Turbulence intensity measurements using particle image velocimetry in diseased carotid artery models: Effect of stenosis severity,plaque eccentricity,and ulceration

Clinical decision-making for the treatment of patients with diseased carotid artery is mainly based on the severity of the stenosis. However, stenosis severity alone is not a sensitive indicator, and other local factors for the assessment of stroke risk are required. Flow disturbance is of particular interest due to its proven association with increased thromboembolic activities. The objective of this study was to investigate the level of turbulence intensity (TI) with regards to certain geometrical features of the plaque – namely stenosis severity, eccentricity, and ulceration. A family of eight carotid-artery bifurcation models was examined using particle image velocimetry. Results showed a marked difference in turbulence intensity among these models; increasing degree of stenosis severity resulted in increased turbulence intensity, going from 0.12 m/s for mild stenosis to 0.37 m/s for severe stenosis (with concentric geometry). Moreover, independent of stenosis severity, eccentricity led to further elevations in turbulence intensity, increasing TI by 0.05–0.10 m/s over the counterpart concentric plaque. The presence of ulceration (in a 50% eccentric plaque) produced a larger portion of moderate turbulence intensity (~0.10 m/s) compared to the non-ulcerated model, more proximal to the bifurcation apex in the post-stenotic recirculation zone. The effect of plaque eccentricity and ulceration in enhancing the downstream turbulence has potential clinical implications for a more sensitive assessment of stroke risk beyond stenosis severity alone.     

Low WSS Induces Intimal Thickening,while Large WSS Variation and Inflammation Induce Medial Thinning,in an Animal Model of Atherosclerosis

Objective

Atherosclerotic plaque development in the arterial wall is the result of complex interaction between the wall’s endothelial layer and blood hemodynamics. However, the interaction between hemodynamic parameters and inflammation in plaque evolution is not yet fully understood. The aim of the present study was to investigate the relation between wall shear stress (WSS) and vessel wall inflammation during atherosclerotic plaque development in a minipig model of carotid stenosis.

Methods

A surgical procedure was performed to create left common carotid artery stenosis by placement of a perivascular cuff in minipigs under atherogenic diet. Animals were followed up on 3T MRI, 1 week after surgery and 3, 6, and 8 months after initiation of the diet. Computational fluid dynamics simulation estimated WSS distribution for the first imaging point. Vascular geometries were co-registered for direct comparison of plaque development and features (Gadolinium- and USPIO-Contrast Enhanced MRI, for permeability and inflammation respectively) with the initial WSS. Histological analysis was performed and sections were matched to MR images, based on spatial landmarks.

Results

Vessel wall thickening, permeability and inflammation were observed distally from the stenosis. They were eccentric and facing regions of normal wall thickness. Histological analysis confirmed eccentric plaque formation with lipid infiltration, intimal thickening and medial degradation. High phagocytic activity in the stenosis region was co-localized with high WSS, corresponding to intense medial degradation observed on histology samples.

Conclusion

Lower WSS promotes atherosclerotic plaque development distal to an induced stenosis. Vascular and perivascular inflammation locations were predominant in the high WSS stenosis segment, where medial thinning was the major consequence.     

Effect of geometrical assumptions on numerical modeling of coronary blood flow under normal and disease conditions

Shear stress plays a pivotal role in pathogenesis of coronary heart disease. The spatial and temporal variation in hemodynamics of blood flow, especially shear stress, is dominated by the vessel geometry. The goal of the present study was to investigate the effect of 2D and 3D geometries on the numerical modeling of coronary blood flow and shear stress distribution. We developed physiologically realistic 2D and 3D models (with similar geometries) of the human left coronary artery under normal and stenosis conditions (30%, 60%, and 80%) using PROE (WF 3). Transient blood flows in these models were solved using laminar and turbulent (k-ω) models using a computational fluid dynamics solver, FLUENT (v6.3.26). As the stenosis severity increased, both models predicted a similar pattern of increased shear stress at the stenosis throat, and in recirculation zones formed downstream of the stenosis. The 2D model estimated a peak shear stress value of 0.91, 2.58, 5.21, and 10.09 Pa at the throat location under normal, 30%, 60%, and 80% stenosis severity. The peak shear stress values at the same location estimated by the 3D model were 1.41, 2.56, 3.15, and 13.31 Pa, respectively. The 2D model underestimated the shear stress distribution inside the recirculation zone compared with that of 3D model. The shear stress estimation between the models diverged as the stenosis severity increased. Hence, the 2D model could be sufficient for analyzing coronary blood flow under normal conditions, but under disease conditions (especially 80% stenosis) the 3D model was more suitable.     

