Cap Stress Research Articles

Plaque Ruptures Are Related to High Plaque Stress and Strain Conditions: Direct Verification by Using In Vivo OCT Rupture Data and FSI Models.

While it has been hypothesized that high plaque stress and strain may be related to plaque rupture, its direct verification using in vivo coronary plaque rupture data and full 3-dimensional fluid-structure interaction models is lacking in the current literature due to difficulty in obtaining in vivo plaque rupture imaging data from patients with acute coronary syndrome. This case-control study aims to use high-resolution optical coherence tomography-verified in vivo plaque rupture data and 3-dimensional fluid-structure interaction models to seek direct evidence for the high plaque stress/strain hypothesis. In vivo coronary plaque optical coherence tomography data (5 ruptured plaques, 5 no-rupture plaques) were acquired from patients using a protocol approved by the local institutional review board with informed consent obtained. The ruptured caps were reconstructed to their prerupture morphology using neighboring plaque cap and vessel geometries. Optical coherence tomography-based 3-dimensional fluid-structure interaction models were constructed to obtain plaque stress, strain, and flow shear stress data for comparative analysis. The rank-sum test in the nonparametric test was used for statistical analysis. Our results showed that the average maximum cap stress and strain values of ruptured plaques were 142% (457.70 versus 189.22 kPa; P=0.0278) and 48% (0.2267 versus 0.1527 kPa; P=0.0476) higher than that for no-rupture plaques, respectively. The mean values of maximum flow shear stresses for ruptured and no-rupture plaques were 145.02 dyn/cm2 and 81.92 dyn/cm2 (P=0.1111), respectively. However, the flow shear stress difference was not statistically significant. This preliminary case-control study showed that the ruptured plaque group had higher mean maximum stress and strain values. Due to our small study size, larger scale studies are needed to further validate our findings.

Impact of residual stress on coronary plaque stress/strain calculations using optical coherence tomography image-based multi-layer models.

Mechanical stress and strain conditions play an important role in atherosclerosis plaque progression, remodeling and potential rupture and may be used in plaque vulnerability assessment for better clinical diagnosis and treatment decisions. Single layer plaque models without residual stress have been widely used due to unavailability of multi-layer image segmentation method and residual stress data. However, vessel layered structure and residual stress have large impact on stress/strain calculations and should be included in the models. In this study, intravascular optical coherence tomography (OCT) data of coronary plaques from 10 patients were acquired and segmented to obtain the three-layer vessel structure using an in-house automatic segmentation algorithm. Multi- and single-layer 3D thin-slice biomechanical plaque models with and without residual stress were constructed to assess the impact of residual stress on stress/strain calculations. Our results showed that residual stress led to a more uniform stress distribution across the vessel wall, with considerable plaque stress/strain decrease on inner wall and increase on vessel out-wall. Multi-layer model with residual stress inclusion reduced inner wall maximum and mean plaque stresses by 38.57% and 59.70%, and increased out-wall maximum and mean plaque stresses by 572.84% and 432.03%. These findings demonstrated the importance of multi-layer modeling with residual stress for more accurate plaque stress/strain calculations, which will have great impact in plaque cap stress calculation and plaque rupture risk assessment. Further large-scale studies are needed to validate our findings.

On the Impact of Residual Strains in the Stress Analysis of Patient-Specific Atherosclerotic Carotid Vessels: Predictions Based on the Homogenous Stress Hypothesis

The identification of carotid atherosclerotic lesion at risk for plaque rupture, eventually resulting in cerebral embolism and stroke, is of paramount clinical importance. High stress in the fibrous plaque cap has been proposed as risk factor. However, among others, residual strains influence said stress predictions, but quantitative and qualitative implications of residual strains in this context are not well explored. We therefore propose a multiplicative kinematics-based Growth and Remodeling (G&R) framework to predict residual strains from homogenizing tissue stress and then investigate its implication on plaque stress. Carotid vessel morphology of four patients was reconstructed from clinical Computed Tomography-Angiography (CT-A) images and equipped with heterogeneous tissue constitutive properties assigned through a histology-based artificial intelligence image segmentation tool. As compared to a purely elastic analysis and depending on patient-specific morphology and tissue distributions, the incorporation of residual strains reduced the maximum wall stress by up to 30%\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$30\\%$$\\end{document} and resulted in a fundamentally different distribution of stress across the atherosclerotic wall. Regardless residual strains homogenized tissue stresses, the fibrous plaque cap may persistently be exposed to spots of high stress. In conclusion, the incorporation of residual strains in biomechanical studies of atherosclerotic carotids may be important for a reliable assessment of fibrous plaque cap stress.

