Atherosclerotic Plaque Growth Research Articles

Acoustic Delivery of Plasma Low-Density Lipoprotein into Liver via ApoB100-Targeted Microbubbles Inhibits Atherosclerotic Plaque Growth.

Atherosclerosis is the main risk factor for cardiovascular disease, which accounts for the majority of mortality worldwide. A significantly increased plasma level of low-density lipoprotein cholesterol (LDL-C), surrounded by a monolayer of phospholipids, free cholesterol, and one apolipoprotein B-100 (ApoB-100) in the blood, plays the most significant role in driving the development of atherosclerosis. Commercially available cholesterol-lowering drugs are not sufficient for preventing recurrent cardiovascular events. Developing alternative strategies to decrease the plasma cholesterol levels is desirable. Herein, we develop an approach for reducing LDL-C levels using gas-filled microbubbles (MBs) that were coated with anti-ApoB100 antibodies. These targeted MBApoB100 could selectively capture LDL particles in the bloodstream through forming LDL-MBApoB100 complexes and transport them to the liver for degradation. Further immunofluorescence staining and lipidomic analyses showed that these LDL-MBApoB100 complexes may be taken up by Kupffer cells and delivered to liver cells and bile acids, greatly inhibiting atherosclerotic plaque growth. More importantly, ultrasound irradiation of these LDL-MBApoB100 complexes that accumulated in the liver may induce acoustic cavitation effects, significantly enhancing the delivery of LDL into liver cells and accelerating their degradation. Our study provides a strategy for decreasing LDL-C levels and inhibiting the progression of atherosclerosis.

Clopidogrel induced reduction in neutrophil count: An overlooked beneficial effect?

Complement-stimulated neutrophils are able to adhere to the endothelium and damage endothelial cells both in vitro and in vivo. These blood cells participate in the early stages, growth and complications of atherosclerotic plaques. Recent findings, based on mendelian randomization analysis, support the concept that high neutrophil counts are a causal risk factor for ischemic heart disease and myocardial infarction . Clopidogrel decreases leukocyte count and inflammatory markers in patients with acute coronary syndromes; this off-target effect, which is independent of the antiplatelet action, may help explaining secondary prevention data showing a superiority of clopidogrel over aspirin in reducing new cardiovascular events.

Evaluating the association between vascular remodeling and plaque calcification patterns of the carotid artery and its effects on ischemic symptoms using CT angiography.

Arterial remodeling is a compensatory mechanism of the vessel wall in response to atherosclerotic plaque growth. However, the clinical significance of vascular remodeling of carotid lesions remains unclear. Through this study, we aimed to evaluate the association between vascular remodeling and ischemic symptoms in patients with an internal carotid artery (ICA) stenosis degree ≥50%, considering the differences in plaque calcification patterns. This retrospective cross-sectional study included adult patients with moderate-to-severe proximal ICA stenosis associated with atherosclerotic plaques admitted to the Zhejiang Hospital between September 2018 and March 2023. Parameters such as lumen diameter, plaque calcification types, calcium scores, and calcification thickness were assessed using non-contrast and contrast-enhanced computed tomography angiography (CTA). The remodeling ratio (RR) was calculated by dividing the maximum distance of the proximal ICA between the inner border of the arterial lumen at the plaque site and the outer borders of the plaque by the luminal diameter. Atherosclerosis risk factors and medications were recorded. The Mann-Whitney U test or chi-square test was used to compare the differences between groups. Correlations were measured using Pearson's correlation coefficient. Predictors of ischemic symptoms were assessed using multivariable logistic regression analysis, with results expressed as odds ratio (ORs) with 95% confidence intervals (CIs). A P value less than 0.05 (two-sided) was considered to indicate statistical significance The differences in RR among plaque calcification types and the association between vascular remodeling and clinical symptoms were analyzed. A total of 242 ICAs in 196 patients were included in this study, and 84 were symptomatic and 158 were asymptomatic. The RR in symptomatic ICA [median, 1.31 (interquartile range, 1.17-1.68)] was significantly greater than that in asymptomatic group [median, 1.20 (interquartile range, 1.05-1.45)], P=0.006). Significant differences in RR existed among plaque calcification types, among which type 5 and 6 plaques had the highest RR. About 71.5% (173/242) of all ICAs showed positive remodeling. Significant correlations were observed between RR and ischemic symptoms and between positive remodeling and calcification thickness (P<0.05 for all variables). On multivariable logistic regression analysis, calcification thickness remained significantly associated with positive remodeling of carotid arteries (OR 2.30; 95% CI: 1.06-5.01; P=0.036). Arterial remodeling exists in the ICA. A significant association between arterial positive remodeling and plaque calcification thickness was established. RR helps predict ischemic symptoms. The results of our study suggest that arterial remodeling serves as a novel measure to help ascertain the risk stratification of ischemic events in carotid atherosclerotic disease.

