Aim. To analyze factors influencing the development of aortic stenosis (AS) in patients with heterozygous familial hypercholesterolemia (heFH).Material and methods. A total of 114 patients with heFH were examined (mean age 54,3±2,7 years, 85 men (69,1%)), of whom 10 (8,8%) had AS. FH was diagnosed according to the Dutch Lipid Clinic Network criteria. Lipid profile parameters, lipoprotein(a) (Lp(a)) level, age, family history of cardiovascular disease, smoking, hypertension (AH), hyperglycemia were analyzed. The history of coronary artery disease (CAD), myocardial infarction (MI), and ischemic stroke was taken into account. Cumulative levels of low-density lipoprotein (LDL) and non-HDL cholesterol were calculated as the total LDL-C over the patient's life, taking into account the levels achieved during lipid-lowering therapy.Results. AS development was influenced by age (odds ratio (OR) 1,1 [1,02; 1,15], p=0,009), HTN (OR 8,15 [1,50; 44,08], p=0,017), lipid profile parameters: total cholesterol (OR 2,09 [1,38; 3,10], p=0,0006; LDL-C (OR 2,8 [1,59; 4,79], p=0,0004), non-HDL-C (OR 1,012 [1,005; 1,019], p=0,003), triglycerides (OR 1,97 [1,33; 2,87], p=0,0007). Cumulative indicators also influenced the risk of AS: cumulative LDL accumulated over the years of life (OR 2,13 [1,31; 3,54], p=0,003), cumulative non-HDL-C level accumulated over life (OR 1,56 [1,01; 2,18], p=0,013), Lp(a) level (AS risk increases by 10,6 times with an increase in Lp(a) by 1 unit of measurement (1 g/l) (OR 10,5 [5,0; 21,9], p=0,0017). The presence of CAD and MI in FH increases the risk of AS (for CAD, OR 8,62 [1,07; 69,113], p=0,044; for MI, OR 3,93 [1,08; 14,36], p=0,034). The combination of MI and cerebrovascular accident increases the risk of AS by 4,94 (OR 4,94 [1,23; 19,62], p=0,021). Tendon xanthomas significantly affects the AS (OR 50,2 [6,03; 413,00], p<0,001).Conclusion. AS detected at a young age can be a manifestation of FH. The development of AS in FH is influenced by age and HTN, and following lipid factors: total cholesterol, LDL, triglycerides, as well as Lp(a) levels and cumulative indicators.

The article presents the up-to-date information on the effect of lipoprotein apheresis (LA) on atherosclerotic lesions. Some studies using modern diagnostic imaging techniques (such as intravascular ultrasound or magnetic resonance imaging) have clearly demonstrated plaque regression. Coronary angiography has also seen reversal or at least slow plaque progression. Plaque regression likely leads to a decrease in the incidence of atherosclerotic cardiovascular events (CVEs). However, this has not yet been fully proven. Recent data indicate that reduction in low-density lipoprotein cholesterol and lipoprotein(a) levels is not a major factor in reducing the incidence of atherosclerotic CVEs in patients undergoing extracorporeal treatment. The most significant risk factors in this case are older age and a greater CVE rate observed before the start of LA, as well as smoking. New studies using modern diagnostic imaging methods in patients receiving LA are necessary.

