Arterial Wall Stress Research Articles

Imminent risk of LVEF decline in asymptomatic patients with primary mitral regurgitation.

2020 American College of Cardiology/American Heart Association (ACC/AHA) Guidelines state that the ideal time for mitral valve surgery in primary mitral regurgitation (PMR) is when the LV approaches but has not yet reached echocardiographic LV ejection fraction (EF) < 60% or LV end-systolic dimension (ESD) > 40 mm. However, it is difficult to know the imminent risk of crossing this threshold when the surgical outcome is less optimal. Using machine learning and statistical models, we have shown that cardiac magnetic resonance (CMR) LV sphericity index (SI) and LV mid circumferential strain rate (SRcirc) added to LVEF and LVESD predict LVEF < 50% after mitral valve surgery. Here we test the hypothesis that these CMR features predict LVEF < 60% in asymptomatic PMR patients at 18 months. 33 asymptomatic PMR patients with moderate to severe mitral regurgitation had CMR with tissue tagging at baseline and every 6 months for 18 months. Two types of models were employed to predict LVEF < 60% at 18 months: a model using CMR features at a single time point (e.g., baseline) and a model utilizing repeated measurements over time. CMR LVEF decreased below 60% in 13 patients over 18 months. LVEF varied over time with an inverse relation to mean arterial pressure and mean end-systolic wall stress. Random Forest models utilizing LV SI, LV mid SRcirc, LVESD, and LVEF at a single time point (baseline) had a predictive accuracy of 64%. LV SI, LV mid SRcirc, LVESD and LVEF at baseline, 6, and 12 months achieved a higher predictive accuracy of 79%, improved sensitivity from 57% to 85% than baseline alone and identified a threshold of CMR LVEF 63%-64% signaling LVEF < 60%. The variability of LVEF due to blood pressure dependence may require a longitudinal study that incorporates LVEF, LVESD, SRcirc at multiple time points to identify the threshold at which LVEF is at risk for decline to less than 60%.

Clustering of vascular aging manifestations and incident cardiovascular events. The Paris Prospective Study III

Abstract Background Vascular aging is a key contributor to cardiovascular disease (CVD). Manifestations of vascular aging are heterogeneous and include atherosclerosis, arterial stiffening, increased arterial wall stress and arterial diameter enlargement. These manifestations have different pathophysiological mechanisms and likely require different prevention strategies. How the different vascular aging manifestations co-exist, or cluster, at the individual level and the association of any such clusters with incident CVD is unknown. Purpose To examine how vascular aging manifestations cluster and whether any such clusters are associated with incident CVD. Methods In the Paris Prospective Study III, a French community-based prospective study on novel determinants of CVD, 10,157 participants underwent a high-resolution carotid echotracking (Artlab, Esaote) between 2008 and 2012, and were thereafter monitored every two years for CVD events up to end 2020 . Hospitalized stroke and coronary heart disease (CHD) events were validated after the review of all medical records. Hierarchical clustering analysis was employed to identify patterns of vascular aging. Hazard ratios (HRs) were quantified in Cox models. Results The study sample included 8,360 participants (39% women, mean age 59.6 years) without prevalent CVD. Three clusters of vascular aging manifestations were identified: - Cluster 1 included 3,995 (47.8%) participants and was characterized by low prevalence of carotid plaques, low carotid intima-media thickness (IMT), low carotid artery stiffness, small carotid diameter and low carotid circumferential wall stress (healthy vascular aging cluster). - Cluster 2 included 2,109 (25.2%) participants and was characterized by high carotid artery stiffness and high carotid circumferential wall stress (arterial stiffness vascular aging cluster). - Cluster 3 included 2,256 (27.0%) participants, and was characterized by high prevalence of carotid plaques and high carotid IMT(atherosclerosis vascular aging cluster). After a median follow-up of 8.5 years, 108 incident stroke events, 218 CHD events and 192 deaths occurred. Compared with cluster 1, cluster 2 (HR 1.76, [95%CI, 1.06-2.94]), but not cluster 3 (HR 1.57, [0.94-2.62]), was associated with a higher risk of stroke. In addition, compared to cluster 1, cluster 3 (HR 1.53, [1.08-2.16]), but not cluster 2 (HR 1.38, [95% CI, 0.96-1.98]), was associated with higher risk of CHD. Both cluster 2 and 3 were associated with higher all-cause mortality (HR for cluster 2: 1.50, [1.02-2.21]; HR for cluster 3: 1.48, [1.01-2.17]). Internal validation using bootstrapping methods (n=1000 samples) provided consistent findings. Conclusion The simultaneous analysis of carotid-echotracking vascular aging parameters identified three patterns of vascular aging that are differentially associated with CHD and stroke in the community.Carotid properties by clustersKM survival curves by clusters

