Automated finite element approach to generate anatomical patient-specific biomechanical models of atherosclerotic arteries from virtual histology-intravascular ultrasound.

Despite advancements in early detection and treatment, atherosclerosis remains the leading cause of death across all cardiovascular diseases (CVD). Biomechanical analysis of atherosclerotic lesions has the potential to reveal biomechanically instable or rupture-prone regions. Treatment decisions rarely consider the biomechanics of the stenosed lesion due in-part to difficulties in obtaining this information in a clinical setting. Previous 3D FEA approaches have incompletely incorporated the complex curvature of arterial geometry, material heterogeneity, and use of patient-specific data. To address these limitations and clinical need, herein we present a user-friendly fully automated program to reconstruct and simulate the wall mechanics of patient-specific atherosclerotic coronary arteries. The program enables 3D reconstruction from patient-specific data with heterogenous tissue assignment and complex arterial curvature. Eleven arteries with coronary artery disease (CAD) underwent baseline and 6-month follow-up angiographic and virtual histology-intravascular ultrasound (VH-IVUS) imaging. VH-IVUS images were processed to remove background noise, extract VH plaque material data, and luminal and outer contours. Angiography data was used to orient the artery profiles along the 3D centerlines. The resulting surface mesh is then resampled for uniformity and tetrahedralized to generate the volumetric mesh using TetGen. A mesh convergence study revealed edge lengths between 0.04 mm and 0.2 mm produced constituent volumes that were largely unchanged, hence, to save computational resources, a value of 0.2 mm was used throughout. Materials are assigned and finite element analysis (FEA) is then performed to determine stresses and strains across the artery wall. In a representative artery, the highest average effective stress was in calcium elements with 235 kPa while necrotic elements had the lowest average stress, reaching as low as 0.79 kPa. After applying nodal smoothening, the maximum effective stress across 11 arteries remained below 288 kPa, implying biomechanically stable plaques. Indeed, all atherosclerotic plaques remained unruptured at the 6-month longitudinal follow up diagnosis. These results suggest our automated analysis may facilitate assessment of atherosclerotic plaque stability.

Assessment with clinical data of a coupled bio-hemodynamics numerical model to predict leukocyte adhesion in coronary arteries.

Numerical simulations of coupled hemodynamics and leukocyte transport and adhesion inside coronary arteries have been performed. Realistic artery geometries have been obtained for a set of four patients from intravascular ultrasound and angiography images. The numerical model computes unsteady three-dimensional blood hemodynamics and leukocyte concentration in the blood. Wall-shear stress dependent leukocyte adhesion is also computed through agent-based modeling rules, fully coupled to the hemodynamics and leukocyte transport. Numerical results have a good correlation with clinical data. Regions where high adhesion is predicted by the simulations coincide to a good approximation with artery segments presenting plaque increase, as documented by clinical data from baseline and six-month follow-up exam of the same artery. In addition, it is observed that the artery geometry and, in particular, the tortuosity of the centerline are a primary factor in determining the spatial distribution of wall-shear stress, and of the resulting leukocyte adhesion patterns. Although further work is required to overcome the limitations of the present model and ultimately quantify plaque growth in the simulations, these results are encouraging towards establishing a predictive methodology for atherosclerosis progress.

Risk stratification of coronary plaques using physiologic characteristics by CCTA: Focus on shear stress.

The identification of factors determining whether a lesion progresses, destabilizes or becomes quiescent remains a challenge. Wall or endothelial shear stress (WSS or ESS, respectively), the frictional force acting on the lumen wall, is strongly associated with changes in the natural history of lesions. Several clinical intravascular imaging studies have shown a clear link between disturbed flow, typically characterized by low WSS, and plaque growth. In support of these studies, in-vitro experiments of shear stress have identified several mechanisms promoting atherosclerosis. More recently, the relationship between WSS and major adverse cardiac events has been explored. Improvements in coronary computed tomography angiography (CCTA) image resolution and quality has allowed for the calculation of WSS from CT. In this review, we provide an introduction to WSS, highlight important human and animal intravascular-based WSS studies, and discuss CT-based WSS studies to date. Finally, we discuss future directions of CCTA and WSS computation.