Objective. The aim of the study was to evaluate the level of expression of the NOS2, NOS3, SONE genes in peripheral blood leukocytes (PBL) of patients with hypertension (HTN) and to study the relationship between the level of transcripts of these genes and the content of nitric oxide metabolites and markers of endothelial dysfunction.Design and methods. The study included healthy people (25 people) and patients with HTN (stages I–II) before prescribing antihypertensive drugs (15 people) and taking cardioselective β-adrenergic receptor blockers for more than a year (metoprolol (25 mg per day) or bisoprolol (5–10 mg per day)) (20 people). The level of gene transcripts was assessed by real-time polymerase chain reaction (PCR). The level of nitric oxide metabolites was determined by the colorimetric method using the Griess reagent. The content of asymmetric dimethylarginine (ADMA), soluble forms of vascular cell adhesion molecule (sVCAM), and intercellular adhesion molecule (sICAM) in blood plasma was determined by ELISA. The content of malondialdehyde (MDA) in blood plasma was determined spectrophotometrically by color reaction with thiobarbituric acid. Statistical processing of the results was carried out using the Statgraphics Centurion XVI software package (version 16.1.11).Results. The level of nitric oxide metabolites in the blood plasma of HTN patients without antihypertensive therapy was 2,1 times higher than in healthy individuals (p = 0,001) and 1,7 times higher than in patients with HTN taking metoprolol or bisoprolol (p = 0,002). The relative content of mRNA of the NOS3 gene in PBL of individuals included in the study did not differ (p > 0,05). The level of NOS2 gene transcripts in PBL of HTN patients before the prescription of antihypertensive drugs exceeded that in healthy individuals (p = 0,0009) and in HTN patients taking metoprolol or bisoprolol (p = 0,0002). The number of SONE transcripts in the PBL of HTN patients was higher than in people with normal blood pressure (p < 0,00001 when comparing patients before the prescription of antihypertensive therapy and individuals from the control group; p = 0,04 when comparing patients with HTN taking antihypertensive drugs and normotensive subjects). The content of MDA, ADMA, sVCAM was higher in the plasma of HTN patients without antihypertensive therapy compared with people from the control group (p = 0,005, 0,003, 0,039, respectively) and patients taking metoprolol or bisoprolol (p = 0,0006, 0,019, 0,016, respectively). The content of nitric oxide metabolites positively correlated with NOS2, SONE, VCAM1 mRNA level in PBL, the content of MDA and ADMA in blood plasma (p < 0,05). A positive correlation was found between the concentration of MDA and ADMA in plasma (p = 0,03).Conclusions. An increase in the level of nitric oxide metabolites in HTN is associated with an increase in the transcriptional activity of the NOS2 gene, a disturbance of the redox balance of the body, and the development of endothelial dysfunction. The SONE gene is probably involved in the modulation of nitric oxide levels in HTN not only as an antisense transcript that destabilizes the mRNA of the NOS3 gene in vascular endothelial cells, but also indirectly, namely, through the regulation of homeostasis of immune system cells through autophagy.

Familial hypercholesterolemia (FH) is one of the most common monogenic diseases that leads to the early development of atherosclerosis and is characterized by a poor prognosis. However, only about 1% of FH cases are diagnosed in Russia. The aim of this study was to determine the genetic defect in the FH family and conduct DNA diagnostics in the proband relatives. The study was performed on blood samples obtained with the informed consent of the patients. Polymerase chain reaction and polyacrylamide gel electrophoresis were used. We report c.683_684insCTGCAAGGA CAAATCTGACGA pathogenic variant of the low-density lipoprotein receptor (LDLR) gene for the first time in Russia and demonstrate its cosegregation in a family with high blood cholesterol. The c.683_684in sCTGCAAGGACAAATCTGACGA insertion is considered as a probable cause of FH.