Duality of jacalin-related lectin: Master regulator and chaperone

Lectins have chaperone-like activity with carbohydrate-binding sites, key in cellular homeostasis. However, the specific interactions of lectin with endoplasmic-reticulum (ER) proteins during stress are unclear. Recently, Das et al. (2023) study reveals lectins' critical role in root cap stress response, through regulating ER stress-responsive proteins, suggesting pathways for enhancing plant resilience.

Combining IVUS + OCT Data, Biomechanical Models and Machine Learning Method for Accurate Coronary Plaque Morphology Quantification and Cap Thickness and Stress/Strain Index Predictions

Assessment and prediction of vulnerable plaque progression and rupture risk are of utmost importance for diagnosis, management and treatment of cardiovascular diseases and possible prevention of acute cardiovascular events such as heart attack and stroke. However, accurate assessment of plaque vulnerability assessment and prediction of its future changes require accurate plaque cap thickness, tissue component and structure quantifications and mechanical stress/strain calculations. Multi-modality intravascular ultrasound (IVUS), optical coherence tomography (OCT) and angiography image data with follow-up were acquired from ten patients to obtain accurate and reliable plaque morphology for model construction. Three-dimensional thin-slice finite element models were constructed for 228 matched IVUS + OCT slices to obtain plaque stress/strain data for analysis. Quantitative plaque cap thickness and stress/strain indices were introduced as substitute quantitative plaque vulnerability indices (PVIs) and a machine learning method (random forest) was employed to predict PVI changes with actual patient IVUS + OCT follow-up data as the gold standard. Our prediction results showed that optimal prediction accuracies for changes in cap-PVI (C-PVI), mean cap stress PVI (meanS-PVI) and mean cap strain PVI (meanSn-PVI) were 90.3% (AUC = 0.877), 85.6% (AUC = 0.867) and 83.3% (AUC = 0.809), respectively. The improvements in prediction accuracy by the best combination predictor over the best single predictor were 6.6% for C-PVI, 10.0% for mean S-PVI and 8.0% for mean Sn-PVI. Our results demonstrated the potential using multi-modality IVUS + OCT image to accurately and efficiently predict plaque cap thickness and stress/strain index changes. Combining mechanical and morphological predictors may lead to better prediction accuracies.

Two analytical structural models of the connecting rod cap

The mathematical models available in the pertinent literature for designing the cap of a connecting rod are critically examined, and it is shown that some currently adopted assumptions are inaccurate. Spurred by these critical remarks, two more realistic mathematical models are developed of the contact between the crankpin and the cap. In both models, the crankpin is modelled as rigid, and the cap is idealized as a purely flexural, curved beam of constant cross-section, in progressive contact with the crankpin. In the first model, the cap is mimicked as a twice-statically redundant structure solved with the Castigliano theorem. The cap structural response is mechanically examined starting from the central part of the cap-crankpin contact. In the second model, the cap is mimicked as a statically determined structure. Particular attention is paid to the cap change of curvature when moving along the cap axis. The beginning of the cap-crankpin contact is determined by requiring that the curvature of the deformed cap equal the curved border of the crankpin. A result common to the two approaches is the definition of a combined factor summarizing the mechanical effect of several variables, namely the total load, the initial clearance, Young’s modulus, and the cap geometry; the last factor is recapped by the radius defining the centre of mass, and by the moment of inertia. To evidence the merits and limits of the two approaches, the extent of the cap-crankpin angular contact, and the value of representative cap stresses, are determined and compared to Finite Element (FE) forecasts. Furthermore, the effect of the ratio between the moment of inertia of the abutment and the cap central cross-section is investigated. This ratio influences the prediction of the contact angle; when the ratio is higher than 4, the numerical FE results significantly differ from the analytical calculations.

The effect of plaque morphology, material composition and microcalcifications on the risk of cap rupture: A structural analysis of vulnerable atherosclerotic plaques.