The influence of multidirectional shear stress on plaque progression and composition changes in human coronary arteries.

AIMS: Local wall shear stress (WSS) plays an important role in the onset of atherosclerotic plaque formation; however, it does not fully explain plaque progression and destabilisation. We aimed to investigate for the first time the influence of multidirectional WSS features on plaque progression and plaque composition changes in human coronary arteries. METHODS AND RESULTS: Coronary artery imaging using biplane angiography and virtual histology intravascular ultrasound (VH-IVUS) was performed in twenty patients with coronary artery disease at baseline and after six-month follow-up. Three-dimensional surfaces of the coronary arteries were generated using the coronary imaging and, together with patient-specific flow measurements, different WSS features (multidirectional and conventional time-averaged WSS [TAWSS]) were determined at baseline using computational fluid dynamics (CFD). The changes in plaque component area over the six-month period were determined from VH-IVUS. Changes in plaque composition rather than plaque size were primarily associated with the (multidirectional) WSS at baseline. Interestingly, regions simultaneously exposed to low TAWSS and low multidirectional WSS showed the greatest plaque progression (p<0.001). CONCLUSIONS: In this patient study, several multidirectional WSS features were found to contribute significantly to coronary plaque progression and changes in plaque composition.

Establishment of an Automated Algorithm Utilizing Optical Coherence Tomography and Micro-Computed Tomography Imaging to Reconstruct the 3-D Deformed Stent Geometry.

Percutaneous coronary intervention (PCI) is the prevalent treatment for coronary artery disease, with hundreds of thousands of stents implanted annually. Computational studies have demonstrated the role of biomechanics in the failure of vascular stents, but clinical studies is this area are limited by a lack of understanding of the deployed stent geometry, which is required to accurately model and predict the stent-induced in vivo biomechanical environment. Herein, we present an automated method to reconstruct the 3-D deployed stent configuration through the fusion of optical coherence tomography (OCT) and micro-computed tomography ( µ CT) imaging data. In an experimental setup, OCT and µ CT data were collected in stents deployed in arterial phantoms ( n=4 ). A constrained iterative deformation process directed by diffeomorphic metric mapping was developed to deform µ CT data of a stent wireframe to the OCT-derived sparse point cloud of the deployed stent. Reconstructions of the deployed stents showed excellent agreement with the ground-truth configurations, with the distance between corresponding points on the reconstructed and ground-truth configurations of [Formula: see text]. Finally, reconstructions required <30 min of computational time. In conclusion, the developed and validated reconstruction algorithm provides a complete spatially resolved reconstruction of a deployed vascular stent from commercially available imaging modalities and has the potential, with further development, to provide more accurate computational models to evaluate the in vivo post-stent mechanical environment, as well as clinical visualization of the 3-D stent geometry immediately following PCI.

Impact of combined plaque structural stress and wall shear stress on coronary plaque progression, regression, and changes in composition.