Emerging Trends in Atherosclerosis: Time to Address Atherosclerosis From a Younger Age.

Over the past two decades, research efforts into cardiovascular disease (CVD) have uncovered findings that fundamentally challenge our understanding of CVD, particularly atherosclerosis. Atherosclerosis was primarily attributed to the well-described abnormal lipid accumulation theory, involving plaque growth with subsequent plaque hemorrhage resulting in acute vessel thrombosis that may or may not rupture. This perspective has now evolved to encompass more complex pathways, wherein the accumulation of abnormal products of oxidation and inflammation is the most likely factor mediating atherosclerotic plaque growth. Furthermore, atherosclerosis was traditionally thought of as a disease in patients aged 40 and older. However, mounting evidence has demonstrated that significant atherosclerosis and CVD events are more prevalent in younger patients than previously realized and accelerating in incidence. With this alarming trend among younger individuals, our review sought to explore why this trend may be happening and what can be done about this developing problem.

The influence of inlet flow asymmetry on the carotid bifurcation hemodynamics

Arterial bifurcations are known to be high-risk areas for the initiation of atherosclerosis. The appearance and growth of atherosclerotic plaques in the bifurcation of the carotid artery can result in severe consequences such as cerebrovascular accidents. The common signs of an atherogenic risk center around the surpassing critical values by certain hemodynamic indices, which are distributed over the artery wall. These indices are related to the effect of blood flow on the arterial wall, and their distribution is influenced by both the bifurcation’s geometric shape and the flow structure at its inlet. The objective of this study is to carry out a comparative analysis of hemodynamic indices in personal-specific models of carotid bifurcation with centrally symmetric and asymmetric input flows. The examined geometric models of bifurcation are based on computed angiography data obtained from the individuals free of apparent pathology. By using computational fluid dynamics within these models, the distribution of hemodynamic indices in a steady periodic flow is calculated and critical zones are determined for them. All the models are divided into two groups – those with symmetric and those with asymmetric input flows. For each model with asymmetric input flow, an alternative geometry is designed to ensure inlet flow symmetry, and comparative numerical calculations of the blood flow are carried out. The results of comparative analysis reveal that the distribution of hemodynamic indices is simpler for the group with symmetric input flow. A comparison of the averages between these two groups with symmetrical and natural asymmetric input flows indicates a 55% better result for the latter group. Furthermore, for almost all models with asymmetric input flow, their alternative models give worse hemodynamic results. Thus, hemodynamic indices in simpler models with symmetrical input flow can serve as an upper estimate for indices in models with natural asymmetric flow. A total of 89 models are included in the study.