Determinants of vascular structure and function in at-risk children born to mothers managed for pre-eclampsia (FINNCARE study).

Pre-eclampsia (PE) is related to elevated blood pressure (BP) in children. The study aims to investigate if elevated BP is reflected in child arterial health and how anthropometrics, body composition, and gestational and perinatal factors influenced this. In this prospective cohort study, we assessed the arteries of 182 children exposed (46 had an early onset, with a diagnosis before 34 gestational weeks, and 136 had a late onset) and 85 children unexposed (non-PE) to PE at 8-12 years from delivery using ultra-high-frequency ultrasound in addition to ambulatory and central BPs, body composition and anthropometrics, and tonometry-derived pulse wave velocity (PWV). No differences were found in intima-media thickness (IMT), adventitia thickness (AT), lumen diameter (LD), local carotid artery stiffness, distensibility, or wall stress between PE-exposed and non-PE-exposed children. All children's brachial, radial, and femoral artery IMTs were associated with 24-h systolic BP (SBP) and pulse pressure, carotid-femoral PWV, and anthropometric measures. The 24-h SBP and anthropometrics, notably lean body mass, were independent predictors of peripheral artery IMTs (brachial R2 = 0.217, radial R2 = 0.208, femoral R2 = 0.214; p < 0.001). Head circumference predicted carotid artery IMT and LD (β = 0.163, p = 0.009; β = 0.417, p < 0.001, respectively), but carotid artery IMT was not associated with BP. No independent associations were found for peripheral artery ATs. Local carotid artery stiffness, distensibility, and wall stress were independently associated with adiposity. No significant associations were found between gestational or perinatal factors and child vascular health parameters. The peripheral artery IMT of PE-exposed children is identical to that of non-PE-exposed children, but associated with BP. Adiposity is related to local carotid artery stiffness. These adverse associations in arterial health may reflect the early progression of cardiovascular disease in PE-exposed children.

Unraveling the Links between Chronic Inflammation, Autoimmunity, and Spontaneous Cervicocranial Arterial Dissection.

Advances in imaging techniques have led to a rise in the diagnosis of spontaneous cervicocranial arterial dissection (SCCAD), which is now considered a common cause of stroke in young adults. However, our understanding of the pathophysiological mechanisms underlying SCCAD remains limited. Prior studies have proposed various factors contributing to arterial wall weakness or stress as potential causes for SCCAD. A combination of biopsies, case reports, and case-control studies suggests that inflammatory changes and autoimmunity may play roles in the cascade of events leading to SCCAD. In this review, we examine the close relationship between SCCAD, chronic inflammation, and autoimmune diseases, aiming to explore potential underlying pathophysiological mechanisms connecting these conditions. While some relevant hypotheses and studies exist, direct evidence on this topic is still relatively scarce. Further investigation of the underlying mechanisms in larger clinical cohorts is needed, and the exploration of animal models may provide novel insights.