AIMS: The focal distribution of atherosclerotic plaques suggests that local biomechanical factors may influence plaque development. METHODS AND RESULTS: We studied 40 patients at baseline and over 12 months by virtual-histology intravascular ultrasound and bi-plane coronary angiography. We calculated plaque structural stress (PSS), defined as the mean of the maximum principal stress at the peri-luminal region, and wall shear stress (WSS), defined as the parallel frictional force exerted by blood flow on the endothelial surface, in areas undergoing progression or regression. Changes in plaque area, plaque burden (PB), necrotic core (NC), fibrous tissue (FT), fibrofatty tissue, and dense calcium were calculated for each co-registered frame. A total of 4029 co-registered frames were generated. In areas with progression, high PSS was associated with larger increases in NC and small increases in FT vs. low PSS (difference in ΔNC: 0.24 ± 0.06 mm2; P < 0.0001, difference in ΔFT: -0.15 ± 0.08 mm2; P = 0.049). In areas with regression, high PSS was associated with increased NC and decreased FT (difference in ΔNC: 0.15 ± 0.04; P = 0.0005, difference in ΔFT: -0.31 ± 0.06 mm2; P < 0.0001). Low WSS was associated with increased PB vs. high WSS in areas with progression (difference in ΔPB: 3.3 ± 0.4%; P < 0.001) with a similar pattern observed in areas with regression (difference in ΔPB: 1.2 ± 0.4%; P = 0.004). Plaque structural stress and WSS were largely independent of each other (R2 = 0.002; P = 0.001). CONCLUSION: Areas with high PSS are associated with compositional changes consistent with increased plaque vulnerability. Areas with low WSS are associated with more plaque growth in areas that progress and less plaque loss in areas that regress. The interplay of PSS and WSS may govern important changes in plaque size and composition.

High Coronary Shear Stress in Patients With Coronary Artery Disease Predicts Myocardial Infarction.

BACKGROUND: Coronary lesions with low fractional flow reserve (FFR) that are treated medically are associated with higher revascularization rates. High wall shear stress (WSS) has been linked with increased plaque vulnerability. OBJECTIVES: This study investigated the prognostic value of WSS measured in the proximal segments of lesions (WSSprox) to predict myocardial infarction (MI) in patients with stable coronary artery disease (CAD) and hemodynamically significant lesions. The authors hypothesized that in patients with low FFR and stable CAD, higher WSSprox would predict MI. METHODS: Among 441 patients in the FAME II (Fractional Flow Reserve Versus Angiography for Multivessel Evaluation II) trial with FFR ≤0.80 who were randomized to medical therapy alone, 34 (8%) had subsequent MI within 3 years. Patients with vessel-related MI and adequate angiograms for 3-dimensional reconstruction (n = 29) were propensity matched to a control group with no MI (n = 29) by using demographic and clinical variables. Coronary lesions were divided into proximal, middle, and distal, along with 5-mm upstream and downstream segments. WSS was calculated for each segment. RESULTS: Median age was 62 years, and 46 (79%) were male. In the marginal Cox model, whereas lower FFR showed a trend (hazard ratio: 0.084; p = 0.064), higher WSSprox (hazard ratio: 1.234; p = 0.002, C-index = 0.65) predicted MI. Adding WSSprox to FFR resulted in a significant increase in global chi-square for predicting MI (p = 0.045), a net reclassification improvement of 0.69 (p = 0.005), and an integrated discrimination index of 0.11 (p = 0.010). CONCLUSIONS: In patients with stable CAD and hemodynamically significant lesions, higher WSS in the proximal segments of atherosclerotic lesions is predictive of MI and has incremental prognostic value over FFR.

Low Coronary Wall Shear Stress Is Associated With Severe Endothelial Dysfunction in Patients With Nonobstructive Coronary Artery Disease.

