Целью данного исследования входила оценка влияния комбинированного препарата розувастатина с эзетимибом на уровни липидов, С-реактивного белка крови и показатели артериальной жесткости у лиц с гиперлипидемией 2а типа. Материал и методы. В исследование включили 40 человек, завершили курс лечения 37 человек (59% женщин, средний возраст 57±8 лет). Перед началом исследования и через 12 недель приема фиксированной комбинации розувастатина с эзетимибом 20/10 мг в сыворотке крови определяли уровни общего холестерина, триглицеридов, ХС ЛВП, глюкозы, ферментов крови, С-реактивного белка. Содержание холестерина липопротеидов низкой плотности (ХС ЛНП) вычисляли по формуле Фридвальда. Для оценки артериальной жесткости применяли три метода: ультразвуковое исследование сонных артерий, аппланационная тонометрия, объемная сфигмография. Результаты. На фоне терапии продемонстрировано значимое снижение общего холестерина, триглицеридов, ХС ЛНП, С-реактивного белка, глюкозы на 41, 25, 56, 38 и 6%, соответственно. Не отмечено изменения параметров артериальной жесткости при УЗИ: индекс жесткости β, коэффициентов растяжимости и податливости. В то же время выявлено снижение показателя артериальной жесткости по данным аппланационной тонометрии - каротидно-феморальной скорости пульсовой волны с 9,4±1,5 до 9,0±1,1 м/с (р< 0,01) на фоне значимого снижения уровня артериального давления, при этом антигипертензиваня терапия не изменялась. Заключение. В результате терапии комбинированным препаратом розувастатина с эзетимибом 20/10 мг в течение 3 месяцев показано значимое снижение уровня холестерина липопротеидов низкой плотности, С-реактивного белка и улучшение показателя артериальной жесткости каротидно-феморальной скорости пульсовой волны

Aim: to measure the echogenicity of atherosclerotic plaques (AP) of carotid arteries to assess the dynamics of atherosclerosis and risk of cardiovascular outcomes (CVO) in patients with different CVD risk. Materials and methods. The study included 223 patients: 80 patients (47 males) with moderate CVD risk (mean age: 53 years, range: 39-66) (Group 1) and 143 patients (123 males) with acute coronary syndrome (ACS) and high CVD risk (mean age: 57, range: 32-83) years (Group 2). All patients were examined at the Chazov National Medical Research Center of Cardiology. Patients underwent a standard clinical examination, biochemical blood test with lipid profile determination, and ultrasound duplex scanning. Patients with ACS were re-examined after 1-1.5 years and patients with moderate CVD risk were re-examined after 1 and 7 years. Results. We analyzed 181 APs in Group 1 and 378 APs in Group 2. Analysis of gray-scale median (GSM) at the first and second visit showed a significant increase in GSM in both groups: from 67.02 [54.13; 82.85] to 73.5 [59.5; 88.7] (p<0.0001) in Group 1, and from 49.3 [39.73;63.64] to 50.7 [40.04;66.54] (p<0.05) in Group 2. An increase in GSM was observed in 79% of patients in Group 1, in 53% of patients in Group 2. Unfavorable CVO (CVO+) developed after 7 years in 7 (8.8%) patients in Group 1, and after 1 year in 23 (23%) patients in Group 2. In Group 1, an increase in GSM was observed only in patients with favorable prognosis (CVO-): from 67.7[52.13; 79.0] to 77.5[64.12; 91.0] (n=148 AP, p<0.05), in patients with CVO+, GSM increased non-significantly from 60.1[53.5; 66.5] to 66.5[55.0; 71.6] (n=18 AP, p=NS). In Group 2, a significant increase in GSM was observed in patients with CVO-: from 48.7[39.0; 63.4] to 51.3[40.0; 67.4] (n=141 AP, p<0.01), in patients with CVO+, GSM decreased from 51.6[42.9; 72.5] to 50.2[40.4; 65.0] (n=43 AP, p=NS). In Group 2, GSM significantly increased by 2.75 (6.05%) from the initial value (p<0.05) in patients with CVO-, while patients with CVO+ showed a significant decrease in the average GSM of AP by 3.33 (7.8%) (p<0.05). Using ROC analysis, a Δ% GSM value of 6.96% was found (area under the curve 0.628 ± 0.0465 [95% CI 0.556 - 0.696], p = 0.0058). According to Cox regression analysis, the risk of CVO increased by 2.16 times with a decrease in GSM AP in the carotid arteries over time by ≥ 6.96% (НR=2.16; 95% CI=1.331 – 3.507); p=0.009. Conclusion. The ultrasound method of measuring the echogenicity of an atherosclerotic plaque of the carotid artery using GSM parameter can be effective for assessing the dynamics of atherosclerosis and prognosis of adverse cardiovascular events in patients with high and moderate CVD risk