Error analysis of a highly efficient and accurate temporal multiscale method for a fractional differential system

This work is concerned with a nonlinear coupled system of fractional ordinary differential equations (FODEs) with multiple scales in time. The micro system is a nonlinear differential equation with a periodic applied force and the macro system is a fractional differential equation. We are interested in the effective long-term computation of the solution. The main challenge is how to obtain the solution of the coupled fractional problem at a lower computational cost, which calls for us to develop an effective analysis and computation framework. We derive a periodic auxiliary system to approximate the original system and give error estimates. Then we propose a numerical scheme based on the auxiliary problem and analyze the discrete error. An efficient multiscale algorithm that is also applicable to 2-D and 3-D problems is designed. The results of numerical experiments demonstrate the accuracy and computational efficiency of the proposed multiscale method. It is observed that, the computational time is significantly reduced and the multiscale method performs very well in comparison to the fully resolved simulation. Furthermore, as a particular example of applications, we consider a simplified model of the atherosclerotic plaque growth problem, and simply evaluate the effect of fractional parameter and damping coefficient on plaque growth and discuss the physical implication.

Design of knowledge-based mechanistic model of atherosclerotic cardiovascular disease for in silico trials

Abstract In silico trials applying a computational model (CM) of atherosclerotic cardiovascular disease (ASCVD) to virtual patients receiving alternative treatments provide an attractive option to complement randomised clinical trials (RCTs) by adding comparative effectiveness data and facilitating the demonstration of drug benefit. In silico modelling allows comparison between treatments with each virtual patient being his own control, and is not limited by the number of patients, comparative arms or trial duration. This study aims at building a knowledge-based mechanistic model of ASCVD. Once validated, the model will be used to run in silico clinical trials to compare the benefit of inclisiran, an siRNA targeting PCSK9 mRNA, vs other lipid-lowering therapies (LLT) on cardiovascular (CV) events in patients with ASCVD. An extensive literature review was performed to identify pathophysiological mechanisms involved in ASCVD and therapeutic mechanisms of action (MOAs). Every piece of knowledge extracted from the literature is awarded a strength of evidence grading to allow tracking of uncertainty in the model. A panel of multidisciplinary experts reviewed knowledge models and subsequent modelling hypotheses to validate their relevance. Knowledge was translated into mathematical equations. Each functional relationship between entities is represented by a biochemical/biophysical reaction with its reaction rate. A system of ordinary differential equations provides dynamics of modelled biological entities. A strategy of model calibration/validation was defined with the expert panel, by selecting relevant RCT and registry data, that the model should be able to reproduce. A virtual population was generated to account for inter-patient variability. A mechanistic CM of ASCVD (including 72 biological entities, 750 parameters) was built from knowledge, describing lipoproteins metabolism and cholesterol homeostasis, dynamics of atherosclerotic plaque growth with lipoproteins infiltration in the intima and evolution of lipidic, necrotic and fibrotic tissues as well as plaque rupture leading to myocardial infarction, ischemic stroke, lower extremity arterial disease or CV death. It also includes the impact of several risk factors (age, sex medical history, diabetes, hypertension, smoking, systemic inflammation, chronic kidney disease) and available LLT (atorvastatin, rosuvastatin, ezetimibe, evolocumab and inclisiran). After calibration, the model and virtual population reproduce pharmacokinetics of LLT, lipoproteins decrease under combinations of LLT and associated reduction in clinical events. ASCVD is ideally suited for in silico modelling: extensive literature is available regarding the pathophysiology, therapeutic MOAs are known and easily integrated in the model, clinically relevant outcomes are adequate model outputs, RCT and registry data exist to calibrate/validate the model. The next step is validation of the model before using it to run in silico trials.Plaque growth and rupture modelMulti-scale in silico model

Trem2 promotes foamy macrophage lipid uptake and survival in atherosclerosis

Atherosclerosis is driven by the expansion of cholesterol-loaded ‘foamy’ macrophages in the arterial intima. Factors regulating foamy macrophage differentiation and survival in plaque remain poorly understood. Here we show, using trajectory analysis of integrated single-cell RNA sequencing data and a genome-wide CRISPR screen, that triggering receptor expressed on myeloid cells 2 (Trem2) is associated with foamy macrophage specification. Loss of Trem2 led to a reduced ability of foamy macrophages to take up oxidized low-density lipoprotein (oxLDL). Myeloid-specific deletion of Trem2 showed an attenuation of plaque progression, even when targeted in established atherosclerotic lesions, and was independent of changes in circulating cytokines, monocyte recruitment or cholesterol levels. Mechanistically, we link Trem2-deficient macrophages with a failure to upregulate cholesterol efflux molecules, resulting in impaired proliferation and survival. Overall, we identify Trem2 as a regulator of foamy macrophage differentiation and atherosclerotic plaque growth and as a putative therapeutic target for atherosclerosis.