Abstract Number ‐ 71: Management of Delayed Carotid Stent Fracture with an Overlapping Open Cell Design Stent: Case Report

Introduction Stent fracture after carotid angioplasty and stenting is rare. Risk factors include presence of angulation, calcification, and restenosis increasing the risk of stent fracture. Although literature indicates that not all carotid stent fractures are associated with adverse outcomes, there is limited details on successful endovascular management of this entity. We describe a unique case of carotid stent fracture with symptomatic restenosis treated with an overlapping open cell stent with no residual stenosis and resolution of symptomology. Methods Case Report. Results A 79‐year‐old man with medical history of right sided symptomatic carotid artery stenosis which had been previously treated with endarterectomy and subsequently carotid stenting after a follow up carotid ultrasound demonstrated recurrence of severe right internal carotid artery (RICA) stenosis. Approximately 2 years after this index procedure, the patient returned with acute onset of left‐hand numbness. Cerebral angiography was performed that demonstrated 85% stenosis with a fractured carotid stent at segment of stenosis (Figure 1A, B). Furthermore, the lesion was found to be heavily calcified. This was determined to be the primary contributing factor in resultant artery wall stress, which over time led to carotid stent fracture. Angioplasty with placement of a new open cell stent and distal embolic protective device was performed successfully. The open cell stent was chosen for this approach as closed cell stents have been associated with an increased odds of in‐hospital stroke/death for carotid lesions, attributable to the lower degree of conformability with closed cell stents. After our stent placement, there was no significant residual stenosis visualized (Figure 1C, D). The patient’s symptoms resolved without any subsequent complaints on follow‐up visit. Conclusions While carotid stent fractures are a rare occurrence, we report a case of symptomatic carotid artery restenosis with a fractured stent due to significant lesion calcification and wall stress. This case was successfully treated with angioplasty and new open cell stent placement due to its potential advantages over closed cell stents in carotid artery lesions. Current literature indicates that carotid stent fractures have a low prevalence. However, there is a paucity of studies on the mechanism of stent fracture as well as optimal management of these fractured stents, suggesting a need for further study and characterization.

Specialty Balloons for Vessel Preparation During Infrainguinal Endovascular Revascularization Procedures: A Review of Literature.

Balloon angioplasty with/without utilizing drug eluting technology or stenting constitutes the treatment of choice for a significant percentage of patients with peripheral artery disease requiring an intervention. However, in cases of diffuse disease and plaque complexity, angioplasty may lead to dissection, recoil, and/or early restenosis, making vessel preparation a key component for successful and durable endovascular revascularization outcome. This review of literature aims to present contemporary data for several commercially available specialty balloons that have been designed to minimize the arterial wall stress of conventional balloon angioplasty and facilitate technical success, as well as long-term patency.

Coupled Multiphysics Simulation using FEA for Complex Fluid-Structure Interaction Problems

In the realm of mechanical engineering, the accurate prediction of fluid-structure interaction (FSI) is paramount for the design and analysis of systems where fluids and structures coexist and interact. This research paper presents a novel approach to address complex FSI problems using coupled multiphysics simulation through Finite Element Analysis (FEA). The proposed methodology integrates advanced computational algorithms to capture the intricate interplay between fluid dynamics and structural mechanics, ensuring a more holistic representation of real-world scenarios. The developed framework was tested on a variety of benchmark problems, ranging from aeroelastic flutter in aircraft wings to blood flow-induced stresses in arterial walls. Results indicate a significant enhancement in prediction accuracy and computational efficiency compared to traditional decoupled methods. Furthermore, the study delves into the challenges faced during the coupling process, offering solutions to mitigate numerical instabilities and enhance convergence rates. The findings of this research not only pave the way for improved design and safety protocols in industries such as aerospace, biomedical, and civil engineering but also underscore the potential of Multiphysics simulation in unravelling the complexities of the natural world.

Comparative Assessment of Biomechanical Parameters in Subjects With Multiple Cerebral Aneurysms Using Fluid-Structure Interaction Simulations.

