Multimorbidity in Severe Mental Illness as Part of the Neurodevelopmental Continuum: Physical Health-Related Endophenotypes of Schizophrenia-A Narrative Review.

BACKGROUND: The majority of deaths in patients with schizophrenia and other severe mental illnesses (SMIs) are caused by natural causes, such as cardiovascular diseases (CVDs). The increased risk of CVD and other somatic diseases in SMIs cannot be fully explained by the contribution of traditional risk factors, behavioral risk factors, patients' lifestyle peculiarities, and the influence of antipsychotics. The present review has the following main objectives: (1) to aggregate evidence that neurodevelopmental disorders are the basis of SMIs; (2) to provide a review of studies that have addressed the shared genetic architecture of SMI and cardiovascular disease; and (3) to propose and substantiate the consideration of somatic diseases as independent endophenotypes of SMIs, which will make it possible to place the research of somatic diseases in SMIs within the framework of the concepts of the "neurodevelopmental continuum and gradient" and "endophenotype". METHODS: A comprehensive literature search was performed on 1 July 2024. The search was performed using PubMed and Google Scholar databases up to June 2024. RESULTS: The current literature reveals considerable overlap between the genetic susceptibility loci for SMIs and CVDs. We propose that somatic diseases observed in SMIs that have a shared genetic architecture with SMIs can be considered distinct physical health-related endophenotypes. CONCLUSIONS: In this narrative review, the results of recent studies of CVDs in SMIs are summarized. Reframing schizophrenia as a multisystem disease should contribute to the activation of new research on somatic diseases in SMIs.

Carotid total plaque area as an independent predictor of short-term subclinical polyvascular atherosclerosis progression and major adverse cardiac and cerebrovascular events.

BACKGROUND: The use of ultrasound-based methods for imaging of subclinical atherosclerosis, including measurement of carotid plaque burden (cPB), is a promising direction for further improvement of major adverse cardiac and cerebrovascular events (MACCE) prediction. OBJECTIVES: The aim of the study was to research the prognostic values' significance of cPB indicators with regard to the short-term progression of polyvascular subclinical atherosclerosis and the long-term onset of MACCE. DESIGN: Single-center prospective cohort study. METHODS: The study included patients 40-64 years of age. All patients underwent duplex scanning (DS) of the carotid and lower limb arteries. The following cPB indicators were determined: carotid plaque score (cPS), maximum carotid plaque thickness (cPTmax), and carotid total plaque area (cTPA). The combined endpoint included the following components: cardiovascular death; nonfatal myocardial infarction; nonfatal stroke or transient ischemic attack (TIA); revascularization of the coronary and/or peripheral arteries. RESULTS: The study included 387 patients, among whom 142 (36.7%) patients underwent repeated DS after 12-24 months. The median follow-up time was 20.0 (13.0; 36.5) months. MACCE were recorded in 33 (8.52%) of patients. cTPA and cPTmax, but not cPS, were independently associated with the progression of subclinical polyvascular atherosclerosis over a period of 13.9 months of follow-up. cTPA, but not cPTmax and cPS, was independently associated with the development of MACCE over a period of 20.0 months of follow-up. Only a cTPA > 42.0 mm2 proved to be an independent predictor of both the progression of subclinical polyvascular atherosclerosis and MACCE. CONCLUSION: In patients from 40 to 64 years of age with various cardiovascular risks, among the indicators of the cPB, only an increase in cTPA > 42.0 mm2 was shown to be independently associated with an increase in the relative risk (RR) of progression of subclinical polyvascular atherosclerosis by 2.38 (1.08-5.25) times, as well as with the development of MACCE by 3.10 (1.54-6.26) times.

Innate and Adaptive Immunity-Related Markers as Predictors of the Short-Term Progression of Subclinical Atherosclerosis in Middle-Aged Patients.

Assessment of inflammation is a promising approach to monitoring the progression of asymptomatic atherosclerosis. The aim of the present study was to investigate the predictive value of innate and adaptive immunity-related markers, in relation to the short-term progression of subclinical atherosclerosis. The study included 183 patients aged 40-64 years who underwent duplex scanning of the carotid and lower limb arteries at two visits with an interval of 12-24 months between examinations. Phenotyping of circulating lymphocytes and monocytes subpopulations were performed through flow cytometry. An increase in the number of circulating TLR4-positive intermediate monocytes (>447.0-467.0 cells/µL) was an independent predictor of the short-term progression of lower limb artery atherosclerosis (p < 0.0001) and polyvascular atherosclerosis (p = 0.003). The assessment of TLR4-positive monocytes significantly improved the prognostic model for the progression of lower limb arterial atherosclerosis (C-index 0.728 (0.642-0.815) versus 0.637 (0.539-0.735); p = 0.038). An increase in the number of circulating TLR4-positive intermediate monocytes was an independent predictor of the short-term progression of lower limb artery and polyvascular atherosclerosis. Their inclusion into models containing conventional risk factors significantly improved their prognostic effectiveness regarding lower limb artery atherosclerosis progression.

