictors of LEAD, whereas the contribution of autoantobodies to Lp(a) in LEAD development is controversial.