BackgroundThe mechanical rupture of an atheroma cap may initiate a thrombus formation, followed by an acute coronary event and death. Several morphology and tissue composition factors have been identified to play a role on the mechanical stability of an atheroma, including cap thickness, lipid core stiffness, remodeling index, and blood pressure. More recently, the presence of microcalcifications (μCalcs) in the atheroma cap has been demonstrated, but their combined effect with other vulnerability factors has not been fully investigated.Materials and methodsWe performed numerical simulations on 3D idealized lesions and a microCT-derived human coronary atheroma, to quantitatively analyze the atheroma cap rupture. From the predicted cap stresses, we defined a biomechanics-based vulnerability index (VI) to classify the impact of each risk factor on plaque stability, and developed a predictive model based on their synergistic effect.ResultsPlaques with low remodeling index and soft lipid cores exhibit higher VI and can shift the location of maximal wall stresses. The VI exponentially rises as the cap becomes thinner, while the presence of a μCalc causes an additional 2.5-fold increase in vulnerability for a spherical inclusion. The human coronary atheroma model had a stable phenotype, but it was transformed into a vulnerable plaque after introducing a single spherical μCalc in its cap. Overall, cap thickness and μCalcs are the two most influential factors of mechanical rupture risk.ConclusionsOur findings provide supporting evidence that high risk lesions are non-obstructive plaques with softer (lipid-rich) cores and a thin cap with μCalcs. However, stable plaques may still rupture in the presence of μCalcs.

Using Optical Coherence Tomography and Intravascular Ultrasound Imaging to Quantify Coronary Plaque Cap Stress/Strain and Progression: A Follow-Up Study Using 3D Thin-Layer Models.

Accurate plaque cap thickness quantification and cap stress/strain calculations are of fundamental importance for vulnerable plaque research. To overcome uncertainties due to intravascular ultrasound (IVUS) resolution limitation, IVUS and optical coherence tomography (OCT) coronary plaque image data were combined together to obtain accurate and reliable cap thickness data, stress/strain calculations, and reliable plaque progression predictions. IVUS, OCT, and angiography baseline and follow-up data were collected from nine patients (mean age: 69; m: 5) at Cardiovascular Research Foundation with informed consent obtained. IVUS and OCT slices were coregistered and merged to form IVUS + OCT (IO) slices. A total of 114 matched slices (IVUS and OCT, baseline and follow-up) were obtained, and 3D thin-layer models were constructed to obtain stress and strain values. A generalized linear mixed model (GLMM) and least squares support vector machine (LSSVM) method were used to predict cap thickness change using nine morphological and mechanical risk factors. Prediction accuracies by all combinations (511) of those predictors with both IVUS and IO data were compared to identify optimal predictor(s) with their best accuracies. For the nine patients, the average of minimum cap thickness from IVUS was 0.17 mm, which was 26.08% lower than that from IO data (average = 0.23 mm). Patient variations of the individual errors ranged from ‒58.11 to 20.37%. For maximum cap stress between IO and IVUS, patient variations of the individual errors ranged from ‒30.40 to 46.17%. Patient variations of the individual errors of maximum cap strain values ranged from ‒19.90 to 17.65%. For the GLMM method, the optimal combination predictor using IO data had AUC (area under the ROC curve) = 0.926 and highest accuracy = 90.8%, vs. AUC = 0.783 and accuracy = 74.6% using IVUS data. For the LSSVM method, the best combination predictor using IO data had AUC = 0.838 and accuracy = 75.7%, vs. AUC = 0.780 and accuracy = 69.6% using IVUS data. This preliminary study demonstrated improved plaque cap progression prediction accuracy using accurate cap thickness data from IO slices and the differences in cap thickness, stress/strain values, and prediction results between IVUS and IO data. Large-scale studies are needed to verify our findings.

Coronary plaque composition influences biomechanical stress and predicts plaque rupture in a morpho-mechanic OCT analysis.

Plaque rupture occurs if stress within coronary lesions exceeds the protection exerted by the fibrous cap overlying the necrotic lipid core. However, very little is known about the biomechanical stress exerting this disrupting force. Employing optical coherence tomography (OCT), we generated plaque models and performed finite-element analysis to simulate stress distributions within the vessel wall in 10 ruptured and 10 non-ruptured lesions. In ruptured lesions, maximal stress within fibrous cap (peak cap stress [PCS]: 174 ± 67 vs. 52 ± 42 kPa, p<0.001) and vessel wall (maximal plaque stress [MPS]: 399 ± 233 vs. 90 ± 95 kPa, p=0.001) were significantly higher compared to non-ruptured plaques. Ruptures arose in the immediate proximity of maximal stress concentrations (angular distances: 21.8 ± 30.3° for PCS vs. 20.7 ± 23.7° for MPS); stress concentrations excellently predicted plaque rupture (area under the curve: 0.940 for PCS, 0.950 for MPS). This prediction of plaque rupture was superior to established vulnerability features such as fibrous cap thickness or macrophage infiltration. In conclusion, OCT-based finite-element analysis effectively assesses plaque biomechanics, which in turn predicts plaque rupture in patients. This highlights the importance of morpho-mechanic analysis assessing the disrupting effects of plaque stress.