Aim. To assess plaque burden according to peripheral artery ultrasound examination in patients with rheumatoid arthritis (RA) with low and moderate disease activity in comparison with the coronary artery condition.Material and methods. The study included 64 patients, of which 43 patients with an established diagnosis of RA and 21 patients with coronary artery disease (CAD) without RA (comparison group). All patients underwent a clinical and paraclinical examination to verify myocardial ischemia and/or CAD according to the 2020 national guidelines, as well as a carotid and femoral artery ultrasound (the latter, only for patients with RA) with determination of plaque burden.Results. In patients with RA in combination with CAD, plaque burden is higher than in patients with RA without coronary artery disease regarding the carotid plaque number 4,0 [4,0; 5,0]/2,0 [1,0; 3,5], proportion of maximum stenosis 35,0 [35,0; 45,0]/30,0 [25,0; 35,0] and the proportion of total stenosis 120,0 [110,0; 152,5]/85,0 [40,0; 110,0]. Three or more carotid plaques determine significant coronary atherosclerosis in RA. In RA patients with CAD, the combination of caro­tid and femoral plaques is associated with significant coronary atherosclerosis in 75% of cases. In a comparative analysis of patients with RA CAD+/RA CAD-, no significant differences were found in the main cardiovascular risk factors, lipid, and inflammatory parameters. When comparing the plaque burden indicators, the severity of coronary atherosclerosis was not revealed between RA patients with CAD+ and the comparison group.Conclusion. Determining the peripheral plaque burden parameters increases the clinical significance of ultrasound as a stage of non-invasive CAD diagnosis in RA.

Aim. To evaluate the prognostic value of GDF-15 in relation the development of bleeding and events in stable CAD patients, receiving combined antithrombotic therapy. Materials and methods. The data was obtained from the prospective registry REGATA, 343 CAD patients (249 males), median age 68 [IQR 62; 75] years) were enrolled. Patients with sinus rhythm and concomitant PAD received acetylsalicylic acid in combination with rivaroxaban 2.5 mg bid (31.8%) or clopidogrel (24.8%). Other 43.4% with concomitant atrial fibrillation (AF) received direct oral anticoagulants in combination with antiplatelet therapy after elective percutaneous coronary interventions. Median follow-up was 12 months [IQR 9.0; 18.0]. The safety end point was major and clinically relevant bleedings (type 2–5) according to the BARC classification. Plasma samples for GDF-15 identification were taken at the inclusion and analyzed using ELISA assay. Results. Frequency of BARC 2–5 bleedings was 16% (BARC 2 – 46; BARC 3 – 9; BARC 4–5 – 0), median GDF-15 level was 1185.0 pg/ml [850.0; 1680.0]. In patients with AF and concomitant MFA, the level of GDF-15 was significantly higher than in the subgroups of patients with only AF or MFA (p=0.0022). According to the quintile analysis, GDF-15 values in the top three quintiles of distribution (cut-off value 943 pg/ml) were associated with higher frequency of bleeding events: 23.2% versus 5.1%; p=0.0001. The multivariable logistic regression model demonstrated that bleeding events were independently associated with GDF-15 level943 pg/ml (OR 2.65, 95% CI 1.11–6.30; p=0.0275), AF (OR 2.61, 95% CI 1.41–4.83; p=0.0023) and chronic kidney disease (OR 1.92, 95% CI 1.03–3.60; p=0.0401). Clinical factors determining the risk of bleeding events also determined a GDF-15 elevation. Conclusion. Assessment of GDF-15 level may improve bleeding risk stratification in CAD patients with concomitant AF and/or PAD receiving combined antithrombotic therapy.

Background and Aims: To determine the frequency of atherosclerotic lesions of the carotid and coronary arteries in rheumatoid arthritis (RA) patients (pts). Methods: To study 64 RApts with suspected CAD (male/female 25/38, mean age 58[52;63] years, with a long history of the disease (9[3;15] years). Results: Carotid ASP was detected in 26% of RApts (Group I). In 74% pts are defined intact carotid arteries (Group II). Groups were comparable in terms of age, disease duration and DAS28. Males prevailed in Group I: 67% vs 33% in Group 2 (p<0,05). The prevalence of traditional risk factors was similar in both groups. Serum HDL-C concentrations in Group I (1,2[1,0;1,5]mmol/l) was lower, than in Group II (1,55 [1,3;2,0]mmol/l, p=0,03). CA stenosis was detected in 34% of pts: in 40% of the Group I (50% - single vessel, 50% - three-vessel damage), and in 33% of the Group II (75% - single vessel, 25% - three-vessel damage). The multiple regression analysis did not established a direct association between CA stenosis and gender, age, activity RA, cholesterol and LDL-C concentrations. The biggest, but not significant value for predicting stenosis spacecraft showed age (OR 0,85;95%CI[0,72-1,0], p=0,05) and HDL-C <1,2mmol/L for women and <1,0mmol/L for men (OR 0.82;95%CI[0,64-0,90], p=0,09). Conclusions: Сarotid ASP were diagnosed in 26% and CA stenosis - in 34% in RApts with suspected CAD. Only a third of RApts have a combined lesion of the carotid and coronary arteries. Male gender, low HDL-C seem to increase the risk of atherosclerotic lesions of the carotid and coronary arteries in RApts.

