Arterial Wall Research Articles

Interaction of a self-expandable stent with the arterial wall in the presence of hypocellular and calcified plaques.

Self-expandable stents manufactured from nitinol alloys are commonly utilized alongside traditional balloon-expandable stents to provide scaffolding to stenosed arteries. However, a significant limitation hampering stent efficacy is restenosis, triggered by neointimal hyperplasia and resulting in the loss of gain in lumen size, post-intervention. In this study, a nonlinear finite element model was developed to simulate stent crimping and expansion and its interaction with the surrounding vessel in the presence of a plaque. The main aim was to determine contact pressures and forces induced at the interface between an artery wall with hypocellular and calcified plaques and an expanded stent. The results demonstrated the drawbacks of plaque calcification, which triggered a sharp contact pressure and radial force surge at the interface as well as a significant rise in von Mises stress within the vessel, potentially leading to rupture and restenosis. A regression line was then established to relate hypocellular and calcified plaques. The adjusted coefficient of determination indicated a good correlation between contact pressures for calcified and hypocellular plaque models. Regarding the directionality of wall properties, contact pressure and force observations were not significantly different between isotropic and anisotropic arteries. Moreover, variations in friction coefficients did not substantially affect the interfacial contact pressures.

Hypercholesterolemia and inflammation-Cooperative cardiovascular risk factors.

Maintaining low concentrations of plasma low-density lipoprotein cholesterol (LDLc) over time decreases the number of LDL particles trapped within the artery wall, slows the progression of atherosclerosis and delays the age at which mature atherosclerotic plaques develop. This substantially reduces the lifetime risk of atherosclerotic cardiovascular disease (ASCVD) events.In this context, plaque development and vulnerability result not only from lipid accumulation but also from inflammation. Changes in the composition of immune cells, including macrophages, dendritic cells, T cells, B cells, mast cells and neutrophils, along with altered cytokine and chemokine release, disrupt the equilibrium between inflammation and anti-inflammatory mechanisms at plaque sites. Considering that it is not a competition between LDLc and inflammation, but instead that they are partners in crime, the present narrative review aims to give an overview of the main inflammatory molecular pathways linked to raised LDLc concentrations and to describe the impact of lipid-lowering approaches on the inflammatory and lipid burden. Although remarkable changes in LDLc are driven by the most recent lipid lowering combinations, the relative reduction in plasma C-reactive protein appears to be independent of the magnitude of LDLc lowering. Identifying clinical biomarkers of inflammation (e.g. interleukin-6) and possible targets for therapy holds promise for monitoring and reducing the ASCVD burden in suitable patients.

Dual-Activated Photoacoustic Probe for Reliably Detecting Hydroxyl Radical in Ischemic Cardiovascular Disease in Mouse and Human Samples.

Cardiovascular disease (CVD) is a chronic disease characterized by the accumulation of lipids and fibrous tissue within the arterial walls, potentially leading to vascular obstruction and an increased risk of heart disease and stroke. Hydroxyl radicals play a significant role in the formation and progression of CVD as they can instigate lipid peroxidation, resulting in cellular damage and inflammatory responses. However, precisely detecting hydroxyl radicals in CVD lesions presents significant challenges due to their high reactivity and short lifespan. Herein, we present the development and application of a novel activatable optical probe, Cy-OH-LP, designed to detect hydroxyl radicals in lipid-rich environments specifically. Built on the Cy7 molecular skeleton, Cy-OH-LP exhibits near-infrared absorption and fluorescence characteristics, and its specific response to hydroxyl radicals enables a turn-on signal in both photoacoustic and fluorescence spectra. The probe demonstrated excellent selectivity and stability in various tests. Furthermore, Cy-OH-LP was successfully applied in an in vivo model to detect hydroxyl radicals in mouse models, providing a potential tool for diagnosing and monitoring AS. The biosafety of Cy-OH-LP was also verified, showing low cytotoxicity and no significant organ damage in mice. The findings suggest that Cy-OH-LP is a promising tool for the specific detection of hydroxyl radicals in lipid-rich environments, providing new possibilities for research and clinical applications in the field of oxidative stress-related diseases.

Arterial Properties and Ventricular-Arterial Interactions in Severe Aortic Stenosis: Impact on Prognosis.