The heterogeneous cellular landscape of atherosclerosis: Implications for future research and therapies. A collaborative review from the EAS young fellows.

Single cell technologies, lineage tracing mouse models and advanced imaging techniques unequivocally improved the resolution of the cellular landscape of atherosclerosis. Although the discovery of the heterogeneous nature of the cellular plaque architecture has undoubtedly improved our understanding of the specific cellular states in atherosclerosis progression, it also adds more complexity to current and future research and will change how we approach future drug development. In this review, we will discuss how the revolution of new single cell technologies allowed us to map the cellular networks in the plaque, but we will also address current (technological) limitations that confine us to identify the cellular drivers of the disease and to pinpoint a specific cell state, cell subset or cell surface antigen as new candidate drug target for atherosclerosis.

Achilles tendon thickness normalized to body surface area as a marker of asymptomatic peripheral arterial disease.

OBJECTIVES: The normalisation of Achilles tendon thickness (ATT) to anthropometric parameters may increase the diagnostic efficiency of the assessment of ATT. The aim of this study was to compare the diagnostic value of AT dimensions depending on their normalization to body surface area (BSA) in patients with asymptomatic peripheral arterial disease (PAD). METHODS: All patients underwent duplex scanning of the carotid arteries and the lower limb arteries. Asymptomatic PAD was defined as the presence of ≥50% stenosis in the carotid and/or lower limb arteries. ATT was measured using a longitudinal scan, width (ATW) and cross-sectional area (AT CSA), which was determined during a cross-sectional scan. RESULTS: The study included 369 patients, among whom asymptomatic PAD was detected in 18 (4.88%) patients. Only the ATT demonstrated diagnostic value for asymptomatic PAD. After normalizing the size of the AT to the BSA, the diagnostic performance of ATT, ATW and AT CSA became statistically significant. Among the studied parameters, only an increase in ATT/BSA >0.29 cm/m2 was associated with a significant increase in the odds ratio (OR) of asymptomatic PAD by 4.11 times (95% CI 1.08-15.7; p = .038) after adjustments. CONCLUSION: An increase in ATT/BSA >0.29 cm/m2 predicted the presence of asymptomatic PAD with a sensitivity of 61.1% and a specificity of 77.9%. ATT/BSA values of less than 0.29 cm/m2 made it possible to exclude asymptomatic PAD with a probability of 97.5%. An increase in ATT/BSA >0.29 cm/m2 was associated with a 4.11-fold increase in the OR of asymptomatic PAD (95% CI 1.08-15.7).

Liver Stiffness Is Associated with the Burden of Carotid and Systemic Atherosclerosis in an Unorganized Cohort of Patients 40-64 Years Old.

Background: The aim of the study is to research the relationship between the severity of liver fibrosis and the burden of carotid and systemic atherosclerosis. Methods: The study includes 163 patients 40 to 64 years of age without atherosclerotic CVD or liver disease. All patients underwent duplex scanning of the carotid and lower limb arteries. All patients underwent transient liver elastometry using the FibroScan (Echosens, France). Results: Carotid plaque was detected in 110 (67.5%) patients. Based on the results of linear regression analysis, relationships between liver stiffness and carotid total plaque area (r = 0.21; p = 0.025) were found. Significant relationships were established between liver stiffness and atherosclerosis burden score based on the results of linear regression (r = 0.17; p = 0.029). Liver stiffness showed moderate diagnostic performance (AUC 0.666; p = 0.01) with regard to generalized atherosclerosis. An increase in liver stiffness >4.5 kPa was associated with an odds ratio of generalized atherosclerosis of 3.48 (95% CI 1.07−11.3; p = 0.038) after adjusting confounding factors. Conclusion: Among patients 40−64 years of age without established atherosclerotic CVD and liver disease, liver stiffness directly correlates with the burden of carotid and systemic atherosclerosis. Liver stiffness showed moderate diagnostic performance (AUC 0.666; p = 0.01) with regard to generalized atherosclerosis.