OBJECTIVES: This study investigated the relationship between low wall shear stress (WSS) and severe endothelial dysfunction (EDFx). BACKGROUND: Local hemodynamic forces such as WSS play an important role in atherogenesis through their effect on endothelial cells. The study hypothesized that low WSS independently predicts severe EDFx in patients with coronary artery disease (CAD). METHODS: Forty-four patients with CAD underwent coronary angiography, fractional flow reserve, and endothelial function testing. Segments with >10% vasoconstriction after acetylcholine (Ach) infusion were defined as having severe EDFx. WSS, calculated using 3-dimensional angiography, velocity measurements, and computational fluid dynamics, was defined as low (<1 Pa), intermediate (1 to 2.5 Pa), or high (>2.5 Pa). RESULTS: Median age was 52 years, 73% were women. Mean fractional flow reserve was 0.94 ± 0.06. In 4,510 coronary segments, median WSS was 3.67 Pa. A total of 24% had severe EDFx. A higher proportion of segments with low WSS had severe EDFx (71%) compared with intermediate WSS (22%) or high WSS (23%) (p < 0.001). Segments with low WSS demonstrated greater vasoconstriction in response to Ach than did intermediate or high WSS segments (-10.7% vs. -2.5% vs. +1.3%, respectively; p < 0.001). In a multivariable logistic regression analysis, female sex (odds ratio [OR]: 2.44; p = 0.04), diabetes (OR: 5.01; p = 0.007), and low WSS (OR: 9.14; p < 0.001) were independent predictors of severe EDFx. CONCLUSIONS: In patients with nonobstructive CAD, segments with low WSS demonstrated more vasoconstriction in response to Ach than did intermediate or high WSS segments. Low WSS was independently associated with severe EDFx.

Oscillatory wall shear stress is a dominant flow characteristic affecting lesion progression patterns and plaque vulnerability in patients with coronary artery disease.

Although experimental studies suggest that low and oscillatory wall shear stress (WSS) promotes plaque transformation to a more vulnerable phenotype, this relationship has not been examined in human atherosclerosis progression. Thus, the aim of this investigation was to examine the association between oscillatory WSS, in combination with WSS magnitude, and coronary atherosclerosis progression. We hypothesized that regions of low and oscillatory WSS will demonstrate progression towards more vulnerable lesions, while regions exposed to low and non-oscillatory WSS will exhibit progression towards more stable lesions. Patients (n = 20) with non-flow-limiting coronary artery disease (CAD) underwent baseline and six-month follow-up angiography, Doppler velocity and radiofrequency intravascular ultrasound (VH-IVUS) acquisition. Computational fluid dynamics models were constructed to compute time-averaged WSS magnitude and oscillatory WSS. Changes in VH-IVUS-defined total plaque and constituent areas were quantified in focal regions (i.e. sectors; n = 14 235) and compared across haemodynamic categories. Compared with sectors exposed to low WSS magnitude, high WSS sectors demonstrated regression of total plaque area (p < 0.001) and fibrous tissue (p < 0.001), and similar progression of necrotic core. Sectors subjected to low and oscillatory WSS exhibited total plaque area regression, while low and non-oscillatory WSS sectors demonstrated total plaque progression (p < 0.001). Furthermore, compared with low and non-oscillatory WSS areas, sectors exposed to low and oscillatory WSS demonstrated regression of fibrous (p < 0.001) and fibrofatty (p < 0.001) tissue and similar progression of necrotic core (p = 0.82) and dense calcium (p = 0.40). Herein, we demonstrate that, in patients with non-obstructive CAD, sectors subjected to low and oscillatory WSS demonstrated regression of total plaque, fibrous and fibrofatty tissue, and progression of necrotic core and dense calcium, which suggest a transformation to a more vulnerable phenotype.

Quantification of the focal progression of coronary atherosclerosis through automated co-registration of virtual histology-intravascular ultrasound imaging data.

The goal of this study was to evaluate the accuracy of a novel algorithm that circumferentially co-registers serial virtual histology-intravascular ultrasound (VH-IVUS) data for the focal assessment of coronary atherosclerosis progression. Thirty-three patients with an abnormal non-invasive cardiac stress test or stable angina underwent baseline and follow-up (6 or 12 months) invasive evaluation that included acquisition of VH-IVUS image data. Baseline and follow-up image pairs (n = 4194) were automatically co-registered in the circumferential direction via a multi-variate cross-correlation algorithm. Algorithm stability and accuracy were assessed by comparing results from multiple iterations of the algorithm (iteration 1 vs. iteration 2) and against values determined manually by two expert VH-IVUS readers (algorithm vs. two expert readers). Furthermore, focal plaque progression values were compared between the algorithm and expert readers following co-registration by the independently determined angles. Strong agreement in circumferential co-registration angles were observed across multiple iterations of the algorithm (stability) and between the algorithm and expert readers (accuracy; all concordance correlation coefficients >0.98). Furthermore, circumferential co-registration angles determined by the algorithm were not statistically when compared to values determined by two expert readers (p = 0. 99). Bland-Altman analysis indicated minimal bias when comparing focal VH-IVUS defined plaque progression in corresponding sectors following circumferential co-registration between the algorithm and expert readers. Finally, average differences in changes in total plaque and constituent areas between the algorithm and readers were within the average range of difference between readers (interobserver variability). We present a stable and validated algorithm to automatically circumferentially co-register serial VH-IVUS imaging data for the focal quantification of coronary atherosclerosis progression.