Haemodynamic assessment of human coronary arteries is affected by degree of freedom of artery movement

Abnormal haemodynamic parameters are associated with atheroma plaque progression and instability in coronary arteries. Flow recirculation, shear stress and pressure gradient are understood to be important pathogenic mediators in coronary disease. The effect of freedom of coronary artery movement on these parameters is still unknown. Fluid–structure interaction (FSI) simulations were carried out in 25 coronary artery models derived from authentic human coronaries in order to investigate the effect of degree of freedom of movement of the coronary arteries on flow recirculation, wall shear stress (WSS) and wall pressure gradient (WPG). Each FSI model had distinctive supports placed upon it. The quantitative and qualitative differences in flow recirculation, maximum wall shear stress (MWSS), areas of low wall shear stress (ALWSS) and maximum wall pressure gradient (MWPG) for each model were determined. The results showed that greater freedom of movement was associated with lower MWSS, smaller ALWSS, smaller flow recirculation zones and lower MWPG. With increasing percentage diameter stenosis (%DS), the effect of degree of freedom on flow recirculation and WSS diminished. Freedom of movement is an important variable to be considered for computational modelling of human coronary arteries, especially in the setting of mild to moderate stenosis.

Abbreviations: 3D: Three-dimensional; 3DR: Three-dimensional Reconstruction; 3D-QCA: Three-dimensional quantitative coronary angiography; ALWSS: Areas of low wall shear stress; CAD: Coronary artery disease; CFD: Computational fluid dynamics; %DS: Diameter stenosis percentage; EPCS: End point of counter-rotating streamlines; FSI: Fluid–structure interaction; IVUS: Intravascular ultrasound; LAD: Left anterior descending; MWSS: Maximum wall shear stress; SST: Shear stress transport; TAWSS: Time-averaged wall shear stress; WSS: wall shear stress; WPG: Wall pressure gradient; MWPG: Maximum wall pressure gradient; FFR: Fractional flow reserve; iFR: Instantaneous wave-free ratio     

Flow pattern analysis in a highly stenotic patient-specific carotid bifurcation model using a turbulence model

The aim of this study is to investigate the blood flow pattern in carotid bifurcation with a high degree of luminal stenosis, combining in vivo magnetic resonance imaging (MRI) and computational fluid dynamics (CFD). A newly developed two-equation transitional model was employed to evaluate wall shear stress (WSS) distribution and pressure drop across the stenosis, which are closely related to plaque vulnerability. A patient with an 80% left carotid stenosis was imaged using high resolution MRI, from which a patient-specific geometry was reconstructed and flow boundary conditions were acquired for CFD simulation. A transitional model was implemented to investigate the flow velocity and WSS distribution in the patient-specific model. The peak time-averaged WSS value of approximately 73 Pa was predicted by the transitional flow model, and the regions of high WSS occurred at the throat of the stenosis. High oscillatory shear index values up to 0.50 were present in a helical flow pattern from the outer wall of the internal carotid artery immediately after the throat. This study shows the potential suitability of a transitional turbulent flow model in capturing the flow phenomena in severely stenosed carotid arteries using patient-specific MRI data and provides the basis for further investigation of the links between haemodynamic variables and plaque vulnerability. It may be useful in the future for risk assessment of patients with carotid disease.     

Hemodynamic impacts of various types of stenosis in the left coronary artery bifurcation: A patient-specific analysis

This study investigates the hemodynamic changes to various types of coronary stenosis in the left coronary artery bifurcation, based on a patient-specific analysis. Twenty two patients with left coronary artery disease were included in this study. All stenoses involving the left coronary artery bifurcation were classified into four types, according to their locations: A) left circumflex (LCx) and left anterior descending (LAD), B) LCx only, C) left main stem only, and D) LAD only. Computational fluid dynamics (CFD) was performed to analyze the flow and wall shear stress (WSS) changes in all reconstructed left coronary geometries. Our results showed that the flow velocity and WSS were significantly increased at stenotic locations. High WSS was found at >70% lumen stenosis, which ranged from 2.5 Pa to 3.5 Pa. This study demonstrates that in patients with more than 50% stenosis in the left coronary artery bifurcation, WSS plays an important role in providing information about the extent of coronary atherosclerosis in the left coronary artery branch.     