Background: The level of IL-1β in blood plasma is determined not only by pro-inflammatory stimuli, but also by allelic polymorphism of the IL1B and NLRP3 genes. Information on the associa-tion of allelic polymorphism of these genes with the risk of arterial hypertension (AH) is scarce and contradictory. The aim of the study: To assess the risk of developing hypertension in carriers of various allelic variants according to the polymorphic markers rs1143634 (c.3953C>T), rs16944 (c.-511T>C), rs1143627 (c.-31C>T) of the IL1B gene and rs35829419 (c.2113C>A) of the NLRP3 gene, as well as to study possible mechanisms for the inclusion of allelic polymorphism of these genes in the etiology and pathogenesis of AH. Materials and methods: 182 DNA samples from healthy people and 180 DNA samples from patients with hypertension (stages I-II) were used for genotyping rs1143634, rs16944, rs1143627 (PCR-RFLP analysis). 215 DNA samples from healthy individuals and 180 hypertensive patients were used to determine alleles and genotypes for rs35829419 of the NLRP3 gene (allele-specific PCR with TaqMan probes). Total RNA obtained from peripheral blood leukocytes (PBL) of 45 healthy people and 50 patients with AH (27 people taking metoprolol or bisoprolol for more than a year and 23 people without antihypertensive thera-py) for assessment of gene expression by real-time PCR was used. The content of pro-inflammatory proteins in the blood plasma of 40 healthy individuals was measured by ELISA. Results: Carriers of the TT genotype for the c.3953C>T marker of the IL1B gene were found to have a 3-fold increased risk of AH (OR=3,239; 95% CI: 1,858-5,649). In healthy individuals with this genotype, the con-tent of IL-1β in blood plasma and the expression of the ICAM1 gene in PBL are higher than in het-erozygotes or homozygotes for the C allele (p=0,029 and p=0,004, respectively). Individuals with the TT genotype for the c.-31C>T marker of the IL1B gene had a reduced risk of АН (OR=0,645; 95% CI: 0,481-0,866). IL1B gene expression and hsCRP levels were lower in healthy individuals with the T allele for rs1143627 (p=0,022, p=0,040, respectively). There were no differences in the distribution of allele and genotype frequencies for markers c.-511T>C of the IL1B gene and c.2113C>A of the NLRP3 gene in the studied groups. Conclusion: Polymorphic markers rs1143634 (c.3953C>T) and rs1143627 (c.-31C>T) of the IL1B gene are probably involved in the predisposi-tion of the inhabitants of Karelia to the development of arterial hypertension.

Семейная гиперхолестеринемия (СГХС) – наиболее частое генетически обусловленное нарушение обмена веществ у человека преимущественно за счет повышения уровня липопротеидов низкой плотности (ЛПНП). Поскольку частота сердечно-сосудистых заболеваний (ССЗ) у пациентов с СГХС значительно различается, помимо пожизненного накопления холестерина ЛПНП в сосудах, высокий сердечно-сосудистый риск развития ССЗ при СГХС, видимо, определяется влиянием других классических факторов риска, таких как возраст, мужской пол, курение, избыточный вес/ожирение, артериальная гипертония и низкий уровень холестерина липопротеидов высокой плотности (ЛПВП) [1–9]. Гиперхолестеринемия индуцирует липидомные и протеомные вариации в частицах ЛПВП, тем самым нарушая их способность стимулировать отток холестерина из макрофагов [10]. Более того, было показано, что частицы ЛПВП пациентов с СГХС менее эффективны в снижении избытка провоспалительных окисленных липидов в ЛПНП по сравнению с частицами, выделенными у пациентов с нормолипидемией [11].