Evaluation of a framework for the co-registration of intravascular ultrasound and optical coherence tomography coronary artery pullbacks.

A growing number of studies have used a combination of intravascular ultrasound (IVUS) and optical coherence tomography (OCT) for the assessment of atherosclerotic plaques. Given their respective strengths these imaging modalities highly complement each other. Correlations of hemodynamics and coronary artery disease (CAD) have been extensively investigated with both modalities separately, though not concurrently due to challenges in image registration. Manual co-registration of these modalities is a time expensive task subject to human error, and the development of an automatic method has not been previously addressed. We developed a framework that uses dynamic time warping for the longitudinal co-registration and dynamic programming for the circumferential co-registration of images and evaluated the methodology in a cohort (n = 12) of patients with moderate CAD. Excellent correlation was seen between the algorithm and two expert readers for longitudinal co-registration (CCC = 0.9964, CCC = 0.9959) and circumferential co-registration (CCC = 0.9688, CCC = 0.9598). The mean error of the circumferential co-registration angle was found to be within 10%. A framework for the co-registration of IVUS and OCT pullbacks has been developed which provides a foundation for comprehensive studies of CAD biomechanics.

Comparison of angiographic and IVUS derived coronary geometric reconstructions for evaluation of the association of hemodynamics with coronary artery disease progression.

Wall shear stress (WSS) has been investigated as a prognostic marker for the prospective identification of rapidly progressing coronary artery disease (CAD) and atherosclerotic lesions likely to gain high-risk (vulnerable) characteristics. The goal of this study was to compare biplane angiographic vs. intravascular ultrasound (IVUS) derived reconstructed coronary geometries to evaluate agreement in geometry, computed WSS, and association of WSS and CAD progression. Baseline and 6-month follow-up angiographic and IVUS imaging data were collected in patients with non-obstructive CAD (n = 5). Three-dimensional (3D) reconstructions of the coronary arteries were generated with each technique, and patient-specific computational fluid dynamics models were constructed to compute baseline WSS values. Geometric comparisons were evaluated in arterial segments (n = 9), and hemodynamic data were evaluated in circumferential sections (n = 468). CAD progression was quantified from serial IVUS imaging data (n = 277), and included virtual-histology IVUS (VH-IVUS) derived changes in plaque composition. There was no significant difference in reconstructed coronary segment lengths and cross-sectional areas (CSA), however, IVUS derived geometries exhibited a significantly larger left main CSA than the angiographic reconstructions. Computed absolute time-averaged WSS (TAWSSABS) values were significantly greater in the IVUS derived geometries, however, evaluations of relative TAWSS (TAWSSREL) values revealed improved agreement and differences within defined zones of equivalence. Associations between VH-IVUS defined CAD progression and angiographic or IVUS derived WSS exhibited poor agreement when examining TAWSSABS data, but improved when evaluating the association with TAWSSREL data. We present data from a small cohort of patients highlighting strong agreement between angiographic and IVUS derived coronary geometries, however, limited agreement is observed between computed WSS values and associations of WSS with CAD progression.

Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients.