Consideration of stiffness of wall layers is decisive for patient-specific analysis of carotid artery with atheroma.

The paper deals with the impact of chosen geometric and material factors on maximal stresses in carotid atherosclerotic plaque calculated using patient-specific finite element models. These stresses are believed to be decisive for the plaque vulnerability but all applied models suffer from inaccuracy of input data, especially when obtained in vivo only. One hundred computational models based on ex vivo MRI are used to investigate the impact of wall thickness, MRI slice thickness, lipid core and fibrous tissue stiffness, and media anisotropy on the calculated peak plaque and peak cap stresses. The investigated factors are taken as continuous in the range based on published experimental results, only the impact of anisotropy is evaluated by comparison with a corresponding isotropic model. Design of Experiment concept is applied to assess the statistical significance of these investigated factors representing uncertainties in the input data of the model. The results show that consideration of realistic properties of arterial wall in the model is decisive for the stress evaluation; assignment of properties of fibrous tissue even to media and adventitia layers as done in some studies may induce up to eightfold overestimation of peak stress. The impact of MRI slice thickness may play a key role when local thin fibrous cap is present. Anisotropy of media layer is insignificant, and the stiffness of fibrous tissue and lipid core may become significant in some combinations.

Moderate thickness of lipid core in shoulder region of atherosclerotic plaque determines vulnerable plaque [sbnd] A parametric study

Peak stress in the fibrous cap of atherosclerotic plaque is largely determined by the cap thickness which cannot be accurately estimated in vivo. This parametric study investigates idealized atherosclerotic plaque geometries. Finite element modeling is applied to search for larger morphological features associated with high cap stresses. By varying seven geometrical and two loading parameters, 100 3D model geometries of atherosclerotic plaques in common iliac artery were generated. In each model peak cap stress was calculated, and statistical comparison of the geometries generating the highest and lowest peak cap stresses was performed. The analysis showed that, compared to geometries generating the lowest stresses, those with high peak cap stress had a significantly lower cap thickness, higher stenosis ratio, lower relative lipid core volume, and cap shoulder radius larger than lipid core radius. High cap stress was observed for cap thicknesses up to 0.13 mm. It can be concluded that vulnerable plaques contain thin fibrous cap, large stenosis ratio and only moderate small-radius lipid core which reaches the shoulder region of the fibrous cap.

Effect of distal thickening and stiffening of plaque cap on arterial wall mechanics.

To investigate the effect of longitudinal variations of cap thickness and tissue properties on wall stresses and strains along the atherosclerotic stenosis, stenotic plaque models (uniformly thick, distally thickened, homogenous, and distally stiffened) were constructed and subjected to computational stress analyses with due consideration of fluid-structure interactions (FSI). The analysis considered three different cap thicknesses-45, 65, and 200μm-and tissue properties-soft, fibrous, and hard. The maximum peak cap stress (PCS) and strain were observed in the upstream throat section and demonstrated increases of the order of 345 and 190%, respectively, as the cap thickness was reduced from 200 to 45μm in uniformly thick models. Distal stiffening increased PCS in the downstream region; however, the overall effect of this increase was rather small. Distal thickening did not affect maximum PCS and strain values for cap thicknesses exceeding 65μm; however, a noticeable increase in maximum PCS and corresponding longitudinal variation (or spatial gradient) in stress was observed in the very thin (45-μm-thick) cap. It was, therefore, inferred that existence of a rather thin upstream cap demonstrating distal cap thickening indicates an increased risk of plaque progression and rupture. Graphical Abstract ᅟ.

Combining IVUS and Optical Coherence Tomography for More Accurate Coronary Cap Thickness Quantification and Stress/Strain Calculations: A Patient-Specific Three-Dimensional Fluid-Structure Interaction Modeling Approach.