Aim . To assess asymptomatic carotid atherosclerosis in patients with moderate cardiovascular risk over a 7-year prospective follow-up using non-invasive ultrasound markers. Material and methods . Eighty patients (47 men and 33 women) aged 53,1±5,9 years with moderate Systematic Coronary Risk Evaluation (SCORE) level, low-density lipoprotein cholesterol (LDL-C) of 2,7-4,8 mmol/l and asymptomatic hemodynamically insignificant (stenosis <50%) carotid atherosclerosis (CA). Patients underwent CA ultrasound (PHILIPS IU22) at baseline and after 7 years. Plaque number, maximum plaque height, total plaque height, total CA stenosis, visual plaque morphology, gray-scale median (GSM), and intima- media thickness of the right and left common CAs were assessed. All patients were prescribed atorvastatin therapy at a dose of 10-40 mg until a target LDL-С level <2,6 mmol/l was achieved. Results. During the follow-up period, a significant increase was noted in the number of plaques, the maximum and total plaque height, total CA stenosis, and intima- media thickness of the right and left common CAs. An increase in GSM was detected in 79% of plaques on statin therapy. Plaque echoicity increased by 4,90 [0,51; 17,41] (p <0,001) or 7,2% [0,7%; 29%] (p<0,001) over seven years. Regression analysis adjusted for sex and age showed the dependence of GSM changes (ΔGSM) on changes in the LDL-C level (ΔLDL-C) (p=0,049). With a decrease in LDL-C by 1 mmol/l, an increase in average GSM was noted by 5,9 (0,03-11,78). The maximum plaque height increased significantly after 7-year follow-up from 1,80 [1,50; 2,20] to 2,00 [1,63; 2,68] mm (p=0,044). In patients who reached a LDL-C level of 1,8 mmol/l, the maximum plaque height decreased more than in patients who did not reach this level (-0,07 [-0,45; 0,14] mm and 0,20 [-0,05; 0,40] mm, respectively (p=0,028)). Regression analysis adjusted for sex and age did not reveal a relationship between the change of maximum plaque height with ΔLDL-C and Δhigh-density lipoprotein cholesterol, but with LDL-C level after 7 years. Conclusion . Statin therapy in patients with CA stenosis <50% stabilizes the plaques due to echogenicity increase. LDL-C <1,8 mmol/l can lead to a decrease in maximum plaque height.

Background and Aims : Endothelial dysfunction plays an important role in the pathogenesis of the novel coronavirus infection (COVID-19) and its complications. The aim of the study was to assess the contribution of obesity to the pathogenesis of endothelial dysfunction as one of the risk factors of a more severe disease.Methods: We examined 19 patients with mild or moderate hypertension 1 month after their recovery from moderate COVID-19 (11m/8f, aged 45.4±9.0 years, without diabetes mellitus, non-smokers). 11 patients with hypertension had obesity (BMI≥30 kg/m2) and 8 had normal body weight (BMI≤25 kg/m2). We compared the endothelium-dependent flow-mediated dilatation (FMD) of the brachial artery in response to reactive hyperemia in the recovered group and in 20 age- and gender-matched healthy controls without cardiovascular risk factors.Results: The FMD in 19 pts with hypertension was significantly lower than in healthy controls (5.3±3.4% vs 9.5±3.9%, p<0.05). FMD in pts with hypertension and obesity was significantly lower than in patients with hypertension and normal body weight (3.9±1.9% vs 7.3±3.7%, p<0.05) and in healthy controls (p<0.05). BMI, SBP, DBP, TC and TG levels were significantly higher in patients with hypertension and obesity than in participants with hypertension and normal body weight: 34.2±3.9 vs 22.7±2.8 kg/m2, 141.3±10 vs 123.5±17.3 mm Hg, 91.6±10.1 vs 79.4±12.8 mm Hg, 6.75±1.88 vs 5.12±0.82 mmol/l and TG 3.75±3.0 vs 1.18±0.24 mmol/l (all p-values <0.05).Conclusions: In conclusion, moderate COVID-19 led to a disruption of the functional state of the endothelium in patients with hypertension, which was more pronounced in patients with obesity. Background and Aims : Endothelial dysfunction plays an important role in the pathogenesis of the novel coronavirus infection (COVID-19) and its complications. The aim of the study was to assess the contribution of obesity to the pathogenesis of endothelial dysfunction as one of the risk factors of a more severe disease. Methods: We examined 19 patients with mild or moderate hypertension 1 month after their recovery from moderate COVID-19 (11m/8f, aged 45.4±9.0 years, without diabetes mellitus, non-smokers). 11 patients with hypertension had obesity (BMI≥30 kg/m2) and 8 had normal body weight (BMI≤25 kg/m2). We compared the endothelium-dependent flow-mediated dilatation (FMD) of the brachial artery in response to reactive hyperemia in the recovered group and in 20 age- and gender-matched healthy controls without cardiovascular risk factors. Results: The FMD in 19 pts with hypertension was significantly lower than in healthy controls (5.3±3.4% vs 9.5±3.9%, p<0.05). FMD in pts with hypertension and obesity was significantly lower than in patients with hypertension and normal body weight (3.9±1.9% vs 7.3±3.7%, p<0.05) and in healthy controls (p<0.05). BMI, SBP, DBP, TC and TG levels were significantly higher in patients with hypertension and obesity than in participants with hypertension and normal body weight: 34.2±3.9 vs 22.7±2.8 kg/m2, 141.3±10 vs 123.5±17.3 mm Hg, 91.6±10.1 vs 79.4±12.8 mm Hg, 6.75±1.88 vs 5.12±0.82 mmol/l and TG 3.75±3.0 vs 1.18±0.24 mmol/l (all p-values <0.05). Conclusions: In conclusion, moderate COVID-19 led to a disruption of the functional state of the endothelium in patients with hypertension, which was more pronounced in patients with obesity.