Circulating Ageing Neutrophils as a Marker of Asymptomatic Polyvascular Atherosclerosis in Statin-Naïve Patients without Established Cardiovascular Disease.

BACKGROUND: Current data on the possible involvement of aging neutrophils in atherogenesis are limited. This study aimed to research the diagnostic value of aging neutrophils in their relation to subclinical atherosclerosis in statin-naïve patients without established atherosclerotic cardiovascular diseases (ASCVD). METHODS: The study was carried out on 151 statin-naïve patients aged 40-64 years old without ASCVD. All patients underwent duplex scanning of the carotid arteries, lower limb arteries and abdominal aorta. Phenotyping and differentiation of neutrophil subpopulations were performed through flow cytometry (Navios 6/2, Beckman Coulter, USA). RESULTS: The number of CD62LloCXCR4hi-neutrophils is known to be significantly higher in patients with subclinical atherosclerosis compared with patients without atherosclerosis (p = 0.006). An increase in the number of CD62LloCXCR4hi-neutrophils above cut-off values makes it possible to predict atherosclerosis in at least one vascular bed with sensitivity of 35.4-50.5% and specificity of 80.0-92.1%, in two vascular beds with sensitivity of 44.7-84.4% and specificity of 80.8-33.3%. CONCLUSION: In statin-naïve patients 40-64 years old without established ASCVD with subclinical atherosclerosis, there is an increase in circulating CD62LloCXCR4hi-neutrophils. It was also concluded that the increase in the number of circulating CD62LloCXCR4hi-neutrophils demonstrated moderate diagnostic efficiency (AUC 0.617-0.656) in relation to the detection of subclinical atherosclerosis, including polyvascular atherosclerosis.

Associations between Circulating VEGFR2hi-Neutrophils and Carotid Plaque Burden in Patients Aged 40-64 without Established Atherosclerotic Cardiovascular Disease.

Background: Neutrophils expressing vascular endothelial growth factor receptor (VEGFR) represent a distinct subtype of neutrophils with proangiogenic properties. The purpose of this study was to identify the interrelations between circulating CD16hiCD11bhiCD62LloCXCR2hiVEGFR2hi-neutrophils and indicators of carotid plaque burden in patients without atherosclerotic cardiovascular diseases (ASCVD). Methods: The study included 145 patients, 51.7% men and 48.3% women, median age-49.0 years. All patients underwent carotid duplex ultrasound scanning. The maximal carotid plaque thickness was used as an indicator of carotid plaque burden. Also, carotid intima-media thickness (cIMT) and femoral IMT were measured. The phenotyping of neutrophil subpopulations was executed by the flow cytometry via the Navios 6/2. Results. The subpopulation of VEGFR2hi-neutrophils accounted for about 5% of the total pool of circulating neutrophils. A decrease in VEGFR2hi-neutrophils with an increase in carotid plaque burden was statistically significant (p = 0.036). A decrease in VEGFR2hi-neutrophils < 4.52% allowed to predict the presence of plaque with a maximum height > 2.1 mm (Q4), with sensitivity of 78.9% and specificity of 61.5% (AUC 0.693; 95% CI 0.575-0.811; p = 0.007). Inverse correlations were established between the carotid and femoral IMT and the absolute and relative number of VEGFR2hi-neutrophils (p < 0.01). Conclusion: In patients aged 40-64 years without established ASCVD, with an increase in indicators of the carotid plaque burden, a significant decrease in the proportion of circulating VEGFR2hi-neutrophils was noticed. A decrease in the relative number of VEGFR2hi-neutrophils of less than 4.52% made it possible to predict the presence of extent carotid atherosclerosis with sensitivity of 78.9% and specificity of 61.5%.

Prognostic Significance of Hypertriglyceridemia in Patients at High and Very High Cardiovascular Risk Depending on the Concentration of Highsensitivity C-reactive Protein.