Our Hidden Enemy: Ultra-Processed Foods, Inflammation, and the Battle for Heart Health.

Over the past few decades, we have witnessed unprecedented growth in new data that has fundamentally changed our traditional understanding of the progression of atherosclerotic plaques, as well as our strategies for preventing cardiovascular diseases, especially atherosclerosis. It was once believed that atherosclerosis was primarily caused by abnormal lipid buildup in the vessel intima, leading to plaque growth and luminal stenosis, with or without rupture. This perspective has now evolved to encompass more complex pathways, wherein the accumulation of abnormal products of oxidation and inflammation are the most likely factors mediating the growth of atherosclerotic plaques. The review aims to provide a comprehensive and detailed exploration of the relationship between ultra-processed foods, chronic inflammation, cardiovascular diseases, obesity, insulin resistance, and the role of the gut microbiota. It touches on several important aspects of modern diet and health.

Macrophage immunometabolism in diabetes-associated atherosclerosis.

Macrophages play fundamental roles in atherosclerotic plaque formation, growth, and regression. These cells are extremely plastic and perform different immune functions depending on the stimuli they receive. Initial in vitro studies have identified specific metabolic pathways that are crucial for the proper function of pro-inflammatory and pro-resolving macrophages. However, the plaque microenvironment, especially in the context of insulin resistance and type 2 diabetes, constantly challenges macrophages with several simultaneous inflammatory and metabolic stimuli, which may explain why atherosclerosis is accelerated in diabetic patients. In this mini review, we discuss how macrophage mitochondrial function and metabolism of carbohydrates, lipids, and amino acids may be affected by this complex plaque microenvironment and how risk factors associated with type 2 diabetes alter the metabolic rewiring of macrophages and disease progression. We also briefly discuss current challenges in assessing macrophage metabolism and identify future tools and possible strategies to alter macrophage metabolism to improve treatment options for diabetes-associated atherosclerosis.

Different stimuli induce endothelial dysfunction and promote atherosclerosis through the Piezo1/YAP signaling axis

Vascular endothelial dysfunction is the initial step in atherosclerosis (AS). AS tends to occur at vascular bifurcations and curves, and endothelial cells(ECs) are highly susceptible to injury due to mechanical forces induced by disturbed flow (DF) with inconsistent blood flow directions. However, the pathogenesis of endothelial cell dysfunction in AS remains unclear and needs further study. Here, we found that Piezo1 expression was significantly increased in DF- and oxidized low-density lipoprotein(ox-LDL)-treated HUVECs in vitro and a model of atherosclerotic plaque growth in ApoE−/− mice fed a Western diet. Furthermore, Piezo1 upregulated autophagy levels in the HUVECs model, which was reversed by Piezo1 knockdown with a lentivirus-mediated shRNA system. Mechanistically, the level of Yes-associated protein (YAP), a transcriptional coactivator in the Hippo pathway, was significantly elevated in the DF- and ox-LDL-induced HUVECs model, and this effect was further inhibited by Piezo1 knockdown. Moreover, the Piezo1 agonist Yoda1 inhibited the protein level of microtubule-associated protein 1 light chain 3-II(LC3-II) and increased the protein level of sequestosome1(p62/SQSTM1) in a dose-dependent manner, while significantly promoting the protein expression and nuclear translocation of YAP. The YAP inhibitor CA3 weakened Yoda1-mediated inhibition of autophagy. Our results suggest that Piezo1 may regulate endothelial autophagy by promoting YAP activation and nuclear translocation, thereby contributing to vascular endothelial dysfunction.