Aim . To evaluate the contribution of subclinical atherosclerosis to the stratification of patients with a SCORE risk of cardiovascular events (CVEs) <5% based on a 10-year follow-up. Material and methods . The study included 379 patients with SCORE risk of CVEs <5% (82 men, 297 women). In 2009, all patients underwent clinical examination, carotid artery (CA) ultrasound with the detection of plaques, total CA occlusion, intima-media thickness (IMT) of the common carotid artery (CCA). The plaque number was determined as the total number of all plaques in 6 following segments: both CCAs, both CCA bifurcations and both internal carotid arteries. The total stenosis was calculated as the sum of stenoses in 6 CA segments in %. In 2019, a telephone survey of patients was conducted with a questionnaire assessing the following CVEs: all-cause death, cardiovascular death, myocardial infarction (MI), stroke, myocardial revascularization, cardiovascular hospitalizations, and composite endpoint. Results . The initial patients’ age ranged from 35 to 67 years (51,1±7,5 years). Plaques from 20% to 50% were detected in 303 participants (79,94%). Over the past 10 years, there have been 5 cardiovascular deaths (1,3%), 7 MIs (1,8%), 5 cases of unstable angina (1,3%), 12 cases of myocardial revascularization (3,2%), 15 strokes (4,0%), 51 cardiovascular hospitalizations (13,5%). The proportion of patients with registered endpoints (CVE+) was 22,4% (n=85). The groups of patients with and without CVEs differed in the level of systolic blood pressure (BP) and blood triglycerides, and did not differ in the level of diastolic BP, lipid profile, glucose, heart rate, smoking status, sex, and age. In the CVE+ group, there were higher values of CCA IMT (0,65 (0,64; 0,70) mm vs 0,62 (0,62; 0,66) mm, p<0,05), total CA stenosis (102,5 (88,1; 120,8)% vs 80 (72,5; 88,1)%, p=0,01), and the CA plaque amount (4,0 (2,8; 3,9) vs 3,0 (2,6; 3,1), p=0,01), respectively. Total CA stenosis was an independent predictor of CVEs when adjusted for sex, age, systolic and diastolic BP (β=0,149; p<0,05), but not for lipid profile. A ROC-analysis revealed a cut-off point for total CA stenosis of 82,5% (AUC=0,598, 95% confidence interval 0,5243-0,673, p<0,05). Conclusion . The total CA stenosis has shown itself to be an independent predictor of CVEs in patients with a SCORE risk <5%.

Background and Aims : We aimed to assess the impact of antithrombotic therapy on long-term prognosis in patients with coronary artery disease (CAD) and concomitant carotid atherosclerosis undergoing coronary artery bypass grafting (CABG).Methods: 189 CAD patients (79.9% males, median age 65 [IQR 60; 71] years) after successful CABG with carotid artery stenosis≥ 50% were enrolled. Carotid endarterectomy was performed in 25.9% of patients. Patients with indications for chronic oral anticoagulation therapy were excluded. Antithrombotic therapy on discharge was chosen at the discretion of physician and include single (ASA) or dual (ASA+clopidogrel) antiplatelets (45.5% and 41.8%) or combination of ASA with oral anticoagulant (mostly warfarin) – dual antithrombotic therapy (DAT) in 12.7%. DAT was prescribed up to 6 months after CABG in patients with higher atherosclerotic burden.Conclusions: DAT is sufficient to prevent TE in high risk patients but increases the risk of bleeding. We supposed that long-term DAT, including ASA and a safer anticoagulant at a lower dose, possibly rivaroxaban 2.5 mg twice daily, may improve outcomes in this category of patients. Background and Aims : We aimed to assess the impact of antithrombotic therapy on long-term prognosis in patients with coronary artery disease (CAD) and concomitant carotid atherosclerosis undergoing coronary artery bypass grafting (CABG). Methods: 189 CAD patients (79.9% males, median age 65 [IQR 60; 71] years) after successful CABG with carotid artery stenosis≥ 50% were enrolled. Carotid endarterectomy was performed in 25.9% of patients. Patients with indications for chronic oral anticoagulation therapy were excluded. Antithrombotic therapy on discharge was chosen at the discretion of physician and include single (ASA) or dual (ASA+clopidogrel) antiplatelets (45.5% and 41.8%) or combination of ASA with oral anticoagulant (mostly warfarin) – dual antithrombotic therapy (DAT) in 12.7%. DAT was prescribed up to 6 months after CABG in patients with higher atherosclerotic burden. Conclusions: DAT is sufficient to prevent TE in high risk patients but increases the risk of bleeding. We supposed that long-term DAT, including ASA and a safer anticoagulant at a lower dose, possibly rivaroxaban 2.5 mg twice daily, may improve outcomes in this category of patients.