Цель. Целью исследования явилась оценка эффективности и приверженности гиполипидемической терапии, частоты развития сердечно-сосудистых осложнений у пациентов с гомо- и гетерозиготной семейной гиперхолестеринемией (СГХС) в течение пятилетнего периода наблюдения в регистре РЕНЕССАНС (Регистр пациентов с СГХС и пациентов очень высокого сЕрдечно-Сосудистого риска с недоСтАточной эффективНоСтью, проводимой гиполипидемической терапии). Материал и методы. РЕНЕССАНС является открытым, национальным, наблюдательным исследованием и включает больных с СГХС. Учитывали наличие факторов риска атеросклероза, анамнез сердечно-сосудистых заболеваний, гиполипидемическую терапию. В каждом центре выполняли определение концентрации: общего холестерина, триглицеридов, холестерина липопротеидов высокой плотности в сыворотке крови. Содержание холестерина липопротеидов низкой плотности (ХС ЛНП) рассчитывали по формуле Фридвальда. В некоторых центрах проводили измерение уровня липопротеида(а). При оценке частоты конечной точки, включавшей фатальные и нефатальные сердечно-сосудистые осложнения (ССО), проводили анализ Каплана-Майера. Результаты. В регистр включено 17 больных с гомозиготной СГХС (средний возраст 22±13 лет, 65% женского пола, 29% дети) и 2288 пациентов с гетерозиготной СГХС (48±16 лет, 57% женского пола, 6% дети). В группе гомозиготной СГХС за период наблюдения 74±13 месяцев ССО зарегистрированы у 5 (29%) пациентов, многокомпонентную гиполипидемическую терапию получали 94% и ни один больной не достиг целевого уровня ХС ЛНП. В группе гетерозиготной СГХС динамическое наблюдение проведено у 1067 (47%) пациентов в течение 32±27 месяцев, конечная точка зарегистрирована у 10% больных. Мужской пол (относительный риск 1,7; 95% доверительный интервал 1,2-2,6 p<0,01), гипертония (3,8; 2,3–6,2; p<0,001), ишемическая болезнь сердца (9,3; 5,6–15,3; p<0,001), отягощенный анамнез по сердечно-сосудистым заболеваниям (ССЗ) (2,6; 1,5–4,5; p<0,001) и концентрация липопротеида(а)≥30 мг/дл (2,2; 1,0–4,7; p<0,05) явились предикторами развития ССО. Частота назначения трехкомпонентной гиполипидемической терапии с ингибиторами PCSK9 возросла с 2 до 9%, а достижение целевого уровня ХС ЛНП − с 2 до 14% (р <0,001 для обоих). Заключение. Пятилетнее наблюдение за участниками регистра РЕНЕССАНС демонстрирует увеличение использования многокомпонентных схем лечения. Мужской пол, гипертония, ишемическая болезнь сердца, отягощенный анамнез по ССЗ и концентрация липопротеида(а) ≥30 мг/дл остаются ведущими факторами, ассоциированными с увеличением риска развития ССО.

A comparative analysis of vascular stiffness indices and the results of blood test was carried out in 85 healthy donors aged 19-64 years, carriers of polymorphic variants of type 1 and type 2 melatonin receptor genes. The associations of polymorphic markers of type 1 MTNR1A (rs34532313) and type 2 MTNR1B (rs10830963) melatonin receptor genes with parameters of vascular stiffness and blood parameters in healthy patients were studied. Genotyping was performed using allele-specific PCR. In all patients, 24-h BP monitoring with assessment of arterial stiffness was performed. Allele C homozygotes of MTNR1A differed significantly from carriers of the major T allele by elevated triglyceride, LDL, and fibrinogen levels. The major allele C of the rs10830963 polymorphic variant of the MTNR1B gene is associated with elevated LDL and triglycerides, as well as with individual differences in the elastic properties of the vascular wall in the examined subjects.

The contribution of polymorphic markers rs2234663 (VNTR) and rs419598 (c.2008T>C) of the IL1RN gene to the predisposition to the development of arterial hypertension among the population of Karelia was studied. The occurrence of alleles and genotypes for these markers was almost the same in the group of healthy people and in patients with arterial hypertension (χ2 = 0.178, p = 0.67; χ2 = 0.540, p = 0.76; χ2 = 0.01, p = 0.93, χ2 = 1.68, p = 0.43, respectively for alleles and genotypes for rs2234663 and rs419598). The level of IL-1β and IL-1α in the plasma of healthy people did not depend on the carriage of these allelic variants of the IL1RN gene. The number of transcripts of the intercellular adhesion molecule ICAM1 gene was higher in peripheral blood leukocytes of healthy individuals with the A1A1 genotype for rs2234663 and TT for rs419598 compared with carriers of alternative genotypes (p < 0.05). The content of the soluble form of ICAM (sICAM) was higher in the plasma of healthy people with the A1A1 genotype than in carriers of the A1A2 and A2A2 genotypes for rs2234663 (p = 0.02). Thus, no association was detected between the polymorphic markers VNTR and c.2008T>C of the IL1RN gene and the risk of developing arterial hypertension in inhabitants of the Republic of Karelia. Nevertheless, the observed effect of the rs2234663 and rs419598 genotypes on ICAM1 level and rs2234663 gene transcripts on sICAM content suggests that these polymorphic loci may be involved in the predisposition to developing steadily high blood pressure, probably through regulation of vascular endothelial functions