Cerebral aneurysm progression is a result of a complex interplay of the biomechanical and clinical risk factors that drive aneurysmal growth and rupture. Subjects with multiple aneurysms are unique cases wherein clinical risk factors are expected to affect each aneurysm equally, thus allowing for disentangling the effect of biomechanical factors on aneurysmal growth. Toward this end, we performed a comparative computational fluid-structure interaction analysis of aneurysmal biomechanics in image-based models of stable and growing aneurysms in the same subjects, using the cardiovascular simulation platform simvascular. We observed that areas exposed to low shear and the median peak systolic arterial wall displacement were higher by factors of 2 or more and 1.5, respectively, in growing aneurysms as compared to stable aneurysms. Furthermore, we defined a novel metric, the oscillatory stress index (OStI), which indicates locations of oscillating arterial wall stresses. We observed that growing aneurysms were characterized by regions of combined low wall shear and high OStI, which we hypothesize to be associated with regions of collagen degradation and remodeling. Such regions were either absent or below 5% of the surface area in stable aneurysms. Our results lay the groundwork for future studies in larger cohorts of subjects, to evaluate the statistical significance of these biomechanical parameters in cerebral aneurysm growth.

Numerical and Probabilistic Methods for Modeling of Abdominal Aortic Aneurysm Rupturing Risk

This study concerns to apply numerical methods and derives a comparative Abdominal Aortic Aneurysm (AAA). An accuracy comparison has been made using the index of rupturing risk versus one computed index. The study examines some factors such as age, Mean Arterial Pressure (MAP), stress-strain via the arterial wall stress (?), wall strength(S), and wall thickness (t). The qualms of AAA wall thickness are the most prevailing endogenous factors, as well as the wall stress and wall strength. A comparison between the Probabilistic Wall Rupture Index (PWRI), diameter-based index, and the output of the numerical method was done considering prediction power. Data records were taken from patients who underwent CT-Scan and ultrasound. Ten patients without rupturing cases were included in the statistical assessments. A matched diameter of a ruptured sample (n=7) and an unruptured sample (n=7) AAA was then considered. All the uncertainties that were observed in the thickness of the AAA wall and its strength were considered based originally on Laplace modified equation and PRRI analysis. The criteria for fitting a straight line to the data points were used for data graphing regarding the random nature of the collected data points. Statistical analysis (and plotting) of data was performed using MinitabTM, SPSSTM, and MatlabTM. The collagen-to- elastin ratio was taken as a measure of the AAA wall stiffness and tensile strength. The obtained results show that modified equations give a considerable coincide and minimum error compared with the original equation, and PRRI indicated a strong sensitivity more than the numerical models.

Atherosclerosis in Fabry Disease-A Contemporary Review.

Fabry disease (FD) is a lysosomal storage disorder characterised by a deficiency in the enzyme α-galactosidase A resulting in sphingolipid deposition which causes progressive cardiac, renal, and cerebral manifestations. The case illustrates a patient with FD who died suddenly, and medical examination demonstrated myocardial scarring and prior infarction. Angina is a frequent symptom in FD. Our own data are consistent with registry data indicating a high prevalence of risk factors for coronary artery disease (CAD) in FD that may accelerate conventional atherosclerosis. Patients with FD also have a higher high-density lipoprotein (HDL)/total cholesterol (T-Chol) ratio which may further accelerate atherosclerosis through expression of early atherosclerotic markers. Patients with FD may develop CAD both via classical atherosclerosis and through formation of thickened fibrocellular intima containing fibroblasts with storage of sphingolipids. Both mechanisms occurring together may accelerate coronary stenosis, as well as alter myocardial blood flow. Our data supports limited data that, although coronary flow may be reduced, the prevalence of epicardial coronary stenosis is low in FD. Microvascular dysfunction and arterial wall stress from sphingolipid deposition may form reactive oxygen species (ROS) and myeloperoxidase (MPO), key atherosclerotic mediators. Reduced myocardial blood flow in FD has also been demonstrated using numerous imaging modalities suggesting perfusion mismatch. This review describes the above mechanisms in detail, highlighting the importance of modifying cardiovascular risk factors in FD patients who likely develop accelerated atherosclerosis compared to the general population.

The up-to-date pathophysiology of Kawasaki disease.