Antioxidant Activity and Heart Diseases

Cardiovascular disease (CVD), which are complex conditions with many pathophysiologic pathways, has increased oxidative stress as a possible common cause. For a cell to function normally, reactive oxygen species (ROS) and antioxidants must coexist in a delicate balance. High levels of ROS damage large cellular molecules including DNA, lipids and proteins, ultimately leading to necrosis and death, although their primary function is essential to shed light on biological processes. Oxidative stress, the leading cause of death globally in people with cardiovascular disease, has an impact on a variety of disorders. An increase in reactive oxygen species leads to a decrease in the availability of nitric oxide, which in turn leads to vasoconstriction and arterial hypertension. Reactive oxygen species also impair myocardial calcium processing by inducing apoptotic and hypertrophic signaling, which promote cardiac remodeling and arrhythmias. Last but not least, ROS has been shown to promote the growth of atherosclerotic plaques. This paper seeks to give an overview of oxidative stress in CVD with a focus on endothelial dysfunction before looking more closely at how it affects the most prevalent of these diseases. In order to reduce the impact of oxidative stress on CVD, appropriate nutrition and diets are reviewed afterwards.

Accurate adventitia reconstruction; significant or not in atherosclerotic plaque growth simulationsƒ A comparative study.

A reform in the diagnosis and treatment process is urgently required as carotid artery disease remains a leading cause of death in the world. To this purpose, all computational techniques are now being applied to enhancing the most cutting-edge diagnosis techniques. Computational modeling of plaque generation and evolution is being refined over the past years to forecast the atherosclerotic progression and the corresponding risk in patient-specific carotid arteries. A prerequisite to their implementation is the reconstruction of the precise three-dimensional models of patient-specific main carotid arteries. Even with the most sophisticated algorithms, accurate reconstruction of the arterial vessel is frequently difficult. Furthermore, there are several works of plaque growth modeling that ignore the reconstruction of the artery's outer layer in favor of a virtual one. In this paper, we investigate the importance of an accurate adventitia layer in plaque growth modeling. This is done as a comparative study by implementing a novel plaque growth model in two reconstructed carotid arterial segments using either their realistic or virtual adventitia layer as input. The results indicate that accurate adventitia reconstruction is of minor importance regarding species distributions and plaque growth in carotid segments, which initially did not contain any plaque regions.Clinical Relevance- The findings of this comparative study emphasize the importance of precise adventitia geometry in plaque growth modeling. As a result, this work sets a higher standard for publishing new plaque growth models.

Towards parallel time-stepping for the numerical simulation of atherosclerotic plaque growth

The numerical simulation of atherosclerotic plaque growth is computationally prohibitive, since it involves a complex cardiovascular fluid-structure interaction (FSI) problem with a characteristic time scale of milliseconds to seconds, as well as a plaque growth process governed by reaction-diffusion equations, which takes place over several months. In this work we combine a temporal homogenization approach, which separates the problem in computationally expensive FSI problems on a micro scale and a reaction-diffusion problem on the macro scale, with parallel time-stepping algorithms. It has been found in the literature that parallel time-stepping algorithms do not perform well when applied directly to the FSI problem. To circumvent this problem, a parareal algorithm is applied on the macro-scale reaction-diffusion problem instead of the micro-scale FSI problem. We investigate modifications in the coarse propagator of the parareal algorithm, in order to further reduce the number of costly micro problems to be solved. The approaches are tested in detailed numerical investigations based on serial simulations.

Haemodynamic Effects on the Development and Stability of Atherosclerotic Plaques in Arterial Blood Vessel.

Studying the formation and stability of atherosclerotic plaques in the hemodynamic field is essential for understanding the growth mechanism and preventive treatment of atherosclerotic plaques. In this paper, based on a multiplayer porous wall model, we established a two-way fluid-solidinteraction with time-varyinginlet flow. The lipid-rich necrotic core (LRNC) and stress in atherosclerotic plaque were described for analyzing the stability of atherosclerotic plaques during the plaque growth by solving advection-diffusion-reaction equations with finite-element method. It was found that LRNC appeared when the lipid levels of apoptotic materials (such as macrophages, foam cells) in the plaque reacheda specified lowerconcentration, and increased with the plaque growth. LRNC was positively correlated with the blood pressure and was negatively correlated with the blood flow velocity. The maximum stress wasmainlylocatedat the necrotic core and graduallymovedtoward the left shoulder of the plaque with the plaque growth, which increases the plaque instability and the risk of the plaque shedding. The computational model may contribute to understanding the mechanisms of early atherosclerotic plaque growth and the risk of instability in the plaque growth.