Background and Aims : COVID 19 infection characterized by activation of the hemostasis system and critical increase D-dimer, which increased risk of deep vein thrombosis (DVT) and pulmonary embolism.Results: The study comprised 114 patients (51% male). CUS was positive for DVT in 31 patients (27%), of whom 17 (54,8%) was proximal DVT, 12 patients (38,7%) had distal DVT. Median days of hospitalization was 19±8,13. 12 patients died (10,5%). Patients with DVT were significant more frequently to be in the ICU (8(26%) vs 7(8,4%), p=0,03), on bed rest (14(45%) vs 18(21,7%), p=0,02). Patients with DVT had significant higher CRP (mg/L) 145,9 [62,7;161,3] vs 90,6 [41,7;150,9] p=0,06, D-dimer (ng/mL) 2596 [1416;4395] vs 1000 [469;2500] p<0,001, fibrinogen (g/L) was lower 3,25[2,44;3,62] vs 4,27[3,32;5,53] p=0,02. D-dimer levels 2497 ng/ml were associated with asymptomatic DVT (sensitivity 62,1%, specificity 74,1%). D-dimer showed an acceptable discriminative capacity (area under the ROC curve 0,707, 95% CI 0,61–0,79 (р˂0,001)).Conclusions: In patients with COVID-19 pneumonia and risk factors for DVT, the frequency of asymptomatic DVT was 27%. D-dimer levels 2497 ng/ml were associated with asymptomatic DVT with sensitivity 62,1%, specificity 74,1%. Background and Aims : COVID 19 infection characterized by activation of the hemostasis system and critical increase D-dimer, which increased risk of deep vein thrombosis (DVT) and pulmonary embolism. Results: The study comprised 114 patients (51% male). CUS was positive for DVT in 31 patients (27%), of whom 17 (54,8%) was proximal DVT, 12 patients (38,7%) had distal DVT. Median days of hospitalization was 19±8,13. 12 patients died (10,5%). Patients with DVT were significant more frequently to be in the ICU (8(26%) vs 7(8,4%), p=0,03), on bed rest (14(45%) vs 18(21,7%), p=0,02). Patients with DVT had significant higher CRP (mg/L) 145,9 [62,7;161,3] vs 90,6 [41,7;150,9] p=0,06, D-dimer (ng/mL) 2596 [1416;4395] vs 1000 [469;2500] p<0,001, fibrinogen (g/L) was lower 3,25[2,44;3,62] vs 4,27[3,32;5,53] p=0,02. D-dimer levels 2497 ng/ml were associated with asymptomatic DVT (sensitivity 62,1%, specificity 74,1%). D-dimer showed an acceptable discriminative capacity (area under the ROC curve 0,707, 95% CI 0,61–0,79 (р˂0,001)). Conclusions: In patients with COVID-19 pneumonia and risk factors for DVT, the frequency of asymptomatic DVT was 27%. D-dimer levels 2497 ng/ml were associated with asymptomatic DVT with sensitivity 62,1%, specificity 74,1%.

Background and Aims : Residual inflammatory risk is identified by hsCRP level ≥2.0 mg/l. Monomeric CRP (mCRP) is an emerging inflammatory biomarker. We studied whether mCRP level is a better predictor of carotid atherosclerosis (CA) progression than hsCRP in patients with low-grade CA and moderate SCORE risk which achieved target LDL cholesterol (LDL-C) level.Methods: The study comprised 80 patients of both genders 53.1±5.8 years old with moderate SCORE risk, LDL-C 2.7-4.8 mmol/l and hemodynamically insignificant (<50% stenosis) subclinical CA. All patients were prescribed statin to achieve LDL-C level <2.6 mmol/l and followed up for 7 years. At the completion of follow up subclinical CA progression, which was defined by the increase in the plaque number, was assessed by ultrasonography by the same operator, hsCRP and mCRP level was measured. Mann-Whitney U Test was used for intergroup comparison.Results: Patients were divided by mCRP level 7.2 μg/l and hsCRP level 2.0 mg/l. The increase in the plaque number was 0.58±0.64 vs. 1.44±1.15 in patients with mCRP <7.2 μg/l and ≥7.2 μg/l, respectively. Thus, mCRP level ≥7.2 μg/l was associated with the 2.5 times higher increase in the plaque number (p=0.006, statistical power =0.88). The increase in the plaque number was 0.67±1.01 vs. 1.06±0.99 in patients with hsCRP <2.0 mg/l and ≥2.0 mg/l, respectively. However, the difference was statistically insignificant (p=0.14, statistical power = 0.27).Conclusions: mCRP level independently of hsCRP correlates with subclinical CA progression in patients with moderate SCORE risk and achieved target LDL-C. This work was supported by the Russian Science Foundation grant # 22-25-00054. Background and Aims : Residual inflammatory risk is identified by hsCRP level ≥2.0 mg/l. Monomeric CRP (mCRP) is an emerging inflammatory biomarker. We studied whether mCRP level is a better predictor of carotid atherosclerosis (CA) progression than hsCRP in patients with low-grade CA and moderate SCORE risk which achieved target LDL cholesterol (LDL-C) level. Methods: The study comprised 80 patients of both genders 53.1±5.8 years old with moderate SCORE risk, LDL-C 2.7-4.8 mmol/l and hemodynamically insignificant (<50% stenosis) subclinical CA. All patients were prescribed statin to achieve LDL-C level <2.6 mmol/l and followed up for 7 years. At the completion of follow up subclinical CA progression, which was defined by the increase in the plaque number, was assessed by ultrasonography by the same operator, hsCRP and mCRP level was measured. Mann-Whitney U Test was used for intergroup comparison. Results: Patients were divided by mCRP level 7.2 μg/l and hsCRP level 2.0 mg/l. The increase in the plaque number was 0.58±0.64 vs. 1.44±1.15 in patients with mCRP <7.2 μg/l and ≥7.2 μg/l, respectively. Thus, mCRP level ≥7.2 μg/l was associated with the 2.5 times higher increase in the plaque number (p=0.006, statistical power =0.88). The increase in the plaque number was 0.67±1.01 vs. 1.06±0.99 in patients with hsCRP <2.0 mg/l and ≥2.0 mg/l, respectively. However, the difference was statistically insignificant (p=0.14, statistical power = 0.27). Conclusions: mCRP level independently of hsCRP correlates with subclinical CA progression in patients with moderate SCORE risk and achieved target LDL-C. This work was supported by the Russian Science Foundation grant # 22-25-00054.

