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Aim. To assess the level of lipoprotein (a) (Lp(a)) and other lipid profile parameters, the composition of blood leukocytes in patients with focal and diffuse coronary atherosclerosis who underwent coronary artery bypass surgery (CABG), as well as to study the effect of Lp(a) on the activation of leukocytes in vitro.Material and methods. The study included 120 male patients (mean age, 67±5 years) with multivessel coronary artery disease after elective CABG surgery. According to the type of coronary artery involvement, patients were divided into groups of diffuse (n=77) and focal (n=43) atherosclerosis. In peripheral blood samples, the content of the main fractions of lipoproteins, including Lp(a), was determined. Activation of neutrophil granulocytes upon addition of Lp(a) was assessed in whole blood and in primary cell culture.Results. In patients with diffuse coronary stenosis, there was a tendency to higher Lp(a) levels; no changes in other lipid profile parameters were detected. In this group of patients, an increase in the absolute leukocyte count was noted due to neutrophilic granulocytes. An absolute neutrophil count >2,9 million/mL was associated with diffuse disease (AUC, 0,69 (95% confidence interval (CI) 0,600,77), p=0,0002, sensitivity 85%, specificity 42%). In patients with Lp(a) ³30 mg/dL, the diagnostic value of a neutrophil count >2,9 million/mL for diffuse stenosis was higher (AUC, 0,74 (95% CI 0,60-0,86), p= 0,005, sensitivity 90%, specificity 48%). According to logistic regression analysis with the introduction of neutrophils and conventional risk factors (age, body mass index, hypertension and smoking) into the model, only the number of neutrophils above the threshold level remained an independent factor in diffuse coronary stenosis. Lp(a) can induce neutrophil activation, detected by increased CD66b overexpression in whole blood, as well as the formation of neutrophil extracellular traps in primary cell culture.Conclusion. Neutrophil granulocytes can participate in the formation of diffuse atherosclerotic coronary lesions. One of the neutrophil activators may be Lp(a). The combination of high neutrophil count and Lp(a) level in the blood increases the risk of diffuse coronary atherosclerosis.

Aim. To investigate on the relation of lipoproteide(a) (Lpa), subfractions of atherogenic lipoproteides and titers of specific autoantibodies (autoAb) with the presence and severity of carotid arteries (CA) lesion in statin-naïve patients with severe hypercholesterolemia.Material and methods. To the study, 133 statin-naïve patients included, age 18 to 75 y.o., with absent clinical signs of coronary heart disease, and with first time diagnosed severe hypercholesterolemia (total cholesterol >7,5 mM/L and/or low density lipoproteides cholesterol >4,9 mM/L) with ultrasound duplex scan data of CA. All patients underwent measurement of Lpa concentration, lipid profile, subfractional content of apoB-100-containing lipoproteides and autoAb titer against them.Results. According to the data from duplex CA scan, patients were selected to 2 groups: control group (n=76) with no CA atherosclerosis; main group — patients with CA stenosis >20% (n=57). The participants of main group were older than controls, with no other clinical or lipid profile differences. Titre of autoAb IgM specific for Lpa and its oxidized modifications was significantly lower in CA atherosclerosis comparing to controls. The grade of CA stenosis in severe hypercholesterolemia patients positively correlated with age (r=0,24, p=0,005) and negatively — with autoAb IgM to apoB100-containing lipoproteides (r=-0,28 and r=-0,26, p

Aim. To investigate on the relation of lipoproteide (a) (Lpa), subfractions of intermediate density lipoproteides (IDL) and low density lipoproteides (LDL) with the probability of familial hypercholestrolemia diagnosis (FHE).Material and methods. Totally, 114 patients included, with severe hypercholesterolemia (LDL-C >4,9 mM/L), with no known coronary heart disease and not taking hypolipidemic therapy. For the probability assessment of FHE, Dutch Lipid Clinics Network criteria were applied. Lipid profile parameters were measured by enzymatic method; Lpa — by immune enzyme method; lipoproteides subfractions — with the Lipoprint® system (Quantimetrix, USA).Results. All patients were selected to subgroups in accordance with the Dutch criteria: I group — with low FHE probability (3-5 points, n=86) and II — with definite and porobable FHE (≥6 points, n=28). Patients from II group had higher atherogenic apoB100-containing lipoproteides (a) levels — 25,5±27,8 and 42,8±41,5 mg/dL (р=0,014), small dense subfractions of LDL — sdLDL: 2,3±3,7 and 7,1±10,1 mg/dL (р

Background. Atherosclerosis is a systemic disease. That is why the damage is not restricted by one vascular area in 18-50% of patients. High serum level of lipoprotein(a) [Lp(a)] is an independent risk factor for coronary, carotid and peripheral atherosclerosis. However the correlation of apoprotein(a) [apo(a)] polymorphism with the multifocal atherosclerosis in coronary heart disease (CHD) is not sufficiently studied.Aim. To study the correlation of apo(a) phenotype with the multifocal atherosclerosis in CHD patients.Material and Methods. 220 patients aged 32- 76 y.o. with the proven coronary and carotid atherosclerosis were split into two groups depending on the presence (n=22) or absence (n=198) of peripheral atherosclerosis. Evaluation of lipid profile, Lp(a) and determination of apo(a) isoforms by SDS electrophoresis in polyacrylamide gel and immunoblotting was performed in all patients.Results. Both groups of patients were comparable by age, sex, classical cardiovascular risk factors, including frequency of hyperlipidemia and diabetes mellitus, lipid profile. The Lp(a) serum level ≥30 mg/dL and low molecular weight (LMW) apo(a) phenotype were found more often in patients with multifocal than coronary and carotid atherosclerosis: 55 and 45% (р=0.372); 73 and 44% (p

Aim. To study the role of lipoprotein(a) [Lp(a)] as a potential autoantigen causing the activation of immunocompetent cells in atherosclerosis. Subjects and methods. A total of 104 men with stable coronary artery (CA) disease and different degrees of progressive coronary atherosclerosis were examined. Clinical blood analysis was carried out and lymphocyte subpopulations (CD4+, Th1, Th17, and Treg) were determined using immunofluorescence and flow cytometry. In addition, the indicators of blood lipid composition, Lp(a), autoantibody (autoAb) titer to Lp(a), and low-density lipoproteins (LDL), and the lymphocyte activation marker sCD25 were also measured. Results. The Lp(a) level was shown to predict the severity of CA lesions (β=0.28, p