Vascular Electrical Stimulation with Wireless, Battery-Free, and Fully Implantable Features Reduces Atherosclerotic Plaque Formation Through Sirt1-Mediated Autophagy.

Electrical stimulation (ES) is a safe and effective procedure in clinical rehabilitation with few adverse effects. However, studies on ES for atherosclerosis (AS) are scarce because ES does not provide a long-term intervention for chronic disease processes. Battery-free implants and surgically mounted them in the abdominal aorta of high-fat-fed Apolipoprotein E (ApoE-/- ) mice are used, which are electrically stimulated for four weeks using a wireless ES device to observe changes in atherosclerotic plaques. Results showed that there is almost no growth of atherosclerotic plaque at the stimulated site in AopE-/- mice after ES. RNA-sequencing (RNA-seq) analysis of Thp-1 macrophages reveal that the transcriptional activity of autophagy-related genes increase substantially after ES. Additionally, ES reduces lipid accumulation in macrophages by restoring ABCA1- and ABCG1-mediated cholesterol efflux. Mechanistically, it is demonstrated that ES reduced lipid accumulation through Sirtuin 1 (Sirt1)/Autophagy related 5 (Atg5) pathway-mediated autophagy. Furthermore, ES reverse autophagic dysfunction in macrophages of AopE-/- mouse plaques by restoring Sirt1, blunting P62 accumulation, and inhibiting the secretion of interleukin (IL)-6, resulting in the alleviation of atherosclerotic lesion formation. Here, a novel approach is shown in which ES can be used as a promising therapeutic strategy for AS treatment through Sirt1/Atg5 pathway-mediated autophagy.

Bruton's Tyrosine Kinase inhibition by Acalabrutinib does not affect early or advanced atherosclerotic plaque size and morphology in Ldlr-/- mice

Atherosclerosis is characterized by the accumulation of lipids and immune cells, including mast cells and B cells, in the arterial wall. Mast cells contribute to atherosclerotic plaque growth and destabilization upon active degranulation. The FcεRI-IgE pathway is the most prominent mast cell activation route. Bruton's Tyrosine Kinase (BTK) is involved in FcεRI-signaling and may be a potential therapeutic target to limit mast cell activation in atherosclerosis. Additionally, BTK is crucial in B cell development and B-cell receptor signaling. In this project, we aimed to assess the effects of BTK inhibition on mast cell activation and B cell development in atherosclerosis.In human carotid artery plaques, we showed that BTK is primarily expressed on mast cells, B cells and myeloid cells. In vitro, BTK inhibitor Acalabrutinib dose-dependently inhibited IgE mediated activation of mouse bone marrow derived mast cells. In vivo, male Ldlr−/− mice were fed a high-fat diet for eight weeks, during which mice were treated with Acalabrutinib or control solvent. In Acalabrutinib treated mice, B cell maturation was reduced compared to control mice, showing a shift from follicular II towards follicular I B cells. Mast cell numbers and activation status were not affected. Acalabrutinib treatment did not affect atherosclerotic plaque size or morphology. In advanced atherosclerosis, where mice were first fed a high-fat diet for eight weeks before receiving treatment, similar effects were observed.Conclusively, BTK inhibition by Acalabrutinib alone did neither affect either mast cell activation nor early- and advanced atherosclerosis, despite the effects on follicular B cell maturation.