Systemic arterial properties contribute to clinical heterogeneity and outcomes in degenerative calcific aortic stenosis (AS). Lumped parameters of afterload have previously been associated with adverse left ventricular remodeling, mortality, and poor exercise tolerance in this population, but most studies did not assess pulsatile aortic pressure-flow relations, the gold standard method for assessing arterial load. Moreover, arterial compliance is highly dependent on non-pulsatile (mean) arterial pressure, which influences prognosis in this population. We retrospectively studied 135 patients with severe AS with same-day catheterization and echocardiogram. Invasive aortic pressures and echocardiographic flow waveforms were used to assess pressure-flow and pressure-volume relations using Windkessel modeling and wave separation analyses. We used Cox regression to assess the relationship between pulsatile load and time to death and heart failure hospital admission (DHFA). Total arterial compliance accounting for pressure-dependence (PD-TAC) was independently predictive of all-cause mortality (HR=0.80, 95%CI=0.66-0.97; p=0.023) and DHFA (HR=0.70; 95%CI=0.50-0.97; p=0.031) even after adjustment for age, race, gender, BMI, and comorbidities, while other arterial parameters were not. In patients with severe AS, pressure-dependent arterial compliance predicts adverse outcomes, while traditional pulsatile arterial load measures do not. Our findings suggest that methods accounting for pressure load on the arterial wall are advantageous in this population in which lower mean pressure can result from severe stenosis and ventricular dysfunction.

Benefit of Probiotics on Cardiovascular Health- A Narrative Review

Coronary artery disease (CAD) is a leading cause of death globally and a prevalent cardiovascular disease (CVD) in which plaque buildup in artery walls results in inadequate blood flow. Risk factors for CAD include hypertension, inflammation, diabetes, and poor diet. In the past few decades, research has emerged on the employment of probiotics in cardiovascular health, particularly focused on methods for using probiotics as preventative measures for the risk factors of CAD. Probiotics can reduce hypertension and inflammation, improve insulin sensitivity, and possibly reduce salt levels in individuals with high-sodium diets. Still, more research needs to be done on the safety and considerations of administering probiotics and their underlying mechanisms since the evidence is predominantly experimental. Probiotics have proven to be a valuable research point given the urgency and incidence rates of coronary artery disease.

Cardiovascular Disease May Be Triggered by Gut Microbiota, Microbial Metabolites, Gut Wall Reactions, and Inflammation

Cardiovascular disease (CVD) may be inherited, as recently shown with the identification of single nucleotide polymorphisms (SNPs or “snips”) on a 250 kb DNA fragment that encodes 92 proteins associated with CVD. CVD is also triggered by microbial dysbiosis, microbial metabolites, metabolic disorders, and inflammatory intestinal epithelial cells (IECs). The epithelial cellular adhesion molecule (Ep-CAM) and trefoil factor 3 (TFF3) peptide keeps the gut wall intact and healthy. Variations in Ep-CAM levels are directly linked to changes in the gut microbiome. Leptin, plasminogen activator inhibitor 1 (PAI1), and alpha-1 acid glycoprotein 1 (AGP1) are associated with obesity and may be used as biomarkers. Although contactin 1 (CNTN1) is also associated with obesity and adiposity, it regulates the bacterial metabolism of tryptophan (Trp) and thus appetite. A decrease in CNTN1 may serve as an early warning of CVD. Short-chain fatty acids (SCFAs) produced by gut microbiota inhibit pro-inflammatory cytokines and damage vascular integrity. Trimethylamine N-oxide (TMAO), produced by gut microbiota, activates inflammatory Nod-like receptors (NLRs) such as Nod-like receptor protein 3 (NLRP3), which increase platelet formation. Mutations in the elastin gene (ELN) cause supra valvular aortic stenosis (SVAS), defined as the thickening of the arterial wall. Many of the genes expressed by human cells are regulated by gut microbiota. The identification of new molecular markers is crucial for the prevention of CVD and the development of new therapeutic strategies. This review summarizes the causes of CVD and identifies possible CVD markers.