Kawasaki disease (KD) is an acute systemic vasculitis of an unknown aetiology. A small proportion of children exposed to severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) or infected by Yersinia reproducibly develop principal symptoms of KD in various ethnic areas, but not in all studies. These microbes provoke a rapid cell‐damaging process, called ‘pyroptosis’, which is characterised by a subsequent release of proinflammatory cellular components from damaged endothelial and innate immune cells. In agreement with these molecular events, patients with KD show elevated levels of damage‐associated molecular patterns derived from cell death. In addition, an overwhelming amount of oxidative stress‐associated molecules, including oxidised phospholipids or low‐density lipoproteins, are generated as by‐products of inflammation during the acute phase of the disease. These molecules induce abnormalities in the acquired immune system and activate innate immune and vascular cells to produce a range of proinflammatory molecules such as cytokines, chemokines, proteases and reactive oxygen species. These responses further recruit immune cells to the arterial wall, wherein inflammation and oxidative stress closely interact and mutually amplify each other. The inflammasome, a key component of the innate immune system, plays an essential role in the development of vasculitis in KD. Thus, innate immune memory, or ‘trained immunity’, may promote vasculitis in KD. Hence, this review will be helpful in understanding the pathophysiologic pathways leading to the development of principal KD symptoms and coronary artery lesions in patients with KD, as well as in subsets of patients with SARS‐CoV‐2 and Yersinia infections.

Influence of Stent Flexibility on Artery Wall Stress and Wall Shear Stress in Bifurcation Lesions.

PurposeStent flexibility can influence clinical outcome, especially in bifurcation lesions. For instance, an overly rigid stent can impose mechanical stress on the artery at the stent edges and alter both arterial geometry and blood flow dynamics in bifurcations. This study investigated the influence of stent flexibility on vessel geometry, histology, wall stress, and blood flow dynamics in arterial bifurcations.Materials and MethodsWe compared arterial angulation, stenosis, histopathology, simulated wall shear stress (WSS), and simulated blood flow velocity distribution in swine coronary artery bifurcations following placement of the less flexible Multi-link 8 or more flexible Kaname stent (4.1 ± 0.5 vs 1.5 ± 0.1 mN, p < 0.05, t-test). Stents were implanted into six coronary artery bifurcations each using the single-stent crossover technique without side branch strut dilatation. Outcomes were examined after 28 days.ResultsImplantation of both stents significantly increased site angulation (Multi-link 8: 148° ± 8° to 172° ± 2°, p < 0.05, paired t-test; Kaname: 152° ± 5° to 164° ± 4°, p < 0.05, paired t-test), but the change tended to be greater after Multi-link 8 stent implantation (24° ± 15° vs 11° ± 7°, p = 0.1, t-test), suggesting greater straightening of the bifurcation. The Multi-link 8 stent induced greater neointimal thickness than the Kaname stent (0.53 ± 0.3 mm vs 0.26 ± 0.1 mm, p < 0.05, t-test). The distribution of neointimal hyperplasia following stent implantation as revealed by longitudinal histopathology matched the distribution of WSS simulated using computational fluid dynamics (CFD). The endothelium at low WSS areas exhibited aberrant cell morphology and leukocyte adhesion. A CFD model of a curved bifurcation suggested that the region of low WSS is expanded by artery straightening.ConclusionIn bifurcated lesions, stent flexibility influences not only mechanical stress on the artery but also WSS, which may induce local neointimal hyperplasia.

P2258Pulse wave velocity, total arterial compliance, and cardiac structure and function in late life