Simulation of particle-hemodynamics in a partially occluded artery segment with implications to the initiation of microemboli and secondary stenoses.

Computational results of laminar incompressible blood-particle flow analyses in an axisymmetric artery segment with a smooth local area constriction of 75 percent have been presented. The flow input waveform was sinusoidal with a nonzero average. The non-Newtonian behavior of blood was simulated with a modified Quemada model, platelet concentrations were calculated with a drift-flux model, and monocyte trajectories were described and compared for both Newtonian and Quemada rheologies. Indicators of "disturbed flow" included the time-averaged wall shear stress (WSS), the oscillatory shear index (OSI), and the wall shear stress gradient (WSSG). Implications of the vortical flow patterns behind the primary stenosis to the formation of microemboli and downstream stenoses are as follows. Elevated platelet concentrations due to accumulation in recirculation zones mixed with thrombin and ADP complexes assumed to be released upstream in high wall shear stress regions, could form microemboli, which are convected downstream. Distinct near-wall vortices causing a local increase in the WSSG and OSI as well as blood-particle entrainment with possible wall deposition, indicate sites susceptible to the onset of an additional stenosis proximal to the initial geometric disturbance.     

Direct numerical simulation of transitional flow in a stenosed carotid bifurcation

The blood flow dynamics of a stenosed, subject-specific, carotid bifurcation were numerically simulated using the spectral element method. Pulsatile inlet conditions were based on in vivo color Doppler ultrasound measurements of blood velocity. The results demonstrated the transitional or weakly turbulent state of the blood flow, which featured rapid velocity and pressure fluctuations in the post-stenotic region of the internal carotid artery (ICA) during systole and laminar flow during diastole. High-frequency vortex shedding was greatest downstream of the stenosis during the deceleration phase of systole. Velocity fluctuations had a frequency within the audible range of 100-300Hz. Instantaneous wall shear stress (WSS) within the stenosis was relatively high during systole ( approximately 25-45Pa) compared to that in a healthy carotid. In addition, high spatial gradients of WSS were present due to flow separation on the inner wall. Oscillatory flow reversal and low pressure were observed distal to the stenosis in the ICA. This study predicts the complex flow field, the turbulence levels and the distribution of the biomechanical stresses present in vivo within a stenosed carotid artery.     

Effects of different stent designs on local hemodynamics in stented arteries

Following the deployment of a coronary stent and disruption of an atheromatous plaque, the deformation of the arterial wall and the presence of the stent struts create a new fluid dynamic field, which can cause an abnormal biological response. In this study 3D computational models were used to analyze the fluid dynamic disturbances induced by the placement of a stent inside a coronary artery. Stents models were first expanded against a simplified arterial plaque, with a solid mechanics analysis, and then subjected to a fluid flow simulation under pulsatile physiological conditions. Spatial and temporal distribution of arterial wall shear stress (WSS) was investigated after the expansion of stents of different designs and different strut thicknesses. Common oscillatory WSS behavior was detected in all stent models. Comparing stent and vessel wall surfaces, maximum WSS values (in the order of 1Pa) were located on the stent surface area. WSS spatial distribution on the vascular wall surface showed decreasing values from the center of the vessel wall portion delimited by the stent struts to the wall regions close to the struts. The hemodynamic effects induced by two different thickness values for the same stent design were investigated, too, and a reduced extension of low WSS region (<0.5Pa) was observed for the model with a thicker strut.     

The effects of stenosis severity on the hemodynamic parameters-assessment of the correlation between stress phase angle and wall shear stress

To study the effects of increase in the degree of stenosis severity and subsequent complexity of hemodynamic patterns on hemodynamic parameters, experimental investigations and numerical simulations were performed. The correlations between the large negative Stress Phase Angle (SPA), the low mean Wall Shear Stress (WSS) and high Oscillatory Shear Index (OSI) were investigated at the distal shoulder and post-stenotic regions as the outcomes of elevated stenosis severity. Models included non-Newtonian fluid flow in stenotic arteries with 30-80% symmetrical stenoses. To study the interactions between pulsatile WSS and pulsatile wall circumferential stress (WCS) acting on endothelial cells, SPA as the phase difference between WSS and WCS waves was used. Moreover, the distribution of SPA on the lumen axis was compared to the distributions of the mean WSS and OSI that have been regarded until now as the determinants of atherosclerosis-prone regions. Results indicate that an increase in stenosis severity, not only affects the mean WSS, mean WCS and pulse amplitudes, but also influences the phase difference between them. The SPA is large negative on the distal shoulder and post-stenotic areas where atherosclerotic plaque develops. The increasing stenosis severity and the subsequent increasing complexity of hemodynamic patterns affect the correlation between any of the low mean WSS and high OSI with large negative SPA, such that it not only leads to create and develop some regions where the correlation between any of the low mean WSS and high OSI with large negative SPA is well but also leads to create and develop other regions where such correlations fail.     