Cardiac allograft vasculopathy (CAV) is one of the leading causes of morbidity and morality in orthotopic heart transplant (HTx) patients. While disturbed flow patterns have been linked to the spatial localization of atherosclerosis, the role of hemodynamics in CAV development has not been examined. HTx patients (n = 5) requiring percutaneous coronary intervention (PCI) for a focal, epicardial lesion were studied. Angiographic images were retrospectively obtained from baseline (i.e., in the presence of no observed disease) and follow-up catheterizations (i.e., at the time of PCI; 12.4 ± 2.6 years post-HTx). Patient-specific computational models were created from baseline images. Computational fluid dynamic techniques were employed to quantify the hemodynamic environment, which was expressed as normalized time-averaged WSS (TAWSSnorm; measure of temporal WSS magnitude) and normalized WSS angle deviation (WSSADnorm; measure of instantaneous WSS vector oscillation) values. Baseline hemodynamic and follow-up angiographic data were co-registered to investigate the association between WSS and subsequent occlusive CAV lesion location. Results indicate a high degree of co-localization between baseline low WSS data and follow-up occlusive CAV lesion. Local minima in TAWSSnorm were located 2.5 ± 0.6 mm from the site of PCI. Furthermore, local maxima in WSSADnorm were located 3.9 ± 0.7 mm from the site of PCI. In 3 patients, the occlusive lesion formed in a region that was subjected to both low and oscillatory WSS at baseline. There was discernable spatial co-localization between baseline disturbed flow patterns and follow-up CAV lesions requiring PCI. These results suggest a role of fluid mechanics in the development of focal, flow-limiting CAV lesions.

An assessment of intra-patient variability on observed relationships between wall shear stress and plaque progression in coronary arteries.

BACKGROUND: Wall shear stress (WSS) has been associated with sites of plaque localization and with changes in plaque composition in human coronary arteries. Different values have been suggested for categorizing WSS as low, physiologic or high; however, uncertainties in flow rates, both across subjects and within a given individual, can affect the classification of WSS and thus influence the observed relationships between local hemodynamics and plaque changes over time. This study examines the effects of uncertainties in flow rate boundary conditions upon WSS values and investigates the influence of this variability on the observed associations of WSS with changes in VH-IVUS derived plaque components. METHODS: Three patients with coronary artery disease underwent baseline and 12 month follow-up angiography and virtual histology-intravascular ultrasound (VH-IVUS) measurements. Coronary artery models were reconstructed from the data and models with and without side-branches were created. Patient-specific Doppler ultrasound (DUS) data were employed as inflow boundary conditions and computational fluid dynamics was used to calculate the WSS in each model. Further, the influence of representative coronary artery flow waveforms upon WSS values was investigated and the concept of treating WSS using relative, rather than actual, values was explored. RESULTS: Models that included side-branch outflows and subject-specific DUS velocities were considered to be the reference cases. Hemodynamic differences were caused by the exclusion of side-branches and by imposing alternative velocity waveforms. One patient with fewer side-branches and a scaled generic waveform had little deviation from the reference case, while another patient with several side-branches excluded showed much larger departures from the reference situation. Differences between models and the respective reference cases were reduced when data were analyzed using relative, rather than actual, WSS. CONCLUSIONS: When considering individual subjects, large variations in patient-specific flow rates and exclusion of multiple side-branches in computational models can cause significant differences in observed associations between plaque evolution and ranges of computed WSS. These differences may contribute to the large variability typically found among subjects in pooled populations. Relative WSS may be more useful than actual WSS as a correlative variable when there is a large degree of uncertainty in flow rate data.

Focal association between wall shear stress and clinical coronary artery disease progression.