Accurate cap thickness and stress/strain quantifications are of fundamental importance for vulnerable plaque research. Virtual histology intravascular ultrasound (VH-IVUS) sets cap thickness to zero when cap is under resolution limit and IVUS does not see it. An innovative modeling approach combining IVUS and optical coherence tomography (OCT) is introduced for cap thickness quantification and more accurate cap stress/strain calculations. In vivo IVUS and OCT coronary plaque data were acquired with informed consent obtained. IVUS and OCT images were merged to form the IVUS + OCT data set, with biplane angiography providing three-dimensional (3D) vessel curvature. For components where VH-IVUS set zero cap thickness (i.e., no cap), a cap was added with minimum cap thickness set as 50 and 180 μm to generate IVUS50 and IVUS180 data sets for model construction, respectively. 3D fluid-structure interaction (FSI) models based on IVUS + OCT, IVUS50, and IVUS180 data sets were constructed to investigate cap thickness impact on stress/strain calculations. Compared to IVUS + OCT, IVUS50 underestimated mean cap thickness (27 slices) by 34.5%, overestimated mean cap stress by 45.8%, (96.4 versus 66.1 kPa). IVUS50 maximum cap stress was 59.2% higher than that from IVUS + OCT model (564.2 versus 354.5 kPa). Differences between IVUS and IVUS + OCT models for cap strain and flow shear stress (FSS) were modest (cap strain <12%; FSS <6%). IVUS + OCT data and models could provide more accurate cap thickness and stress/strain calculations which will serve as basis for further plaque investigations.

Intima heterogeneity in stress assessment of atherosclerotic plaques.

Atherosclerotic plaque rupture is recognized as the primary cause of cardiac and cerebral ischaemic events. High structural plaque stresses have been shown to strongly correlate with plaque rupture. Plaque stresses can be computed with finite-element (FE) models. Current FE models employ homogeneous material properties for the heterogeneous atherosclerotic intima. This study aimed to evaluate the influence of intima heterogeneity on plaque stress computations. Two-dimensional FE models with homogeneous and heterogeneous intima were constructed from histological images of atherosclerotic human coronaries (n = 12). For homogeneous models, a single stiffness value was employed for the entire intima. For heterogeneous models, the intima was subdivided into four clusters based on the histological information and different stiffness values were assigned to the clusters. To cover the reported local intima stiffness range, 100 cluster stiffness combinations were simulated. Peak cap stresses (PCSs) from the homogeneous and heterogeneous models were analysed and compared. By using a global variance-based sensitivity analysis, the influence of the cluster stiffnesses on the PCS variation in the heterogeneous intima models was determined. Per plaque, the median PCS values of the heterogeneous models ranged from 27 to 160 kPa, and the PCS range varied between 43 and 218 kPa. On average, the homogeneous model PCS values differed from the median PCS values of heterogeneous models by 14%. A positive correlation (R2 = 0.72) was found between the homogeneous model PCS and the PCS range of the heterogeneous models. Sensitivity analysis showed that the highest main sensitivity index per plaque ranged from 0.26 to 0.83, and the average was 0.47. Intima heterogeneity resulted in substantial changes in PCS, warranting stress analyses with heterogeneous intima properties for plaque-specific, high accuracy stress assessment. Yet, computations with homogeneous intima assumption are still valuable to perform sensitivity analyses or parametric studies for testing the effect of plaque geometry on PCS. Moreover, homogeneous intima models can help identify low PCS, stable type plaques with thick caps. Yet, for thin cap plaques, accurate stiffness measurements of the clusters in the cap and stress analysis with heterogeneous cap properties are required to characterize the plaque stability.