Numerical simulation of blood pulsatile flow in a stenosed carotid artery using different rheological models

Symmetrical 30-60% stenosis in a common carotid artery under unsteady flow condition for Newtonian and six non-Newtonian viscosity models are investigated numerically. Results show power-law model produces higher deviations, in terms of velocity and wall shear stress in comparison with other models while generalized power-law and modified-Casson models are more prone to Newtonian state. Comparing separation length of recirculation region at different critical points of cardiac cycle confirms the necessity of considering blood flow in unsteady mode. Increasing stenosis intensity causes flow patterns more disturbed downstream of the stenosis and WSS appear to develop remarkably at the stenosis throat.     

Myocardial bridging and endothelial dysfunction – Computational fluid dynamics study

Myocardial bridging (MB) is associated with endothelial dysfunction in patients with angina and non-obstructive coronary artery disease. This study aims to determine if there is a link between abnormal blood flow patterns and endothelial dysfunction in patients with MB. Ten patients with MB in their left anterior descending (LAD) artery were selected, 5 of whom had endothelial dysfunction and 5 had no endothelial dysfunction based on their response to acetylcholine. Similarly, 10 patients without MB in their LAD, 5 of whom had endothelial dysfunction and 5 of whom had no endothelial dysfunction, were studied as a control group. Transient computational fluid dynamics simulations were performed to derive wall shear stress (WSS) over the entire vessel including proximal, middle and distal segments. Patients with MB and endothelial dysfunction had lower WSS in the proximal LAD and greater WSS in the mid-LAD than patients with MB but without endothelial dysfunction. When comparing patients with endothelial dysfunction, those with MB had significantly lower shear stress in the proximal LAD (0.32 ± 0.14 Pa (with MB) vs 0.71 ± 0.38 Pa (without MB), p = 0.01) and greater shear stress in the mid-LAD (2.81 ± 1.20 Pa (with MB) vs 1.66 ± 0.31 Pa (without MB), p = 0.014) than patients without MB. Our findings demonstrated that the presence of MB significantly contributes to low WSS and endothelial dysfunction relationship.     

Transient blood flow in elastic coronary arteries with varying degrees of stenosis and dilatations: CFD modelling and parametric study

In this paper, we have analysed pulsatile flow through partially occluded elastic arteries, to determine the haemodynamic parameters of wall shear stress (WSS), wall pressure gradient and pressure drops (ΔP), contributing to enhanced flow resistance and myocardial ischaemic regions which impair cardiac contractility and cause increased work load on the heart. In summary, it can be observed that stenoses in an artery significantly influence the haemodynamic parameters of wall shear stress and pressure drop in contrast to dilatations case. This deduces that stenosis plays a more critical role in plaque growth and vulnerability in contrast to dilatation, and should be the key element in cardiovascular pathology and diagnosis. Through quantitative analysis of WSS and ΔP, we have provided a clearer insight into the haemodynamics of atherosclerotic arteries. Determination of these parameters can be helpful to cardiologists, because it is directly implicated in the genesis and development of atherosclerosis.     

Advanced human carotid plaque progression correlates positively with flow shear stress using follow-up scan data: An in vivo MRI multi-patient 3D FSI study