Objective: Obesity is a major risk factor for asthma in children. Obese children have an increased risk of asthma; have more frequent and severe exacerbations, decreased lung function, and poor quality of life. However, the relationship between obesity, lung function, and asthma control remains unclear in obese asthmatic Indian children. Therefore, we examined the relationship of body mass index (BMI) with lung function, asthma control, and quality of life in obese asthmatic children. Design and method: Forty-seven children (8–15 years) with asthma according to Global Initiative for Asthma (GINA) guidelines were enrolled in the study from the Pediatric Chest Clinic of All India Institute of Medical Sciences, New Delhi, India. Weight was recorded to the nearest 0.1 kg and height was measured using a stadiometer nearest to 0.1 cm. The measurements of height and weight were used to calculate BMI. BMI derived was categorized by using Z score tables of WHO-BMI for age standards for boys and girls between 5 and 19 years. Lung function was assessed using spirometry parameters (Super spiro MK2 Micro Medical Ltd, UK), HRQoL was assessed using Juniper’s Pediatric Asthma Quality of Life Questionnaire (PAQLQ), and level of asthma control was assessed by Juniper’s Asthma control questionnaire (ACQ). ACQ score ranges from 0 (well controlled) to 6 (extremely poorly controlled). Spearman’s rank correlation analysis was performed to study the relationship between BMI, lung function parameters, PAQLQ score, and asthma control score Results: Obese children had mean (SD) age of 10.7 (2.5) years, BMI = 25.9 ± 7.5 kg/m2, forced expiratory volume-1 second (FEV1)/ forced vital capacity (FVC) was 82.8 ± 10.7%, ACQ score of 1.5 (0.8), and PAQLQ score of 5.5 (1.1).BMI was significantly directly correlated with ACQ score (r = 0.610, p < 0.001), and inversely correlated with predicted FEV1/FVC (r = -0.537, p = 0.002) and PAQLQ score (r = -0.625, p < 0.002). Conclusions: In obese asthmatic children, obesity is associated with a reduction in lung function and poor asthma control, and quality of life. Early weight-loss interventions could play role in preventing obesity and related pulmonary function impairment in asthmatic children.

Aim . To study predictors of radial artery occlusion (RAO) and ways to prevent it after interventions using radial access. Material and methods . The study consisted of prospective and retrospective parts. The total number of included patients was 2284. Patients undergoing interventions by radial access in various medical organizations were retrospectively considered. The prospective study included 1284 patients who were subject to interventional treatment. Patients were randomized into two groups as follows: in group 1, hemostasis was performed within 4 hours, in group 2 — >6 hours. All patients underwent a bedside Barbeau test with a pulse oximeter and an ultrasound of access arteries to determine the radial artery patency/occlusion. Results . The RAO rate in the retrospective part was 21,8%, while in the prospective one — 10,1% with long-term hemostasis and 1,4% with short-term hemostasis (p<0,001). Predictors of RAO were type 2 diabetes (odds ratio (OR), 1,9, 95% confidence interval (CI), 1,1-3,4, p=0,03) and an increase in hemostasis duration by 1 hour (OR, 1,2, 95% CI, 1,1-1,3, p<0,001). When analyzing the retrospective part, the predictors of RAO were body mass index (OR, 1,06, 95% CI, 1,02-1,09, p=0,002), female sex (OR, 0,6, 95% CI, 0,4-0,9, p=0,02), smoking (OR, 1,38, 95% CI, 1-1,91, p=0,047). The administration of statins in different dosages, as well as antihypertensive and anti-ischemic agents, did not have a significant effect on the RAO rate. Conclusion . The main predictors of RAO were type 2 diabetes, an increase in hemostasis duration, female sex, smoking, and the artery-to-introducer diameter ratio. Taking statins, anti-ischemic and antihypertensive agents does not have a protective effect on RAO rate.

Aim To study the relationship between monomeric C-reactive protein (mCRP) and the progression of asymptomatic carotid atherosclerosis in patients with a moderate risk for cardiovascular diseases (CVD) as assessed with the SCORE model.Material and methods The study included 80 men and women aged 53.1±5.8 years assigned to the category of a moderate risk for CVDs by the SCORE model with a low-density lipoprotein cholesterol (LDL-C) level of 2.7–4.8 mmol/l and asymptomatic, hemodynamically insignificant (<50% luminal narrowing) carotid atherosclerosis according to ultrasonic data. All patients were prescribed atorvastatin to achieve a LDL-C level <2.6 mmol/l. After 7 years of follow-up, ultrasonic examination of carotid arteries was performed, and concentrations of high-sensitivity C-reactive protein (hsCRP) and mCRP were measured.Results A concentration of LDL-C <2.6 mmol/l was achieved in all patients. The progression of atherosclerosis as determined by an increased number of atherosclerotic plaques (ASPs), was observed in 45 (56 %) patients. At 7 months of follow-up, concentrations of cCRP were higher in the group of patients with progressive carotid atherosclerosis, while the levels of hsCRP did not differ between the groups. Increased mCRP concentrations were associated with changes in variables of the “atherosclerotic load”, including the number of ASPs, total ASP height, and the intima-media thickness (IMT). In patients with a median mCRP concentration of 5.2 [3.3; 7.1] µg/l and more, the increases in mean ACP number and total ASP height were considerably higher than in patients with mCRP concentrations lower than the median (3.9 and 2.7 times, respectively), whereas the odds ratio for the progression of asymptomatic carotid atherosclerosis was 5.5 (95 % confidence interval, CI: 2.1–14.6; p=0.001). ROC analysis showed that the concentration of hsCRP had no predictive value for prognosis of asymptomatic carotid atherosclerosis (p=0.16), while the area under the ROC curve (AUC) for mCRP was 0.75±0.056 (95 % CI: 0.64–0.86; p=0.001).Conclusion According to the results of 7-year follow-up, the plasma concentration of mCRP was significantly higher in patients with an increased number of ASPs than in patients without this increase. An increased level of mCRP may indicate a higher inflammatory risk of CVD.