Wall shear stress (WSS) has been investigated as a potential prospective marker to identify rapidly progressing coronary artery disease (CAD) and potential for lesions to acquire vulnerable characteristics. Previous investigations, however, are limited by a lack of understanding of the focal association between WSS and CAD progression (i.e., data are notably spatially averaged). Thus, the aim of this investigation was to examine the focal association between WSS and coronary atherosclerosis progression, and compare these results to those determined by spatial averaging. Five patients with CAD underwent baseline and 6-month follow-up angiographic and virtual histology-intravascular ultrasound imaging to quantify CAD progression. Patient-specific computational fluid dynamics models were constructed to compute baseline WSS values, which were either averaged around the entire artery circumference or examined in focal regions (sectors). Analysis of data within each sector (n = 3871) indicated that circumferentially averaged and sector WSS values were statistically different (p < 0.05) and exhibited poor agreement (concordance correlation coefficient = 0.69). Furthermore, differences were observed between the analysis techniques when examining the association of WSS and CAD progression. This investigation highlights the importance of examining spatially heterogeneous variables at a focal level to reduce the affect of data reduction and warrants implementation in a larger clinical study to determine the predictive power in prospectively identifying rapidly progressing and/or vulnerable coronary plaques.

Fluid-structure interaction of a patient-specific abdominal aortic aneurysm treated with an endovascular stent-graft.

BACKGROUND: Abdominal aortic aneurysms (AAA) are local dilatations of the infrarenal aorta. If left untreated they may rupture and lead to death. One form of treatment is the minimally invasive insertion of a stent-graft into the aneurysm. Despite this effective treatment aneurysms may occasionally continue to expand and this may eventually result in post-operative rupture of the aneurysm. Fluid-structure interaction (FSI) is a particularly useful tool for investigating aneurysm biomechanics as both the wall stresses and fluid forces can be examined. METHODS: Pre-op, Post-op and Follow-up models were reconstructed from CT scans of a single patient and FSI simulations were performed on each model. The FSI approach involved coupling Abaqus and Fluent via a third-party software - MpCCI. Aneurysm wall stress and compliance were investigated as well as the drag force acting on the stent-graft. RESULTS: Aneurysm wall stress was reduced from 0.38 MPa before surgery to a value of 0.03 MPa after insertion of the stent-graft. Higher stresses were seen in the aneurysm neck and iliac legs post-operatively. The compliance of the aneurysm was also reduced post-operatively. The peak Post-op axial drag force was found to be 4.85 N. This increased to 6.37 N in the Follow-up model. CONCLUSION: In a patient-specific case peak aneurysm wall stress was reduced by 92%. Such a reduction in aneurysm wall stress may lead to shrinkage of the aneurysm over time. Hence, post-operative stress patterns may help in determining the likelihood of aneurysm shrinkage post EVAR. Post-operative remodelling of the aneurysm may lead to increased drag forces.

Geometrical enhancements for abdominal aortic stent-grafts.

PURPOSE: To compare the function of 2 stent-graft designs for endovascular abdominal aortic aneurysm repair. METHODS: Computational fluid dynamics was used to investigate the performance of a conventional stent-graft versus one with a novel tapered configuration (equal area ratios at the inlet and bifurcation). Idealized geometries (uniplanar) were formed first for both devices. To mimic the clinical setting with pulsatile blood flow, a realistic model (multiplanar) was created for the conventional stent-graft based on computed tomography scans from 3 patients with different aortic geometries. A similar model was created for the tapered stent-graft by mimicking the deployment of the conventional stent-graft through its centerline. RESULTS: The tapered stent-graft model demonstrated reduced secondary flow vortices and wall shear stresses in the iliac limbs compared to the conventional graft in the idealized scenario. The drag forces in the idealized models were similar for both designs, though the tapered stent-graft showed a 4% reduction. Flow was split more evenly between the tapered stent-graft limbs in the realistic scenario. CONCLUSION: The novel tapered design reduced flow velocities and secondary flows due to its smooth trunk-to-limb transition, while also splitting the flow between the iliac limbs more evenly. In multiplanar models, the out-of-plane curvature was the greatest cause of skewed flow, which reduced the benefits of the tapered stent-graft.