Although it has been well-accepted that atherosclerosis initiation and early progression correlate negatively with flow wall shear stresses (FSS), increasing evidence suggests mechanisms governing advanced plaque progression are not well understood. Fourteen patients were scanned 2–4 times at 18 month intervals using a histologically validated multi-contrast magnetic resonance imaging (MRI) protocol to acquire carotid plaque progression data. Thirty-two scan pairs (baseline and follow-up scans) were formed with slices matched for model construction and analysis. 3D fluid–structure interaction (FSI) models were constructed and plaque wall stress (PWS) and flow shear stress (FSS) were obtained from all matching lumen data points (400–1000 per plaque; 100 points per matched slice) to quantify correlations with plaque progression measured by vessel wall thickness increase (WTI). Using FSS and PWS data from follow-up scan, 21 out of 32 scan pairs showed a significant positive correlation between WTI and FSS (positive/negative/no significance ratio=21/8/3), and 26 out of 32 scan pairs showed a significant negative correlation between WTI and PWS (positive/negative/no significance ratio=2/26/4). The mean FSS value of lipid core nodes (n=5294) from all 47 plaque models was 63.5 dyn/cm², which was 45% higher than that from all normal vessel nodes (n=27553, p<0.00001). The results from this intensive FSI study indicate that flow shear stress from follow-up scan correlates positively with advanced plaque progression which is different from what has been observed in plaque initiation and early-stage progression. It should be noted that the correlation results do not automatically lead to any causality conclusions.     

Carotid geometry effects on blood flow and on risk for vascular disease

It has been widely observed that atherosclerotic diseases occur at sites with complex hemodynamics, such as artery bifurcations, junctions, and regions of high curvature. These regions usually have very low or highly oscillatory wall shear stress (WSS). In the present work, 3D pulsatile blood flow through a model of the carotid artery bifurcation was simulated using a finite volume numerical method. The goal was to quantify the risk of atherogenesis associated with different carotid artery geometries. A risk scale based on the average WSS on the sinus wall of the internal carotid artery was proposed-a scale that can be used to quantify the effect of the carotid geometry on the relative risk for developing vascular disease. It was found that the bifurcation angle and the out-of-plane angle of the internal carotid artery affect the formation of low stress regions on the carotid walls. The main conclusions are: (a) larger internal carotid artery angles (theta(IC)) generally increase the frequency and the area of blood recirculation and lower the WSS on the sinus wall, hence increasing the risk of plaque build-up; (b) off-plane angles were found to lower the WSS on the sinus for geometries with theta(IC)25 degrees . Larger off-plane angles generally increase the danger of plague build-up; (c) for theta(IC) < 25 degrees , the off-plane angle does not have an obvious effect on the hemodynamic WSS; (d) symmetric bifurcations were found to increase the WSS on the sinus wall and ease the risk of vascular disease.     

Hemodynamics and wall mechanics in human carotid bifurcation and its consequences for atherogenesis: investigation of inter-individual variation

Finite element simulations of fluid-solid interactions were used to investigate inter-individual variations in flow dynamics and wall mechanics at the carotid artery bifurcation, and its effects on atherogenesis, in three healthy humans (normal volunteers: NV1, NV2, NV4). Subject-specific calculations were based on MR images of structural anatomy and ultrasound measurements of flow at domain boundaries. For all subjects, the largest contiguous region of low wall shear stress (WSS) occurred at the carotid bulb, WSS was high (6-10 Pa) at the apex, and a small localized region of WSS > 10 Pa occurred close to the inner wall of the external carotid artery (ECA). NV2 and NV4 had a "spot" of low WSS distal to the bifurcation at the inner wall of the ECA. Low WSS patches in the common carotid artery (CCA) were contiguous with the carotid bulb low WSS region in NV1 and NV2, but not in NV4. In all three subjects, areas of high oscillatory shear index (OSI) were confined to regions of low WSS. Only NV4 exhibited high levels of OSI on the external adjoining wall of the ECA and CCA. For all subjects, the maximum wall shear stress temporal gradient (WSSTG) was highest at the flow divider (reaching 1,000 Pa/s), exceeding 300 Pa/s at the walls connecting the ECA and CCA, but remaining below 250 Pa/s outside of the ECA. In all subjects, (maximum principle) cyclic strain (CS) was greatest at the apex (NV1: 14%; NV2: 11%; NV4: 6%), and a second high CS region occurred at the ECA-CCA adjoining wall (NV1: 11%, NV2: 9%, NV4: 5%). Wall deformability was included in one simulation (NV2) to verify that it had little influence on the parameters studied. Location and magnitude of low WSS were similar, except for the apex (differences of up to 25%). Wall distensibility also influenced OSI, doubling it in most of the CCA, separating the single high OSI region of the carotid bulb into two smaller regions, and shrinking the ECA internal and external walls' high OSI regions. These observations provide further evidence that significant intra-subject variability exists in those factors thought to impact atherosclerosis.     