BACKGROUND: It has been established that an increase in triglyceride-rich lipoprotein levels is associated with the development of systemic low-grade inflammation. Data on the prognostic role of hypertriglyceridemia (HTG) dependent on the state of low-grade inflammation are limited. OBJECTIVE: The study's objective was to evaluate the predictive value of mild-to-moderate HTG (2.3- 11.2 mmol/L) regarding the development of cardiovascular events in patients at high and very high cardiovascular risk (CVR), depending on the high-sensitivity C-reactive protein (hsCRP) values. METHODS: The study included 185 patients with high and very high CVR. The concentration of hsCRP in blood serum was measured using an enzyme-linked immunosorbent assay kit. The combined endpoint was cardiovascular death, nonfatal myocardial infarction or unstable angina (which required hospitalization), nonfatal stroke, and coronary revascularization. RESULTS: HTG was revealed in 17.3% of the patients. An increase in hsCRP ≥2.0 mg/L was observed in 51.9% of the patients. The event-free survival of patients with HTG was not statistically different from that in patients with TG <2.3 mmol/L (RR 1.61; 95% CI 0.86-3.00; p=0.133). In the subgroup of patients with hsCRP <2.0 mg/L, patients with HTG were not significantly different from patients without HTG. In the subgroup of patients with hsCRP≥2.0 mg/L, the presence of HTG was associated with a 4.63 times increase in the RR of adverse cardiovascular events (95% CI 1.35-15.8; p=0.015) after adjusting for potential confounders. CONCLUSION: In patients with high and very high CVR, an increase in TG ≥2.3 mmol/L was associated with the development of adverse cardiovascular events only in the subgroup of patients with an increase in hsCRP ≥2.0 mg/L. The presence of HTG was associated with a 4.63 times increase in RR of adverse cardiovascular events (95% CI 1.35-15.8; p=0.015).

Associations between Hypertriglyceridemia and Circulating Neutrophil Subpopulation in Patients with Dyslipidemia.

BACKGROUND: There is strong evidence to suggest that the negative influence of triglyceride-rich lipoproteins (TRLs) on atherosclerosis development and progression is at least partially mediated by their proinflammatory effects. However, the effect of hypertriglyceridemia (HTG) on the subpopulation composition of circulating neutrophils has not been studied so far. The aim of this study was to examine correlations between the level of triglycerides (TGs) and the subpopulation composition of circulating neutrophils in middle-aged patients with dyslipidemia without established atherosclerotic cardiovascular diseases (ASCVDs). METHODS: Ninety-one patients with dyslipidemia, including 22 (24.2%) patients with HTG, were enrolled in the study. Phenotying of neutrophil subpopulations was performed through flow cytometry (Navios 6/2, Beckman Coulter, USA). For phenotyping of neutrophil subpopulations, conjugated monoclonal antibodies were used: CD16, PE-Cyanine7 (Invitrogen, USA); CD11b-FITC (Beckman Coulter, USA); CD62L-PE (Beckman Coulter, USA); and CD184 (CXCR4)-PE-CF594 (BD Biosciences, USA). RESULTS: Following the correlation analysis, the TG level directly correlated with the number of circulating leukocytes (r = 0.443; p < 0.0001) and neutrophils (r = 0.311; p=0.008). HTG patients displayed a significantly high number of circulating neutrophils with CD16hiCD11bhiCD62Lhi and CD16hiCD11bloCD62Lbr phenotypes. TG levels directly correlated with the number of circulating neutrophils having CD16hiCD11bhiCD62Lhi and CD16hiCD11bloCD62Lbr phenotypes. Following the linear regression analysis, statistically significant correlations between TG levels and neutrophil subpopulations having CD16hiCD11bloCD62Lbr and CD16hiCD11bbrCD62LloCXCR4hi phenotypes were established. Changes in TG levels could explain up to 19.1% of the variability in the number of studied neutrophil subpopulations. CONCLUSION: Among middle-aged patients without established ASCVDs, patients with HTG demonstrated a significantly higher overall number of neutrophils and neutrophils having CD16hiCD11bhiCD62Lhi (mature neutrophils) and CD16hiCD11bloCD62Lbr (immunosuppressive neutrophils) than patients with normal TG levels. The TG level was associated with an increase in the number of CD16hiCD11bloCD62Lbr and CD16hiCD11bbrCD62LloCXCR4hi (ageing neutrophils) neutrophils, adjusted for the sex and age of the patients.

Relationship between the abdominal aortic diameter and carotid atherosclerosis in middle-aged patients without established atherosclerotic cardiovascular diseases.