Aim. To evaluate the results of two-year use of alirokumab in Karelia Republic. Materials and methods. The observation group consisted of 27 patients (17 patients with familial hypercholesterolemia, 10 patients with the history of myocardial infarction), mean age 53.44.3 years, 70.3% men, follow-up duration from one year to 2.5 years, 18 (66.6%) patients received therapy for more than 2 years. 19 patients received alirocumab at a dose of 75 mg/ml once every 2 weeks, eight at a dose of 150 mg/ml once every 2 weeks. Before the start of therapy, the majority received maximally tolerated statin therapy, 10 patients received statin therapy in combination with ezetemibe, 3 patients received ezetemibe monotherapy due to statin intolerance. The target levels of LDL cholesterol were considered for very high risk patients less than 1.4 mmol/L, high risk less than 1.8 mmol/L, extreme risk less than 1 mmol/L. Results. The reduction of LDL on therapy with alirocumab was 58%; target levels of LDL were achieved in 77.8%. The level of decrease in LDL cholesterol less than 50% was noted only in 7.4% of cases. Patients requiring a large dose of the drug were classified as very high risk, had higher cholesterol and LDL-C levels. The level of Lp(a) decrease on 29.7% by 612 months. No destabilization of coronary heart disease, new cases of stroke were registered. Conclusion. The inclusion of alirocumab in the treatment regimen contributed to the stable course of atherosclerosis-associated diseases, the achievement of LDL cholesterol targets in 77.8% of patients, was not accompanied by side effects during 2.5 years therapy.

Background and Aims : to evaluate the safety of extremely low LDL-C (low density cholesterol) concentration on iPCSK9 therapy.

In patients with familial hypercholesterolemia (FH) the exposure of very high LDL-C concentration and cumulative LDL-C level (cum LDL-C) can play a significant role in the prognosis. Objective: to analyze the contribution of “cum LDL-C for all life” and the index “cum LDL-C/age” to the development of coronary heart disease (CHD), myocardial infarction (MI), and a combined end point: MI, stroke, unstable angina in FH patients. Methods: 188 patients (mean age 49.2 years, males 45.7%) with FH were examined (Dutch Lipid Clinic Criteria). We had evaluated cumulative LDL-C and index “cum DL-C/age” along with other classical risk factors. Cum LDL-C was calculated as LDL-Cmax × (age at initiating of hypolipidemic therapy) + LDL-C at inclusion age at initiation/correction therapy). Cumulative LDL-C and “cum LDL-C/age” were calculated as the ratio cum LDL-C to age. The follow-up period was 5.4 (from 3 to 10) years. Results: The index “cum LDL-C/age” was higher in patients with CHD 58.7 ± 10.4 mmol/L/years vs. 40.1 ± 11.7 mmol/L/years in patients without CHD (p < 0.001). According to our data based on the results of the logistic regression analysis in patients with FH, cumulative LDL-C and the cumulative index “cum LDL–C/age” played a strong predictive role in the development of CHD in FH patients; it was greater than the role of TC and LDL-C concentrations. We present ROC curves for CHD, MI and combined end point in FH patients, and a prognostic scale for CHD development, which is based on classical cardiovascular risk factors. Conclusion: cumulative LDL-C level plays an important role in the development of CHD in FH patients.