Abstract Background Coupled abnormalities in arterial and left ventricular (LV) stiffness characterize aging and heart failure with preserved ejection fraction. We hypothesized that two measures of aortic stiffness, pulse wave velocity (PWV; reflecting segmental arterial wall stress in late systole) and total arterial compliance (TAC; reflecting distensibility of entire arterial system) differentially relate to cardiac structure and function in the elderly. Methods Among participants in the Atherosclerosis Risk In Community (ARIC) study, we assessed the cross-sectional relationship of carotid-femoral PWV (cfPWV) and TAC with echocardiographic measures of cardiac structure and function using multivariable linear regression adjusting for demographics and co-morbidities. TAC defined as stroke volume over pulse pressure [mL/mmHg]. Exclusions were LVEF &lt;50%, prevalent HF, ≥moderate valvular disease. Results Of the 4,141 participants included in this study, mean age was 75±5 years, 41% were male, and 80% were white. Mean values were: cfPWV: 11.7±3.4 m/sec; TAC: 1.1±0.3 mL/mmHg. Greater cfPWV was associated with greater LV mass, worse systolic function, and worse diastolic function (Table). In contrast, worse TAC was not related to LV structure and did not demonstrate consistent relationships with measures of LV diastolic function, but was associated with worse LV longitudinal strain. Echo measures cfPWV (1SD increase) TAC (1SD decrease) β Coefficient p-value β Coefficient p-value Cardiac structure Mean wall thickness, cm 0.10 &lt;0.001 -0.01 0.499 LVMI, g/m2 0.04 0.016 0.02 0.299 LVEDVI, ml/m2 -0.07 &lt;0.001 -0.02 0.332 LV systolic function LVEF (Simpson's), % -0.04 0.01 -0.16 &lt;0.001 Longitudinal strain, % 0.14 &lt;0.001 0.19 &lt;0.001 LV diastolic function Septal e', cm/sec -0.08 &lt;0.001 -0.02 0.169 E/e' septal 0.04 0.005 -0.02 0.138 LAVI, ml/m2 -0.05 0.003 -0.04 0.026 Conclusion Two non-invasive measures of aortic stiffness, cfPWV and TAC, demonstrate differential associations with LV structure and function in late life. Greater cfPWV is more robustly associated with LV structure and function than TAC.

Abstract P416: Objectively Measured Snoring is Not Associated With Maladaptive Arterial Remodeling in Overweight and Obese Adults

Introduction: We previously reported that snoring severity was related to carotid arterial remodeling as characterized by wider inter-adventitial diameter (IAD) and greater intima-media thickness (IMT) in overweight and obese adults without obstructive sleep apnea (OSA). Considered to be an adaptive mechanism to maintain circumferential wall and shear stress homeostasis and a natural process in the setting of aging, early arterial remodeling is associated with cardiovascular morbidity and mortality. Elevations in arterial circumferential wall tension (CWT) and stress (CWS) in the setting of this compensatory arterial remodeling is considered maladaptive. We aimed to examine the association between snoring severity and CWT and CWS in adults with or without OSA. Methods: Cross-sectional analyses were conducted using 24-month follow up data from the Slow Adverse Vascular Effects lifestyle intervention study. The original population consisted of 349 overweight/obese (BMI 25-40 kg/m 2 ) adults aged 20-45 years old without hypertension or diabetes. The snoring index (SI) and oxygen desaturation index (ODI) were measured by the ResMed ApneaLink device among 122 participants. Snoring/OSA was categorized into three groups: OSA (ODI≥5; n=41), heavy snoring (ODI&lt;5, ≥median SI; n=40), and low snoring (ODI&lt;5, below-median SI; n=41). B-mode carotid ultrasound was used to measure end-diastole mean common carotid artery (CCA) IMT and lumen diameter (LD). Mean CWT (kPa*mm) and CWS (kPa) were calculated using Laplace’s law: CWT=MAP*(LD/2) and CWS= CWT/IMT; CCA wall to lumen ratio (WLR) = IMT/ LD. We used multiple linear regression to assess the association between snoring/OSA categories and CWT, CWS, and WLR adjusting for intervention group, age, sex, race, pulse pressure, BMI, non-HDL cholesterol, and fasting glucose, . Results: Participants were, on average, 40.1 ± 5.9 years old with a BMI of 31.6 ± 4.4 kg/m 2 ; 76.2% were women and 82% were white. Most CVD risk factors differed across snoring/OSA categories, including age, BMI, lipids, and fasting glucose, with risk factors worse in the OSA and heavy snoring groups compared to the low snoring group (all p &lt;0.05). In unadjusted analyses, CWT was higher in both heavy snoring (32.71 ± 4.74) and OSA (33.74 ± 5.09) groups compared to the low snoring group (29.94 ± 4.51; all p&lt;0.01). Differences were also noted in WLR between the low snoring and OSA groups (0.11 ± 0.01 vs. 0.12 ± 0.02; p&lt;0.05). Between-group differences in CWT were attenuated (p=0.09) and eliminated in WLR after multivariable adjustment. Differences in CWS across snoring/OSA categories were not observed. Conclusion: Our findings suggest that, in overweight and obese young to middle-aged adults without hypertension or diabetes, objectively measured snoring may not be associated with maladaptive arterial remodeling after accounting for traditional CVD risk factors.