BACKGROUND: The purpose of our research was to study the relationship between the diameter of abdominal aorta (AA) and subclinical atherosclerosis in patients without established atherosclerotic cardiovascular diseases (ASCD) in the absence of pathological enlargement of AA. METHODS: The study included 136 patients (52.9% male, 47.1% female), median age was 51.0 (45.5; 58.0) years. The maximum diameter of AA was measured in the infrarenal region at a level between the place of origin of the lower renal artery and bifurcation in cross section. Measurement of the anteroposterior diameter of AA was carried out from the outer-to-outer edge (OTO). Also, we determined the Aortic Size Index (ASI) with respect to body surface area (BSA), using the values of BSA obtained by five different formulas validated for use in clinical practice. All patients underwent carotid duplex ultrasound scanning with assessment of degree of carotid stenosis (according to ECST criteria). RESULTS: An increase in the anteroposterior diameter of AA was directly correlated with maximum stenosis of carotid arteries (r=0.186; P=0.030). According to the results of a logistic regression analysis an increase in the diameter of AA by 1 mm was associated with an increase in the relative risk of carotid stenosis ≥50% by 1.37 times (95% CI: 1.01-1.85; P=0.041) after adjustment. Thus, an increase in diameter of AA of more than 1.75 cm with a sensitivity of 71.4% and a specificity of 73.0% made it possible to predict the presence of stenosis of the carotid arteries ≥50%. An increase in ASIBoyd (BSA was calculated using Boyd's formula) of more than 0.84 allowed predicting the presence of stenosis of the carotid arteries ≥50% with a sensitivity of 85.7% and a specificity of 65.6%. CONCLUSIONS: In middle-aged patients without established ASCD, the diameter of AA and ASI directly correlated with the degree of carotid stenosis (according to ECST criteria). The diameter of AA and ASI demonstrated good sensitivity and specificity for the presence of asymptomatic carotid stenosis of ≥50%.

Achilles Tendon Thickness Is an Independent Predictor of Carotid Atherosclerosis and Is Associated With a Carotid Plaque Burden.

The aim of the study was to research the relationship between carotid atherosclerosis markers and ultrasound parameters of Achilles tendons (AT). The study included 150 patients at high and very high cardiovascular risk (CVR). All patients underwent a carotid ultrasound scanning. We evaluated carotid plaque, carotid plaque score (cPS), carotid total plaque area (cTPA), and the percentage of stenosis. All patients underwent AT ultrasound with an assessment of thickness (Achilles tendon thickness [ATT]), width (Achilles tendon width), and cross-sectional area. An increase in the ATT ≥5.07 mm was associated with a 4.55-fold increase in the relative risk of carotid atherosclerosis (sensitivity 68.3% and specificity 62.5%). Direct correlations between the ATT and carotid stenosis (r = 0.277; P = .004), cPS (r = 0.225; P = .035), and cTPA (r = 0.305; P = .004) were determined. An increase in the mean ATT by 1 mm was associated with an increase in cTPA by 8.09 mm2 (95% CI: 2.26-13.9; P = .007) and carotid stenosis by 4.11% (95% CI: 0.64-7.60; P = .021). Thus, in patients with high and very high CVR, an increase in ATT is an independent predictor of carotid atherosclerosis. The ATT directly correlates with the markers of carotid plaque burden.

Conceptualization of Heterogeneity of Chronic Diseases and Atherosclerosis as a Pathway to Precision Medicine: Endophenotype, Endotype, and Residual Cardiovascular Risk.

The article discusses modern approaches to the conceptualization of pathogenetic heterogeneity in various branches of medical science. The concepts of endophenotype, endotype, and residual cardiovascular risk and the scope of their application in internal medicine and cardiology are considered. Based on the latest results of studies of the genetic architecture of atherosclerosis, five endotypes of atherosclerosis have been proposed. Each of the presented endotypes represents one or another pathophysiological mechanism of atherogenesis, having an established genetic substrate, a characteristic panel of biomarkers, and a number of clinical features. Clinical implications and perspectives for the study of endotypes of atherosclerosis are briefly reviewed.

Multivessel spontaneous coronary artery dissection in a patient after mild COVID-19: A case report.