Arterial stiffness indicators (reflected wave propagation time (RWTT), aortic pulse wave velocity (PWV), arterial stiffness index (ASI), augmentation index (AIx)) were assessed in healthy people and patients with arterial hypertension with different allelic variants of the NOS2 gene (rs1730017 (C>T), rs1800482 (G>C)). We examined healthy individuals (64 people, age 38.58 ± 2.19 years, 28 men and 36 women) and patients with AH (stage I-II) (36 people, age 38.04 ± 1.20 years , 20 men and 16 women). In the group of patients with AH, differences in ASI values between carriers of the T allele and CC genotype of rs1730017 (p = 0.036) and daily average AIx, AIx daily values in individuals with GG and GC + CC genotypes rs1800482 (G> C) were revealed (p = 0.049, p = 0.017, respectively). In the group of healthy people, a significant increase in daily AIx was found in carriers of the C allele at rs1800482 (p = 0.048). Carriage of the T allele by rs1730017, for which a protective effect on the development of AH has been previously shown, causes lower values of the arterial stiffness index in patients with this disease. The presence of the C allele of by rs1800482 in the genotype of healthy and sick people, associated with an increased risk of hypertension, is probably one of the reasons for the increase in AIx, as one of the indicators of arterial stiffness.

Aim      To compare results of clinical, laboratory, and genetic examination of patients with familial hypercholesterolemia (FHC).Material and methods  112 patients aged 40.2±17.9 years (49 men) were examined. The gene of low-density lipoprotein receptor (LDLR) was analyzed and evaluated using the Dutch Lipid Clinic Network (DLCN) criterion of lipid score ≥6. The LDLR gene mutation was searched for using the conformational polymorphism analysis followed by sequencing of the DNA of isolated LDLR gene exons.Results Mean variables of the blood lipid profile were total cholesterol (C), 10.12±2.32 mmol/l, LDL-C, 7.72±2.3 mmol/l. Corneal arcus was observed in 15 % of patients, tendon xanthomas in 31.8 %, and xanthelasma palpebrarum in 5.3 %. The types of LDLR gene mutations included missense mutations (42.8 %), mutations causing a premature termination of protein synthesis (41.1 %), and frameshift mutations (16.1 %). In the presence of a mutation in exon 4, patients with IHD compared to patients with no IHD had significantly higher levels of total C (10.88±2.08 mmol/l vs. 8.74±1.57 mmol/l, respectively, р=0.001) and LDL-C (8.60±2.14 mmol/l vs. 6.62±1.79 mmol/l, respectively, р=0.005). Patients with IHD compared to patients with no IHD and a mutation in LDLR gene exon 9 had only a higher LDL-C level (8.96±1.53 mmol/l vs. 6.92±1.59 mmol/l, respectively, р=0.022). A differentiated comparison of IHD patients using a logistic regression depending on the identified type of LDLR gene mutation produced formulas for calculating the odds ratio of IHD and myocardial infarction (MI) with adjustments for the patient's age and baseline LDL.Conclusion      The detection rate of the LDLR gene mutations was 42.8 % for missense mutations, 41.1 % for mutations causing a premature termination of protein synthesis, and 16.1 % for frameshift mutations. Blood lipid profiles did not differ between patients from different cities and with different types of LDLR gene mutations. Blood lipid profiles were different in IHD patients depending on the mutation type.

Impaired balance of T regulatory and T effector lymphocytes has recently been considered as an important pathogenetic link in arterial hypertension (AH). There are, however, contradictory literature data about contents of these cells in the patients with hypertension, or obtained in experimental animal models of induced hypertension. Most results about changed patterns of immune cells in cardiovascular diseases were obtained by means of flow cytometry. There are also some works on expression of genes encoding surface and cytoplasmic differentiation antigens of immune cells in the patients with cardiovascular pathologies. These results coincide with the data obtained with flow cytometric techniques. Purpose of the present study was to analyze of the levels of gene transcripts encoding differentiation markers of regulatory (FOXP3, IL2R) T cells, effector T subpopulations (T helpers 17 (RORγ), and CD8 lymphocytes (CD8A) in healthy subjects and the patients with arterial hypertension (stages I-II). We examined healthy individuals (40 people, 20 men and 20 women), 27 patients with hypertension who did not receive antihypertensive therapy (14 men and 13 women), 26 hypertensive patients taking β-adrenergic receptor blockers (metoprolol or bisoprolol), including 12 men and 14 women. The relative levels of transcripts in peripheral blood leukocytes were assessed by real-time RT-PCR. It was shown that the transcriptional activity of FOXP3, IL2R, RORγ, and CD8A genes in peripheral blood leukocytes of the diseased people was significantly higher than in healthy individuals (p < 0.01). This finding may indicate an increased number of circulating T regulatory lymphocytes, CD8+ cells and T helpers 17 in hypertensive patients, and activation of T cell immunity in these patients. There were no statistically significant gender differences in FOXP3, IL2R, RORγ and CD8A gene expression in leukocytes, both in the group of healthy people and in hypertensive patients. The patients receiving cardioselective β-adrenergic receptor blockers (metoprolol and bisoprolol) exhibited lower expression of these genes, thus, probably, indicating antiinflammatory and immunomodulatory properties of these drugs.