Finite element simulation of three dimensional residual stress in the aortic wall using an anisotropic tissue growth model

Residual stress is believed to play a significant role in the in vivo stress state of the arterial wall, but quantifying residual stress in vivo is challenging. Based on the well-known assumptions that residual stress is a result of heterogeneous arterial growth and that it homogenizes the transmural distribution of arterial wall stress, we propose a new anisotropic tissue growth model for the aorta to recover the three-dimensional residual stress field in a bi-layer human aortic wall. Finite element simulations showed that the predicted residual stress magnitude with this method are within the documented range for human aorta. Particularly, the homeostatic inter-layer stress difference is identified as a key parameter to quantify the opening angle. To the authors’ knowledge, this is the first finite element study employing anisotropic growth of aortic tissue in a bi-layer model to generate three-dimensional residual stress field, and the resultant opening angle can match with the experiments. A parametric study found that inter-layer stress homogeneity, arterial blood pressure, axial pre-stretch, and material stiffness strongly affect the residual stress field.

A combined growth and remodeling framework for the approximation of residual stresses in arterial walls

AbstractA combined model of multiplicative growth and fiber remodeling in the sense of a reorientation of the collagen fibers is proposed for the simulation of adaptation processes in arterial tissues, where both mechanisms are supposed to be governed by the intensity and the direction of the principal stresses. The generalized formulation of the growth tensor includes up to three perpendicular anisotropy directions, which are defined based on the local principal stress state. Remodeling is incorporated in a straightforward manner by formulating a scalar evolution equation for the angle between the existing and the target fiber orientation vectors. In numerical examples on idealized arterial segments, the fiber remodeling algorithm is illustrated and a comparison of different approaches for the growth tensor with respect to stresses in the loaded state, fiber angles and residual stresses is conducted.

Common Carotid Artery Diameter and Risk of Cardiovascular Events and Mortality: Pooled Analyses of Four Cohort Studies.

Carotid arterial diameter enlargement is a manifestation of arterial remodeling and may be a risk factor for cardiovascular disease (CVD). We evaluated the association between carotid artery diameter and risk of stroke, coronary heart disease, CVD, and all-cause mortality and explored whether the associations could be explained by processes involved in arterial remodeling, that is, blood pressure-related media thickening, arterial stiffness, arterial wall stress, and atherosclerosis. We included 4887 participants (mean age 67±9 years; 54% women) from 4 cohort studies: Rotterdam Study, NEPHROTEST, Hoorn Study, and a study by Blacher et al. Common carotid artery properties were measured using echotracking. Incident cases were recorded based on medical records. We used Cox proportional hazard models adjusting for cardiovascular risk factors and estimates of processes underlying arterial remodeling. During follow-up (mean, 11 years), 379 (8%) individuals had a stroke, 516 had a (11%) coronary heart disease, 807 had a (17%) CVD, and 1486 (30%) had died. After adjustment for cardiovascular risk factors, individuals in the highest tertile of carotid diameter (diameter >8 mm) compared with those in the lowest tertile (diameter <7 mm) had a higher incidence of stroke (hazard ratio, 1.5; 95% confidence interval, 1.1-2.0). From all estimates of processes underlying arterial remodeling, adjustment for carotid intima-media thickness attenuated this association (hazard ratio after adjustment for intima-media thickness, 1.2; 95% confidence interval, 0.9-1.6). Larger carotid diameter was associated with risk of CVD and mortality but not clearly with coronary heart disease risk. We showed that a larger carotid diameter is associated with incident stroke, CVD, and mortality. Carotid intima-media thickness, a measure of blood pressure-related media thickening, partially explained the association with stroke incidence.