The role of biomarkers on hemodynamics in atherosclerotic artery

Atherosclerosis, a chronic inflammatory cardiovascular disease, leads to arterial constriction caused by the accumulation of lipids, cholesterol, and various substances within artery walls. Such plaque can rupture, resulting in a blood clot that obstructs major arteries and may initiate myocardial infarction, ischemic stroke, etc. Atherosclerotic plaque formation begins with the accumulation of foam cells and macrophages within the intima layer of the arterial wall. At the latter stage, the smooth muscle cells migrated from deeper artery wall layers, contributing to the fibrous cap formation and plaque stabilizing. A developed plaque gradually enters the lumen and narrows down the lumen to impede blood flow. We introduce a two-phase and macroscopic model to investigate the progression of plaque growth in its advanced stage and analyze the minimum gap (Lumen Clearance) within an atherosclerotic artery so that blood cells can pass through. Cardiac troponin, a high specificity and sensitivity biomarker, facilitates early detection of elevated myocardial infarction, ischemic stroke risks, etc. This study aims at establishing a relationship between the troponin concentration in atherosclerotic arteries and their internal clearance, which could significantly improve our understanding of disease progression. Our observations show that the plaque undergoes rapid evolution in its initial stages, gradually slowing down over time to reach a stable state. A positive correlation exists between the maximum plaque depth and cardiac troponin concentration in the blood. However, the lumen clearance exhibits the opposite behavior. The speed of blood cells slows down at an enhanced plaque depth within atherosclerotic arteries.

CBL-b E3 ligase-mediated neddylation and activation of PARP-1 induce vascular calcification

Vascular calcification (VC) refers to the accumulation of mineral deposits on the walls of arteries and veins, and it is closely associated with increased mortality in cardiovascular disease patients, particularly among high-risk patients with diabetes and chronic kidney disease (CKD). Neuronal precursor cell-expressed developmentally downregulated protein 8 (NEDD8) is a ubiquitin-like protein that plays a pivotal role in various cellular functions, primarily through its conjugation to target proteins and subsequent relay of biological signals. However, the role of NEDDylation in VC has not been investigated. In our study, we observed that MLN4924, an inhibitor of the NEDD8-activating E1 enzyme, effectively impedes the progression of VC. LC‒MS/MS analysis revealed that poly(ADP‒ribose) polymerase 1 (PARP-1) is subjected to NEDD8 conjugation, leading to an increase in PARP-1 activity during VC. We subsequently revealed that PARP-1 NEDDylation is mediated by the E3 ligase CBL proto-oncogene B (CBL-b) and is reversed by NEDD8-specific protease 1 (NEDP-1) during VC. Furthermore, the CBL-b C373 peptide effectively mitigated the inactive form of the E3 ligase activity of CBL-b, ultimately preventing VC. These findings provide compelling evidence that the NEDD8-dependent activation of PARP-1 represents a novel mechanism underlying vascular calcification and suggests a promising new therapeutic target for VC.

Simulation of plaque formation in a realistic geometry of a human aorta: effects of endothelial layer properties, heart rate, and hypertension.

Nowadays, cardiovascular diseases are the most common cause of death worldwide. Besides, atherosclerosis is a cardiovascular disease that occurs with persistent narrowing of arteries, especially medium and large-sized arteries. Atherosclerosis begins with a local elevation in the permeability of the arterial wall as a result of endothelial inflammation. Subsequently, excess LDL permeates into the arterial wall. Then, through several chemical responses and reactions, foam cells are produced. These foam cells serve as a crucial indicator for assessing the development of atherosclerosis within the arteries. In this study, the effect of endothelial layer modeling, heart rate (HR) and hypertension on the foam cell accumulation is numerically investigated in a patient-specific geometry of the human thoracic aorta. Navier-Stokes, Darcy, and mass transfer equations are used to obtain the velocity and concentration field within the domain. Regarding the dependence of endothelial cell properties on time-averaged wall shear stress, it is observed that foam cells are mainly concentrated in the outer curvature of the aortic arch, downstream of the left subclavian artery. However, considering oscillatory-shear-rate as the determinant of endothelial cell properties leads to the accumulation of foam cells in the inner curvature of the descending aorta. Regarding the HR, with the increase of HR, the volume average concentration of the foam cell decreases. However, there is no substantial difference between the cases of different HRs. Moreover, foam cell concentration significantly increases in the hypertension case. This result implies that a slight increase in the blood pressure may induce irreparable problems in the circulatory system.