Model-based cap thickness and peak cap stress prediction for carotid MRI

A rupture-prone carotid plaque can potentially be identified by calculating the peak cap stress (PCS). For these calculations, plaque geometry from MRI is often used. Unfortunately, MRI is hampered by a low resolution, leading to an overestimation of cap thickness and an underestimation of PCS. We developed a model to reconstruct the cap based on plaque geometry to better predict cap thickness and PCS.We used histological stained plaques from 34 patients. These plaques were segmented and served as the ground truth. Sections of these plaques contained 93 necrotic cores with a cap thickness <0.62mm which were used to generate a geometry-based model. The histological data was used to simulate in vivo MRI images, which were manually delineated by three experienced MRI readers. Caps below the MRI resolution (n=31) were (digitally removed and) reconstructed according to the geometry-based model. Cap thickness and PCS were determined for the ground truth, readers, and reconstructed geometries.Cap thickness was 0.07mm for the ground truth, 0.23mm for the readers, and 0.12mm for the reconstructed geometries. The model predicts cap thickness significantly better than the readers. PCS was 464kPa for the ground truth, 262kPa for the readers and 384kPa for the reconstructed geometries. The model did not predict the PCS significantly better than the readers.The geometry-based model provided a significant improvement for cap thickness estimation and can potentially help in rupture-risk prediction, solely based on cap thickness. Estimation of PCS estimation did not improve, probably due to the complex shape of the plaques.

Abstract 383: Patient-Specific Coronary Models Combining Intravascular Ultrasound and Optical Coherence Tomography Lead to More Accurate Plaque Cap Thickness and Stress/Strain Quantifications

Accurate cap thickness and stress/strain quantifications are of fundamental importance for vulnerable plaque research. An innovative modeling approach combining intravascular ultrasound (IVUS) and optical coherence tomography (OCT) is introduced for more accurate patient-specific coronary morphology and stress/strain calculations. In vivo IVUS and OCT coronary plaque data were acquired from two patients with informed consent obtained. IVUS and OCT images were segmented, co-registered, and merged to form the IVUS+OCT data set, with OCT providing accurate cap thickness. Biplane angiography provided 3D vessel curvature. Due to IVUS resolution (150 μm), original virtual histology (VH) IVUS data often had lipid core exposed to lumen since it sets cap thickness as zero when cap thickness &lt;150 μm. VH-IVUS data were processed with minimum cap thickness set as 50 and 180 μm to generate IVUS50 and IVUS180 data sets for modeling use. 3D fluid-structure interaction models based on IVUS+OCT, IVUS50 and IVUS180 data sets were constructed to investigate the impact of OCT cap thickness improvement on stress/strain calculations. Figure 1 is a brief summary of results from 27 slices with cap covering lipid cores from 2 patients. Mean cap thickness (unit: mm) from Patient 1 was 0.353 (OCT), 0.201 (IVUS50), and 0.329 (IVUS180), respectively. Patient 2 mean cap thickness was 0.320 (OCT), 0.224 (IVUS50), and 0.285 (IVUS180). IVUS50 underestimated cap thickness (27 slices) by 34.5%, compared to OCT cap values. IVUS50 overestimated mean cap stress (27 slices) by 45.8%, compared to OCT cap stress (96.4 vs. 66.1 kPa). IVUS50 maximum cap stress was 59.2% higher than that from IVUS+OCT model (564.2 vs. 354.5 kPa). Differences between IVUS and IVUS+OCT models for mean cap strain and flow shear stress were modest (cap strain: &lt;12%; FSS &lt;2%). Conclusion: IVUS+OCT data and models could provide more accurate cap thickness and stress/strain calculations which will serve as basis for plaque research.

Cellular strain avoidance is mediated by a functional actin cap - observations in an Lmna-deficient cell model.

In adherent cells, the relevance of a physical mechanotransduction pathway provided by the perinuclear actin cap stress fibers has recently emerged. Here, we investigate the impact of a functional actin cap on the cellular adaptive response to topographical cues and uniaxial cyclic strain. Lmna-deficient fibroblasts are used as a model system because they do not develop an intact actin cap, but predominantly form a basal layer of actin stress fibers underneath the nucleus. We observe that topographical cues induce alignment in both normal and Lmna-deficient fibroblasts, suggesting that the topographical signal transmission occurs independently of the integrity of the actin cap. By contrast, in response to cyclic uniaxial strain, Lmna-deficient cells show a compromised strain avoidance response, which is completely abolished when topographical cues and uniaxial strain are applied along the same direction. These findings point to the importance of an intact and functional actin cap in mediating cellular strain avoidance.