Currently used X-ray and laboratory methods for monitoring the effectiveness of TB treatment are not always convenient, because they give a delayed result, as in the case of sputum culture or are difficult to perform, for example, in patients with poor sputum production or patients not following instructions. The aim of the study was to develop mathematical model for predicting the treatment effectiveness of MDR-TB based on Human-beta-defensin-1 level Materials and methods: 50 patients with pulmonary MDR-TB were included in the study. A mathematical model was generated by discriminant functional analysis using Human-beta-defensin-1 (HBD-1) level at baseline, after 30 doses, and after 60 doses of treatment. Results: As a result of the discriminant functional analysis, a mathematical model was obtained for predicting the MDR-TB treatment effectiveness based on the HBD-1 levels at the beginning, after 30 doses and after 60 doses of anti-TB treatment: А = 0,1513*Def0 + 0,2661*Def30 + 0,1946Def60 - 28,4089 В = -0,01995*Def0 + 0,12139*Def30 + 0,03918*Def60 - 1,37308 where Def0 – HBD-1 at the treatment onset, Def30 – HBD-1 after 30 doses, Def60 – HBD-1 after 60 doses. If А>В, the prognosis is unfavorable. If А<В, the prognosis is favorable. Conclusions: The obtained mathematical model allows predicting MDR-TB treatment effectiveness based on Human-beta-defensin-1 level.

Background: Development of carotid atherosclerotic plaques (CAP) in patients (pts) with rheumatoid arthritis (RA) is associated with accumulation of traditional risk factors and immunological disorders. CAP neovascularization is associated with its’ inflammation and increasing vulnerability. Therefore, early detection of CAP neovascularization is important for prevention of potential cardiovascular complications, preferably using a non-invasive technique, such as contrast-enhanced ultrasound (CEUS) of the carotid arteries. Objectives: to identify the relationship between the severity of CAP neovascularization, lipid parameters and RA-related parameters. Methods: Evaluation of 23 RA pts, 8 males and 15 females, mean age 61 [58; 65] years, with a longstanding disease (7 [3;12] years), seropositivity for IgM rheumatoid factor (RF) (76%) and anti-cyclic citrullinated peptide (ACCP) (62%) and moderate clinical disease activity (DAS 28 3,9 [3,2;4,8]). Nineteen RA pts (83%) received Methotrexate, 35% - biological agents, 35% - low-dose glucocorticoids. All patients underwent bilateral CEUS of the carotid arteries using a PHILIPS IU22 ultrasound system with 3-9 MHz linear array transducer and i/v administration of SonoVue contrast agent. The severity of carotid intraplaque neovascularization (IPN) was visually assessed on a scale from 0 to 3 (Shah et al. 2007): 0 - no neovascularization, 1 (mild) - limited to moderate neovascularization, 2 (severe) - extensive appearance of neovascularization, 3 - in the presence of a pulsating vessel in the plaque image. Results: Carotid IPN was found in all RA pts. Grade 1 of neovascularization was established in 39% pts (group I) and Grade 2 - in 61% pts (group II). Groups were comparable in terms of age, sex, body mass index, smoking, disease duration and activity RA (DAS 28 score). The degree of carotid IPN positively correlated with the LDL-C level (R = 0,46, p=0,04), and the TG level (R=0,56, p=0,01) and negatively correlated with the HDL-C level (R= -0,52, p=0,02) in all pts. The degree of neovascularization was also associated with RA duration (R=0,52, p<0,05) and ACCP-positivity (R=0,57, p=0,007). Aforementioned correlations were significant for both groups of RA pts. No association was found between the severity of IPN and the levels of RF, DAS28. Association between the degree of carotid stenosis and CRP concentrations (R=-0,73, p<0,05) was found in pts of group II. Conclusion: CEUS of carotid arteries demonstrated the presence of a predominantly extensive carotid IPN in RA pts. Cases of more severe carotid IPN were associated with lipid parameters (positively with the LDL-C, TG levels and negatively with the HDL-C level), RA duration and ACCP-positivity. The relationship between the degree of carotid artery stenosis and CRP requires additional studies to determine the role of immunological disorders in the development of carotid intraplaque neovascularization in RA pts. References: [1]Shah F., Balan P., Weinberg M., Reddy V., Neems R., Feinstein M., Dainauskas J., Meyer P., Goldin M., Feinstein S.B. Contrast-enhanced ultrasound imaging of atherosclerotic carotid plaque neovascularization: a new surrogate marker of atherosclerosis? Vasc Med. 2007;12(4):291-7. https://doi.org/10.1177/1358863x07083363 Disclosure of Interests: None declared