Contribution of the arterial cells to atherosclerosis and plaque formation.

Atherosclerosis is commonly known as an inflammatory disease that is characterized by lipid deposition in the arterial wall, causing gradual restriction or complete blockade of blood flow, which can cause complications such as myocardial infarction, stroke, or peripheral artery disease. Several factors contribute to initiation and progression of atherosclerotic plaque formation. The role of macrophages and leukocytes in atherosclerosis has been well explored. Here, we provide an overview of what has been reported on the role and impact of the arterial cells on plaque formation, and vice versa. The atherogenic environment can trigger transformation and dedifferentiation of the endothelial cells (ECs), smooth muscle cells, and fibroblasts (FBs) whereby they can either directly contribute to plaque formation or influence its composition. Recent studies have demonstrated the plasticity in the identity of the arterial cells, the formation of intermediate cell types that share the characteristics of multiple cell types, and have revealed novel roles and functions for these cells in atherosclerosis. The potential for all vascular cells to cross-transdifferentiate, and detection of cells with mosaic characteristics in the atherosclerotic plaques reveal that the plaque environment is a complex and dynamic environment that could regulate the disease progression independent from the circulating lipid levels. We will also provide an overview on the interplay between sex and atherosclerosis, which has remained an underexplored area.

Understanding the Complex Interplay of Epigenetic Factors in Atherosclerosis: A Review

This review focuses on the epigenetic factors that play a vital role in the formation of plaques and lead to atherosclerosis and related diseases in humans during current times. Apart from the epigenetics there are plenty more factors that influence the atherosclerotic risk in the older population of the current era. Lack of physical activities has become one of the most commonly found traits that causes obesity in people especially the middles aged adults. People working 9 - 5 in an office, or an IT firm tend spend idle time with their computer for 4 - 5 consecutive hours with barely changing their position. Lack of exercise tends to affect not only the physical health but also stress a person mentally. Chronic inflammatory diseases like atherosclerosis have a major role in the morbidity and mortality from cardiovascular disease worldwide. Atherosclerotic plaques are created by the pathophysiological process of lipids, inflammatory cells and fibrous components gradually accumulating within artery walls. Endothelial dysfunction signals the start of atherosclerosis and allows low-density lipoproteins (LDL) to enter the subendothelial region. Oxidative stress-induced changes in retained low-density lipoprotein (LDL) set off an inflammatory cascade that draws T cells and monocytes to the site of the lesion. The interaction of these immune cells with the local vascular cells encourages the production of foam cells, which fills the plaque’s centre with lipids. Smooth muscle cells multiply and help produce fibrous caps as the lesion ages, which affects the stability of the plaque. Studies shows how the brain responds to physical labour and how differently the effectively the enzymes and hormones are secreted, and their actions are vastly guided based on the physical stress an individual undergoes. Among the most prominent causes of atherosclerosis epigenetics has been focussed majorly in this review, where we focus on the underlying genetic factors that play a vital role in atherosclerosis and related cardiovascular diseases and also the genetic approach to a treatment is also elaborated. A number of miRNAs are involved in the cause/cure for the atherosclerosis, the following tables give an outlook regarding the same. This review aims to focus on the causes, risk factors, pathophysiology and the treatment and therapies that are currently available all the way concentrating on the genetic approach in the above-mentioned perspective. HIGHLIGHTS The review revolves around the modifiable and non-modifiable risk factors leading to atherosclerosis. Key risk factors and epigenetics causes of atherosclerosis and atherosclerosis related Cardio vascular Diseases (CVD). The article explains in detail regarding the pathophysiology of atherosclerosis. The progression and stages of atherosclerosis. GRAPHICAL ABSTRACT