A simple method of incorporating the effect of the Uniform Stress Hypothesis in arterial wall stress computations.

Residual stress has a great influence on the mechanical behaviour of arterial wall. Numerous research groups used the Uniform Stress Hypothesis to allow the inclusion of the effects of residual stress when computing stress distributions in the arterial wall. Nevertheless, the available methods used for this purpose are very computationally expensive, due to their iterative nature. In this paper we present a new method for including the effects of residual stress on the computed stress distribution in the arterial wall. The new method, by using the Uniform Stress Hypothesis, enables computing the effect of residual stress by averaging stresses across the thickness of the arterial wall. Being a post-processing method for the computed stress distributions, the proposed method is computationally inexpensive, and thus, better suited for clinical applications than the previously used ones. The resulting stress distributions and values obtained using the proposed method based on the Uniform Stress Hypothesis are very close to the ones returned by an existing iterative method.

Arterial Wall Stress Induces Phenotypic Switching of Arterial Smooth Muscle Cells in Vascular Remodeling by Activating the YAP/TAZ Signaling Pathway

Background/Aims: Increasing wall stress or biomechanical stretch experienced by arteries influences the initiation of atherosclerotic lesions. This initiation is mediated by Yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ), which are both effectors of the Hippo pathway. In this study, the functional roles of YAP/TAZ proteins in the regulation of the stretch-mediated programing of human umbilical arterial smooth muscle cells (HUASMCs) to a proliferative phenotype were examined. Methods: HUASMCs were seeded on a Matrigel-coated silicone chamber and subjected to biomechanical stretch for 24 h after 48 h of growth. YAP/TAZ small interfering RNA was used to specifically knockdown YAP/ TAZ expression in HUASMCs. Results: We observed that YAP/TAZ activation via biomechanical stretching is involved in the regulation of critical aspects of the HUASMC phenotypic switch. YAP/TAZ knockdown significantly attenuated the stretch-induced proliferative and pro-inflammatory phenotypes in HUASMCs. Furthermore, treatment with atorvastatin, an anti-atherosclerotic drug, attenuated the stretch-induced phenotypic switch of HUASMCs from the contractile to synthetic state by suppressing YAP/TAZ expression. Additional investigations demonstrated the role of stretch in inhibiting the Hippo pathway, leading to the activation of PI3-kinase (PI3K) and phosphoinositide dependent kinase (PDK1); the key molecule for the regulation of the PDK1 and Hippo complex interaction was Sav1. These results showed the importance of YAP/TAZ activation, induced by biomechanical stretch, in promoting atheroprone phenotypes in HUASMCs. Conclusion: Taken together, our findings revealed a mechanism by which YAP/TAZ activation contributes to the pathogenesis of atherosclerosis.

Numerical simulation of low-density lipoprotein mass transport in human arterial stenosis - Calculation of the filtration velocity.

Accumulation of cholesterol and other atherogenic lipids such as low-density lipoprotein (LDL) in artery wall causes reduction of vessel diameter and artery stenosis. The study of the mass transfer of these large molecules in the wall with considering effective factors on lumen flow and different physiological factors is the subject considered nowadays. In this paper, results of two dimensional and axi-symmetric simulations of three different models of the artery with 60% stenosis under pulsatile blood flow are presented. Filtration velocity of LDL mass transport in the permeable artery wall and shear stress of blood flow are investigated using ADINA software Three different flow models are considered. In the first and second models, the filtration velocity considered as a given parameter and constant in arterial wall boundary, while in third model arterial wall considered as porous wall, the filtration velocity is calculated from pressure difference as an input parameter of the model. The results show that filtration velocity is strongly depend on geometry and it is not constant along the wall, contrary to simplified models. The results of concentration variations in lumen and wall illustrate the increase in near wall LDL concentration or concentration polarization.