Background and Aims : to evaluate some characteristics in patients, who received iPCSK9 in Karelia RepublicMethods: we analyzed the data from Karelian registry about 55 patients, who received iPCSK9 (28 alirocumab, 27 evolocumab). We had developed special questionnaire, it included age, gender, smoking, diabetes mellitus, body mass index (BMI), lipid profile before and after treatment, data about education, marital status, adherence to therapy. Mean age of patients was 46.3±2.7 y.o., 65% male, 47 patients had ischemic heart disease, 32 patients had myocardial infarction, 25 had revascularization procedures.Results: Eleven (20%) patients younger 40 y.o., 14 (25%) patients older 60 y.o., 39 (71%) patients had high education; 47 (85.7%) patients lived in the city. More often specialties: 21 (38%) engineer, 6 (11%) has medical education, 5 (9%) teachers. Five (9%) patients live in own house, 3 (5.5%) rent a flat, and others 47 (85.7%) lives in own flats, 49 (89% patients) did not smoke, 8 (14%) patients had diabetes mellitus, 13 (24%) patients had BMI 25-29.9 kg/m2, 14 (25.4%) had obesity. It was 45 (82%) patients, who had achieved the target LDL-cholesterol level. Adherence to statin therapy was 3.5±0.3 balls and adherence to iPCSK9 was 3.99±0.01, it did not depend on availability of cardiovascular disease and age.Conclusions: Patients who received iPCSK9 in Karelia characterized by high education (85.7%), living on own flats (87.5%), 89% of them did not smoke. Adherence to iPCSK9 was higher than to statin and did not depend on availability of cardiovascular disease and age. Background and Aims : to evaluate some characteristics in patients, who received iPCSK9 in Karelia Republic Methods: we analyzed the data from Karelian registry about 55 patients, who received iPCSK9 (28 alirocumab, 27 evolocumab). We had developed special questionnaire, it included age, gender, smoking, diabetes mellitus, body mass index (BMI), lipid profile before and after treatment, data about education, marital status, adherence to therapy. Mean age of patients was 46.3±2.7 y.o., 65% male, 47 patients had ischemic heart disease, 32 patients had myocardial infarction, 25 had revascularization procedures. Results: Eleven (20%) patients younger 40 y.o., 14 (25%) patients older 60 y.o., 39 (71%) patients had high education; 47 (85.7%) patients lived in the city. More often specialties: 21 (38%) engineer, 6 (11%) has medical education, 5 (9%) teachers. Five (9%) patients live in own house, 3 (5.5%) rent a flat, and others 47 (85.7%) lives in own flats, 49 (89% patients) did not smoke, 8 (14%) patients had diabetes mellitus, 13 (24%) patients had BMI 25-29.9 kg/m2, 14 (25.4%) had obesity. It was 45 (82%) patients, who had achieved the target LDL-cholesterol level. Adherence to statin therapy was 3.5±0.3 balls and adherence to iPCSK9 was 3.99±0.01, it did not depend on availability of cardiovascular disease and age. Conclusions: Patients who received iPCSK9 in Karelia characterized by high education (85.7%), living on own flats (87.5%), 89% of them did not smoke. Adherence to iPCSK9 was higher than to statin and did not depend on availability of cardiovascular disease and age.