San-wei-tan-xiang capsule attenuates atherosclerosis by increasing lysosomal activity in adipose tissue macrophages

Ethnopharmacological relevanceDyslipidemia is the leading risk factor of atherosclerosis (AS). Adipose tissue macrophages (ATMs) can regulate postprandial cholesterol levels via uptake and hydrolyzation of lipids and regulation of macrophage cholesterol efflux (MCE). San-wei-tan-xiang (SWTX) capsule, a Traditional Chinese medicine, exerts clinical benefits in patients with atherosclerotic cardiovascular diseases. Aim of the studyThis work is aimed to evaluate the chemical ingredients and mechanisms of SWTX in anti-AS. Materials and methodsThe chemical ingredients of SWTX identified by liquid chromatography coupled with tandem mass spectrometry were used for network pharmacological analysis. The atheroprotective function of SWTX was evaluated in ApoE−/− mice fed a cholesterol-enriched diet. ResultsThe chemical ingredients identified in SWTX were predicated to be important for lipid metabolism and AS. Animals studies suggested that SWTX effectively attenuated the atherosclerotic plaque growth, elevated postprandial HDL cholesterol levels, elevated the proportion of Tim4 and CD36-expressed ATMs, and upregulated the uptake of lipid and lysosomal activity in ATMs. SWTX-induced elevation of postprandial HDL cholesterol levels was dependent on increased lysosomal activity, since chloroquine, an inhibitor of lysosomal function, blocked the effect of SWTX. Lastly, some predicated bioactive compounds in SWTX can elevate lysosomal activity in vitro. ConclusionSWTX could attenuate atherosclerotic plaque formation by elevating lysosomal activity and enhancing MCE in ATMs.

Ulcerative colitis and cardiovascular disease. Case report

This article describes a clinical case of a patient suffering from ulcerative colitis and cardiovascular pathology for a long time. In the clinical case, a patient with a late onset of ulcerative colitis and a sharp deterioration in cardiovascular pathology is presented. This combination of diseases is of clinical interest, because according to existing data, inflammatory bowel diseases (IBD) are predictors of increased cardiovascular risk. The clinical case describes the therapy of inflammatory bowel diseases, which can stop the symptoms of the disease and thereby reduce the risk of progression of cardiovascular pathology, describes the hypotensive, hypolipidemic therapy received by the patient. Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), affect not only the gastrointestinal tract, but also have extra-intestinal manifestations. For example, IBD develops chronic inflammation syndrome, which leads to the development of endothelial dysfunction and accelerated growth of atherosclerotic plaques. Given that inflammation triggers the early stages of atherogenesis, and an increase in inflammatory cytokines is accompanied by a higher cardiovascular risk, today there is an assumption that patients suffering from IBD have a higher risk of developing cardiovascular events than healthy ones. In our clinical case, the latest data on IBD as a risk factor for cardiovascular diseases are presented. Infl mmation plays a key role in the development of IBD and cardiovascular pathology. Understanding the main mechanisms underlying these diseases and leading to increased cardiovascular risk and worsening prognosis in patients with IBD will optimize treatment tactics and, thus, reduce the number of adverse events and mortality in this cohort of patients. The purpose of our clinical case is to attract special attention to this cohort of patients from cardiologists, gastroenterologists and therapists in order to be able to consider starting preventive prevention as early as possible.

Wall Shear Stress Measurement in Carotid Artery Phantoms with Variation in Degree of Stenosis Using Plane Wave Vector Doppler

Wall shear stress (WSS) plays an important role in the formation, growth, and rupture of atherosclerotic plaques in arteries. This study measured WSS in diseased carotid artery phantoms with degrees of stenosis varying from 0 to 60% with both steady and pulsatile flow. Experiments were performed using in silico and real flow phantoms. Blood velocities were estimated using plane wave (PW) vector Doppler. Wall shear stress was then estimated from the velocity gradient near the wall multiplied by the viscosity of a blood-mimicking fluid. The estimated WSS using the in silico phantom agreed within 10% of the ground-truth values (root-mean-square error). The phantom experiment showed that the mean WSS and maximum WSS increased with the increasing degree of stenosis. The simulation and experiment results provide the necessary validation data to give confidence in WSS measurements in patients using the PW vector Doppler technique.