Unsteady solute dispersion in large arteries under periodic body acceleration

The present study investigates the effect of periodic body acceleration on solute dispersion in blood flow through large arteries. Transport coefficients (i.e., exchange, convection, and dispersion coefficients) and mean concentration of the solute are analyzed in the presence of wall absorption. The solute is quickly transported to the wall of arteries with a smaller radius, whereas the opposite is true for arteries with a larger radius. In the presence of body acceleration, the amplitude of fluctuations of the convection coefficient K1(t) increases significantly as the radius of the artery increases. In contrast, an opposite scenario exists for the dispersion coefficient K2(t). The solute dispersion process becomes more effective in arterial blood flow as the radius of the artery decreases. More interestingly, in large arteries with body acceleration, the solute is convected, dispersed, and distributed more toward the upstream direction owing to flow reversal during the diastolic phase of pressure pulsation. Note that this important feature of flow reversal is solely due to periodic body acceleration. For an artery with a small radius, under the influence of periodic body acceleration, the mean concentration of solute Cm is the minimum, and more axial spread is noticed in the axial direction. In contrast, an opposite scenario arises in the artery with a large radius. Additionally, the effect of body acceleration on the shear-induced diffusion of red blood cells is discussed in blood flow.

Relationship Between Early and Established Rheumatoid Arthritis Vascular Change of the Dorsalis Pedis Artery Observed with Ultrasound Imaging

BackgroundDespite early treatment of rheumatoid arthritis (RA) being well established to prevent erosive joint damage, studies report persistent moderate to high disease activity. Other pathologies, for example, rheumatoid vasculitis (RV) may contribute symptoms that may not be captured by existing clinical assessment. ObjectivesTo investigate ultrasound-observed changes in the proximal dorsalis pedis artery (DPA) between early (≤ 5 y) and established (>5 y) RA and the RA Disease Activity Index-5 (RADAI-5). MethodsParticipants with early (n = 20) and established RA (n = 20) were recruited. Five parameters of the DPA were examined with a previously established ultrasound method. Independent t-tests and Cohen d statistics assessed differences and effect size between ultrasound parameters and RADAI-5, and the two groups. Pearson correlation assessed associations between ultrasound parameters and RADAI-5. ResultsMajority of participants (98%) demonstrated arterial wall thickening regardless of disease duration. However, lumen diameter (Cohen's d = 0.972, p = 0.004) and artery diameter (Cohen's d = 0.694, p = 0.034) were decreased in established RA compared to early RA. No strong associations were found between RADAI-5 and ultrasound parameters, except for lumen diameter in early RA demonstrating a fair association to RADAI-5 (r = 0.445). The mean RADAI-5 score indicated moderate to high disease activity with no difference between early and established RA (p = 0.283). ConclusionArterial wall thickening of the DPA indicating the precursory changes of RV was observed in most RA participants, with reductions in artery and lumen diameter occurring in established disease. However, the long-standing instrument RADAI-5 may not reflect symptoms and clinical impacts related to vascular changes among people with RA.

Whole-body insulin resistance leads to accelerated atherosclerosis: role for Nox2 NADPH oxidase.

Insulin resistance underpins the progression of type 2 diabetes mellitus and leads to a collection of risk factors for the development of atherosclerosis. Whether or not insulin resistance at a whole-body level per se leads to accelerated atherosclerosis is unclear. To answer this question, we generated atherosclerosis-prone mice with whole-body insulin resistance secondary to haploinsufficiency of the insulin receptor (IR+/-) deficient in ApoE-/- (IR+/-/ApoE-/-). IR+/-/ApoE-/- and ApoE-/- littermates had similar weight, lipids, and glucose tolerance at baseline. After 12 weeks of Western high-cholesterol diet, IR+/-/ApoE-/- had significantly more atherosclerosis in the thoracoabdominal aorta and at the level of the aortic sinus than ApoE-/- littermates. Excess Nox2 NADPH oxidase (Nox2) derived superoxide has been suggested to underpin diabetes-related atherosclerosis. In IR+/-/ApoE-/- we examined the effect of inhibiting Nox2 using genetic or pharmacological approaches on the development of atherosclerosis. To genetically delete Nox2, we generated IR+/-/ApoE-/-/Nox2-/y and to inhibit Nox2 pharmacologically, we treated IR+/-/ApoE-/- with the peptide Nox2 inhibitor gp91dstat. IR+/-/ApoE-/-/Nox2-/y had significant disruption of the aortic wall with increased thoracoabdominal atherosclerosis when compared to IR+/-/ApoE-/-/Nox2+/y littermates. Inhibition of Nox2 using gp91dstat reduced atherosclerosis in the thoracoabdominal aorta of IR+/-/ApoE-/-. Whole-body insulin resistance accelerates the development of atherosclerosis. Genetic inhibition of Nox2 leads to disruption of the aortic wall in IR+/-/ApoE-/- mice with accelerated atherosclerosis, whereas pharmacological Nox2 inhibition reduces atherosclerosis in IR+/-/ApoE-/- without disruption of the arterial wall.