Coronavirus disease 2019 (COVID-19) is characterized by heterogeneity of possible cardiovascular manifestations. Spontaneous coronary artery dissection is a rare cause of acute coronary syndrome, the development of which in patients with COVID-19 has been described and studied insufficiently. A 35-year-old male patient presented to our hospital with an acute coronary syndrome a few weeks after mild COVID-19. According to coronary angiography, a dissection of ramus intermedius was detected. Successful stenting was performed. Subsequently, the patient had relapses of chest pain, which led to two repeated coronary angiographies. The patient had been diagnosed with consecutive dissections of right coronary artery and distal branch of ramus intermedius. Repeated stenting of dissected segments of right coronary artery and ramus intermedius was not performed. Afterward, the patient's condition remained stable and he was successfully discharged. One of the main pathophysiological mechanisms of cardiovascular complications in COVID-19 is probably the virus-triggered hyperinflammation and massive release of cytokines. A systemic inflammatory response may initiate inflammation of the vascular wall and other target tissues. The results of histological studies confirm the direct infection of endothelial cells 2019-nCoV with the development of diffuse endothelial inflammation (endotheliitis). It is possible that in patients with a genetic predisposition to artery dissection, COVID-19 may be a trigger of spontaneous coronary artery dissection.

Biomechanical Forces and Atherosclerosis: From Mechanism to Diagnosis and Treatment.

The article provides an overview of current views on the role of biomechanical forces in the pathogenesis of atherosclerosis. The importance of biomechanical forces in maintaining vascular homeostasis is considered. We provide descriptions of mechanosensing and mechanotransduction. The roles of wall shear stress and circumferential wall stress in the initiation, progression and destabilization of atherosclerotic plaque are described. The data on the possibilities of assessing biomechanical factors in clinical practice and the clinical significance of this approach are presented. The article concludes with a discussion on current therapeutic approaches based on the modulation of biomechanical forces.

The prognostic value of various carotid ultrasound parameters in patients at high and very high cardiovascular risk.

BACKGROUND: According to the current guidelines the visualization of atherosclerotic plaques in the carotid arteries is the only option that carotid ultrasound provides for the assessment of cardiovascular risk (CVR). The direction devoted to the development and implementation of markers based on the quantification of atheroma, is promising. The aim of the study was to evaluate the prognostic value of various carotid ultrasound parameters in patients at high and very high CVR. METHODS: Patients at high and very high CVR were included. All patients underwent carotid ultrasound. We evaluated carotid intima-media thickness (cIMT), carotid plaque, carotid plaque score (cPS) and carotid total plaque area (cTPA). The combined endpoint was cardiovascular death, non-fatal myocardial infarction or unstable angina, non-fatal stroke and coronary revascularization. RESULTS: The study included 100 patients. The duration of the follow-up period was 24.4 (14.1-34.3) months. Endpoint events occurred in 34.0% patients. cIMT and cPS were not significantly associated with the risk of cardiovascular events. The presence of carotid plaque in accordance with Cox regression after adjusting for possible confounders was associated with an increase in the relative risk of cardiovascular events by 10.5 times (95% CI 1.27-86.5; p = 0.008). CTPA ≥69 mm2 according to adjusted analysis was associated with an increase in the risk of cardiovascular events by 5.86 times (95% CI 2.09-16.4; p = 0.001). CONCLUSION: In patients at high and very high CVR among carotid atherosclerosis markers only carotid plaque and cTPA had an independent predictive value regarding the development of adverse cardiovascular events.

Association between Carotid Wall Shear Rate and Arterial Stiffness in Patients with Hypertension and Atherosclerosis of Peripheral Arteries.

AIM: To evaluate carotid wall shear rate (WSR) in association with local and regional vascular stiffness in patients with hypertension (HTN) and atherosclerosis of peripheral arteries and to study the pattern of change of WSR in patients with HTN with increasing severity of peripheral artery atherosclerosis. MATERIALS AND METHODS: Study involved 133 patients with HTN, 65 men and 48 women, aged in average 57.9±10.8 years. All patients were divided into four groups in accordance with ultrasound morphologic classification of vessel wall. Duplex scanning of carotid and lower limb arteries was performed. Carotid-femoral (cfPWV) and carotid-radial (crPWV) pulse wave velocity (PWV) were measured. Local carotid stiffness was evaluated by carotid ultrasound. RESULTS: WSR of patients with plaques without and with hemodynamic disturbance was 416±128 s-1 and 405±117 s-1, respectively, which was significantly less than the WSR in patients with intact peripheral arteries - 546±112 s-1. Decreased carotid WSR was associated with increased crPVW, cfPWV, Peterson's elastic modulus, decreased distensibility, and distensibility coefficient. CONCLUSION: In patients with HTN and atherosclerotic lesions of peripheral arteries, it is registered that the carotid WSR decreased with increasing severity of atherosclerosis. Decreased carotid WSR is associated with increased local carotid stiffness, regional vascular stiffness of muscular, and elastic vessels.