Aim To determine in a prospective study factors of progressive atherosclerotic lesion of blood vessels in patients with rheumatoid arthritis (RA). Material and methods This prospective study included 124 patients with RA and suspected ischemic heart disease (IHD) and 30 patients with IHD (comparison group) aged 58 [52; 63] years. On enrollment to the study and at 3 years of follow-up, all patients underwent clinical and instrumental examination according to European and Russian guidelines for diagnosis and treatment of stable IHD (2013), including coronography as indicated. For all RA patients of the comparison group, risk factors (RF) were evaluated, including arterial hypertension, smoking, excessive body weight, family history of cardiovascular diseases (CVD), diabetes mellitus, and dyslipidemia. The following laboratory data were evaluated: blood count; biochemistry, including total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), rheumatoid factor (RhF), cyclic citrullinated peptide antibodies, and high-sensitivity C-reactive protein (hsCRP). Proinflammatory cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF- α), were measured in RA patients once, at 3 years of follow-up. Results Incidence of FRs for CVD was similar in RA patients and in the comparison group. Median RA duration before inclusion into the study was 11 years, and median DAS28 index score was 3.8. Incidence of dyslipidemia due to increased TC, LDL-C, and HDL-C was higher for RA patients at baseline. The LDL-C goal (<1.8 mmol/l) was achieved only in 3 (10 %) patients of the comparison group and 10 (8 %) RA patients. RA patients had higher levels of the inflammation indexes, hsCRP (0.75 mg/dl vs . 0.16 mg/dl; p<0.05) and erythrocyte sedimentation rate (ESR) (15 mm/h vs . 11.5 mm/h; p<0.05). In the RA group at baseline, atherosclerotic plaques with carotid artery (CTA) stenosis of 20% or more were found in 94 (77 %) patients; in 3 of them, CA stenosis was >50%. Patients with RA frequently had unchanged or slightly changed coronary arteries (CA) (47% of patients), and less frequently they had hemodynamically significant multi-arterial coronary atherosclerotic lesions (7 % vs. 57 % of patients in comparison group). At 37.5 months, 21 (23 %) of 94 RA patients had progressive atherosclerosis in CA and/or CTA; 12 (13 %) RA patients had only progressive CA atherosclerosis; 7 (8 %) had only progressive CTA atherosclerosis; and 2 (2 %) had simultaneous progression of CA and CTA atherosclerosis. Two groups of RA patients were formed, with the progression of atherosclerosis (n=21) and without the progression of atherosclerosis (n=69). RFs for the development/progression of atherosclerosis in RA patients included smoking, family history of CVD, and duration of the disease. Levels of lipids did not differ. Levels of proinflammatory cytokines (IL-1β, IL-6, TNF-α) were higher in RA patients with progressive atherosclerosis. No effects of the anti-rheumatic therapy on the progression of atherosclerosis were observed. Conclusion Progression of atherosclerosis in RA remains in disease with low and moderate activity during the anti-rheumatic and hypolipidemic treatment. The development of atherosclerosis in RA is determined by lipid, inflammatory, and immune disorders.

Objective: The main aim of study was to investigate the association between subcutaneous (SF), visceral (VF), periaortic (PF), epicardial (EF) fat and carotid artery intima-media thickness (CIMT) in patients with abdominal obesity (AO) and whith metabolic syndrome (MS). Design and method: 127 patients 18–45 y.o. (average age 38,4 ± 6,0) with AO (men (M) – 58,3%) were enrolled in study. Height, weight, BMI, waist circumference, blood tests (fast glucose (FG) and glucose tolerance (GT), lipid profile) were measured. MS was defined as AO (cut-off of > 80 cm in women (W) and > 94 cm in M) plus > 1 sign: HDL < 1,30 (w)/1,04 (m)mmol/l; triglycerides > 1,7mmol/l; FG > 5,6mmol/l; violation GT; BP > 140/90mmHg. The averaged TIM was measured on both sides in a longitudinal section in the distal third of thein left and right carotid artery at a distance of 1 cm proximal to the bifurcation, calculated as the maximum value of the two average values obtained during two successive measurements and direct access two consecutive measurements lateral access. SF, VF, PF, EF (range: -150 to -30 HU) was measured by computed tomography. We calculated ratio subcutaneous to visceral fat (RSV). 24 hour blood pressure monitoring was performed. We formed 2 groups: AO (AO plus 1 or less sing of MS) and MS. Results: No statistically significant difference between the groups was found in the assessment of TIM.Tab. 1. Correlations CIMT with age r = 0,406 (p = 0,000), BMI r = 0,225 (p = 0,000), WC r = 0,031 (p = 0,000), TG r = 0,215 (p = 0,013), daytime SBPm r = 0,187 (p = 0,031), with volume of VF r = 0,326 (p = 0,000), EF r = 0,329 (p = 0,000), PF r = 0,440 (p = 0,000), LDL r = 0,182 (p = 0,037) were found. An inverse correlation was found with RSV r = -0,241 (p = 0,005) and with HDL r = -0,239 (p = 0,005). Conclusions: This study shows the role of PVT and other fat depots in the development of structural and functional disorders of the vascular wall in young people. The revealed correlations prove the existence of a close pathogenetic relationship between obesity, lipid metabolism disorders and the state of the vascular wall.