Cap inflammation leads to higher plaque cap strain and lower cap stress: An MRI-PET/CT-based FSI modeling approach

Plaque rupture may be triggered by extreme stress/strain conditions. Inflammation is also implicated and can be imaged using novel imaging techniques. The impact of cap inflammation on plaque stress/strain and flow shear stress were investigated. A patient-specific MRI-PET/CT-based modeling approach was used to develop 3D fluid-structure interaction models and investigate the impact of inflammation on plaque stress/strain conditions for better plaque assessment. 18FDG-PET/CT and MRI data were acquired from 4 male patients (average age: 66) to assess plaque characteristics and inflammation. Material stiffness for the fibrous cap was adjusted lower to reflect cap weakening causing by inflammation. Setting stiffness ratio (SR) to be 1.0 (fibrous tissue) for baseline, results for SR=0.5, 0.25, and 0.1 were obtained. Thin cap and hypertension were also considered. Combining results from the 4 patients, mean cap stress from 729 cap nodes was lowered by 25.2% as SR went from 1.0 to 0.1. Mean cap strain value for SR=0.1 was 0.313, 114% higher than that from SR=1.0 model. The thin cap SR=0.1 model had 40% mean cap stress decrease and 81% cap strain increase compared with SR=1.0 model. The hypertension SR=0.1 model had 19.5% cap stress decrease and 98.6% cap strain increase compared with SR=1.0 model. Differences of flow shear stress with 4 different SR values were limited (<10%). Cap inflammation may lead to large cap strain conditions when combined with thin cap and hypertension. Inflammation also led to lower cap stress. This shows the influence of inflammation on stress/strain calculations which are closely related to plaque assessment.

Effects of Residual Stress, Axial Stretch, and Circumferential Shrinkage on Coronary Plaque Stress and Strain Calculations: A Modeling Study Using IVUS-Based Near-Idealized Geometries.

Accurate stress and strain calculations are important for plaque progression and vulnerability assessment. Models based on in vivo data often need to form geometries with zero-stress/strain conditions. The goal of this paper is to use IVUS-based near-idealized geometries and introduce a three-step model construction process to include residual stress, axial shrinkage, and circumferential shrinkage and investigate their impacts on stress and strain calculations. In Vivo intravascular ultrasound (IVUS) data of human coronary were acquired for model construction. In Vivo IVUS movie data were acquired and used to determine patient-specific material parameter values. A three-step modeling procedure was used to make our model: (a) wrap the zero-stress vessel sector to obtain the residual stress; (b) stretch the vessel axially to its length in vivo; and (c) pressurize the vessel to recover its in vivo geometry. Eight models were constructed for our investigation. Wrapping led to reduced lumen and cap stress and increased out boundary stress. The model with axial stretch, circumferential shrink, but no wrapping overestimated lumen and cap stress by 182% and 448%, respectively. The model with wrapping, circumferential shrink, but no axial stretch predicted average lumen stress and cap stress as 0.76 kPa and -15 kPa. The same model with 10% axial stretch had 42.53 kPa lumen stress and 29.0 kPa cap stress, respectively. Skipping circumferential shrinkage leads to overexpansion of the vessel and incorrect stress/strain calculations. Vessel stiffness increase (100%) leads to 75% lumen stress increase and 102% cap stress increase.

Quantify patient-specific coronary material property and its impact on stress/strain calculations using in vivo IVUS data and 3D FSI models: a pilot study.

Computational models have been used to calculate plaque stress and strain for plaque progression and rupture investigations. An intravascular ultrasound (IVUS)-based modeling approach is proposed to quantify in vivo vessel material properties for more accurate stress/strain calculations. In vivo Cine IVUS and VH-IVUS coronary plaque data were acquired from one patient with informed consent obtained. Cine IVUS data and 3D thin-slice models with axial stretch were used to determine patient-specific vessel material properties. Twenty full 3D fluid-structure interaction models with ex vivo and in vivo material properties and various axial and circumferential shrink combinations were constructed to investigate the material stiffness impact on stress/strain calculations. The approximate circumferential Young's modulus over stretch ratio interval [1.0, 1.1] for an ex vivo human plaque sample and two slices (S6 and S18) from our IVUS data were 1631, 641, and 346kPa, respectively. Average lumen stress/strain values from models using ex vivo, S6 and S18 materials with 5% axial shrink and proper circumferential shrink were 72.76, 81.37, 101.84kPa and 0.0668, 0.1046, and 0.1489, respectively. The average cap strain values from S18 material models were 150-180% higher than those from the ex vivo material models. The corresponding percentages for the average cap stress values were 50-75%. Dropping axial and circumferential shrink consideration led to stress and strain over-estimations. In vivo vessel material properties may be considerably softer than those from ex vivo data. Material stiffness variations may cause 50-75% stress and 150-180% strain variations.