Management of patients developing axillary pseudoaneursym after ductal stenting: Report of three cases

Pseudoaneurysms develop as a result of disruption of the arterial wall due to trauma or iatrogenic reasons such as catheterization, and it is important due to the high risk of bleeding and rupture. Until recently, the main treatment of pseudoaneurysms was surgical repair. However, in recent years, minimally invasive methods such as ultrasound-guided compression and percutaneous thrombin injection have been used more frequently. In this article, the clinical course and findings of three different cases who developed pseudoaneurysm as a result of stenting the ductus arteriosus via the axillary artery were discussed.

Comparison of Laminar and Turbulent K–Omega Shear Stress Transport Models Under Realistic Boundary Conditions Using Clinical Data for Arterial Stenosis

Abstract Early diagnosis of cardiovascular diseases (CVDs), including arterial stenosis, enables targeted treatments that reduce CVD mortality. It is vital to improve the accuracy of early diagnostic tools. Current computational studies of stenosis use mathematical models, such as laminar and k–omega shear stress transport (SST) models, available in ansys (Fluent and CFX), openfoam, and comsol software packages. Users can adjust boundary conditions, such as inlet velocity and outlet pressure using user-defined functions (UDFs) with different expressions and constant values. However, currently there is no rule over what to impose at these boundaries, and previous studies have used various assumptions, such as rigid artery wall, one-way fluid–structure interaction (FSI) or two-way FSI, and the blood's Newtonian or non-Newtonian material properties. This variety in construction has associated deviations of the models from the clinical data and lessens the value of the models as potential diagnostic or predictive tools for medical practitioners. In this study, we examine arterial stenosis models, with severities of 20%, 40%, and 50%, compared with the healthy artery analyzed in terms of strain energy to the artery wall. Additionally, we investigate elastic walls using one-way FSI, comparing with laminar and k–omega SST. These boundary conditions are based on clinical data. The results regarding the strain energy (mJ) behavior along the artery wall show that the k–omega SST model outperforms the laminar model for short arterial segments and under the Newtonian assumption with a no-slip boundary wall and turbulent flow.

Morphological rationale for surgical treatment of patients with true splenic artery aneurysm

Aim. To study the morphological features of the wall structure of the splenic artery aneurysm in order to identify the safest and most effective method of surgical treatment.Materials and methods. From 2020 to 2023, 43 patients underwent surgery for true splenic artery aneurysm. Interventions involved laparoscopic clipping of aneurysm branches, laparoscopic resection of aneurysm, laparoscopic splenectomy, and resection of giant splenic artery aneurysm. A clinical and morphological study of 16 slides of splenic artery aneurysm was performed. The aneurysm wall and the adjacent wall of the splenic artery without macroscopic signs of lumen dilatation for 1 cm from the aneurysmal dilatation were examined.Results. Microscopic study revealed fragments of loose, edematous wall of large elastic arteries with atherosclerosis, atheromatosis and calcification. Atherosclerotic plaques were observed in the intima; calcium deposits were detected in 81.25% of slides, and defects in elastic fibers – in all slides. The elastic membrane was thinned or had a discontinuous structure. Morphological changes in the wall of the splenic artery persisted up to 1.0 ± 0.2 cm proximal and distal to the aneurysm.Conclusion. Taking into account the revealed features of the morphological structure of the aneurysm, the formation of an end-to-end vascular anastomosis of the splenic artery, clipping or suturing of the aneurysm neck pose a significant risk of aneurysm recurrence. Laparoscopic clipping of splenic artery aneurysm branches at a distance of >1.5 cm from the edges of the aneurysm becomes the operation of choice for patients in this category.

Nonlinear biomechanical behaviour of extracranial carotid artery aneurysms in the framework of Windkessel effect via FSI technique

Extracranial carotid artery aneurysms (ECCA) lead to rupture and neurologic symptoms from embolisation, with potentially fatal outcomes. Investigating the biomechanical behaviour of EECA with blood flow dynamics is crucial for identifying regions more susceptible to rupture. A coupled three-dimensional (3D) Windkessel-framework and hyperelastic fluid-structure interaction (FSI) analysis of ECCAs with patient-specific geometries, was developed in this paper with a particular focus on hemodynamic parameters and the arterial wall's biomechanical response. The blood flow has been modelled as non-Newtonian, pulsatile, and turbulent. The biomechanical characteristics of the aneurysm and artery are characterised employing a 5-parameter Mooney-Rivlin hyperelasticity model. The Windkessel effect is also considered to efficiently simulate pressure profile of the outlets and to capture the dynamic changes over the cardiac cycle. The study found the aneurysm carotid artery exhibited the high levels of pressure, wall shear stress (WSS), oscillatory shear index (OSI), and relative residence time (RRT) compared to the healthy one. The deformation of the arterial wall and the corresponding von Mises (VM) stress were found significantly increased in aneurysm cases, in comparison to that of no aneurysm cases, which strongly correlated with the hemodynamic characteristics of the blood flow and the geometric features of the aneurysms. This escalation would intensify the risk of aneurysm wall rupture. These findings have critical implications for enhancing treatment strategies for patients with extracranial aneurysms.

Myogenic response of the cerebral vessel: a mathematical model

The myogenic response is most typical for small arterial vessels and consists in constriction of the vessel with an increase in transmural pressure, the pressure difference between the inner and outer surfaces of the vascular wall. There are many models describing this response. In models of last decades, in addition to macrostretchings and macrostrains, their microanalogues are introduced into consideration, that significantly complicates the description. In the presented work a simple model of the wall of the small cerebral artery is described, which includes the main parameters that control the myogenic response and corresponds to physiological processes underlining this response. It is believed that active stresses depend on stretching and the concentration of free calcium ions in the cytoplasm of the smooth muscle cell. In turn, the calcium content depends on the membrane potential, determined by the pressure. An axisymmetric stationary problem is considered; the wall material in the non-activated state is assumed to be pseudoelastic. Calculations showed a qualitative difference in the dependence of active stress on stretching and its distribution in the radial direction before and after the development of the vascular response. The calculated diameter values before and after exposure to substances affecting the polarization of the smooth muscle cell membrane are within the range of experimental values. These results indicate that the introduction of the dependence of calcium concentration on membrane potential expands the area of applicability of simple models of this kind for evaluating the value of vascular diameter.

Development and approval of a mobile test bench for the study of the mechanical properties of biological tissues

The determination of the mechanical properties of vessel walls and atherosclerotic plaques is a recurring issue in the numerical modelling of vessel sections. Testing machines are usually located in specialised laboratories outside medical facilities, and transporting samples from the clinic is difficult. Therefore, the task of developing mobile testing devices that can be installed directly in the clinic to perform tests immediately after surgery is relevant. This paper presents the results of the development and validation of a mobile test bench for performing mechanical experiments on uniaxial compression and tension of biological tissues. The purpose of the work is to perform mechanical tests on tissues in the clinic, avoiding their transport to the laboratory and/or freezing. Arduino UNO hardware platform is used as the control element of the test bench, which controls the main elements (motor, load cell), records data on SD card and displays information about the experiment on the computer screen. Structurally, the test bench is an analogue of a two-column testing machine. All mechanisms are assembled in a portable case, the control module is in the form of a remote plastic box. Verification of the test bench was carried out using an Instron 3342 universal testing machine with a 500 N load cell. A total of 121 soft tissue tests (including arterial wall and atherosclerotic plaque) were performed on the bench. The Young's modulus and ultimate strength values obtained are summarised in a table. The mean Young's modulus for the wall of the internal carotid artery was 0.32 ± 0.24 MPa, for soft plaque 0.30 ± 0.17 MPa, and for hard plaque 0.85 ± 0.39 MPa; a tensile strength of 1.12 ± 0.67 MPa was also determined for hard plaques in carotid arteries. The result is a unique database of tissue Young's moduli obtained from freshly collected material. The methodology and its implementation on the mobile test bench show good agreement with literature data.