Numerical analysis of hemodynamics in spastic middle cerebral arteries

Cerebral vasospasm (CVS) is the most common serious complication of subarachnoid hemorrhage. Among the many factors that are associated with the pathogenesis of CVS, hemodynamics plays an important role in the initiation and development of CVS. Numerical simulation was carried out to obtain the flow patterns and wall shear stress (WSS) distribution in spastic middle cerebral arteries. The blood was assumed to be incompressible, laminar, homogenous, Newtonian, and steady. Our simulations reveal that flow velocity and WSS level increase at the stenosis segment of the spastic vessels, but further downstream of stenosis, the WSS significantly decreases along the inner wall, and flow circulation and stagnation are observed. The hydrodynamic resistance increases with the increase of vessel spasm. Moreover, the change of flow field and hydrodynamic forces are not linearly proportional to the spasm level, and the rapid change of hemodynamic parameters is observed as the spasm is more than 50%. Accordingly, in the view of hemodynamic physiology, vessels with less than 30% stenosis are capable of self-restoration towards normal conditions. However, vessels with more than 50% stenosis may eventually lose their capacity to adapt to differing physiologic conditions due to the extreme non-physilogic hemodynamic environment, and the immediate expansion of the vessel lumen might be needed to minimize serious and non-reversible effects.     

Effect of a lipid pool on stress/strain distributions in stenotic arteries: 3-D fluid-structure interactions (FSI) models

Nonlinear 3-D models with fluid-structure interactions (FSI) based on in vitro experiments are introduced and solved by ADINA to perform flow and stress/strain analysis for stenotic arteries with lipid cores. Navier-Stokes equations are used as the governing equations for the fluid. Hyperelastic Mooney-Rivlin models are used for both the arteries and lipid cores. Our results indicate that critical plaque stress/strain conditions are affected considerably by stenosis severity, eccentricity, lipid pool size, shape and position, plaque cap thickness, axial stretch, pressure, and fluid-structure interactions, and may be used for possible plaque rupture predictions.     

Influence of the Accuracy of Angiography-Based Reconstructions on Velocity and Wall Shear Stress Computations in Coronary Bifurcations: A Phantom Study

Introduction

Wall shear stress (WSS) plays a key role in the onset and progression of atherosclerosis in human coronary arteries. Especially sites with low and oscillating WSS near bifurcations have a higher propensity to develop atherosclerosis. WSS computations in coronary bifurcations can be performed in angiography-based 3D reconstructions. It is essential to evaluate how reconstruction errors influence WSS computations in mildly-diseased coronary bifurcations. In mildly-diseased lesions WSS could potentially provide more insight in plaque progression.

Materials Methods

Four Plexiglas phantom models of coronary bifurcations were imaged with bi-plane angiography. The lumens were segmented by two clinically experienced readers. Based on the segmentations 3D models were generated. This resulted in three models per phantom: one gold-standard from the phantom model itself, and one from each reader. Steady-state and transient simulations were performed with computational fluid dynamics to compute the WSS. A similarity index and a noninferiority test were used to compare the WSS in the phantoms and their reconstructions. The margin for this test was based on the resolution constraints of angiography.

Results

The reconstruction errors were similar to previously reported data; in seven out of eight reconstructions less than 0.10 mm. WSS in the regions proximal and far distal of the stenosis showed a good agreement. However, the low WSS areas directly distal of the stenosis showed some disagreement between the phantoms and the readers. This was due to small deviations in the reconstruction of the stenosis that caused differences in the resulting jet, and consequently the size and location of the low WSS area.

Discussion

This study showed that WSS can accurately be computed within angiography-based 3D reconstructions of coronary arteries with early stage atherosclerosis. Qualitatively, there was a good agreement between the phantoms and the readers. Quantitatively, the low WSS regions directly distal to the stenosis were sensitive to small reconstruction errors.     

Computer simulations of atherosclerotic plaque growth in coronary arteries

A three dimensional mathematical model with a linear plaque growth function was developed to investigate the geometrical adaptation of atherosclerotic plaques in coronary arteries and study the influences of flow wall shear stress (WSS), blood viscosity and the inlet flow rate on the growth of atherosclerotic plaques using computational plaque growth simulations. The simulation results indicated that the plaque wall thickness at the neck of the stenosis increased at a decreasing rate in the atherosclerosis progression. The simulation results also showed a strong dependence of the plaque wall thickness increase on the blood viscosity and the inlet flow rate. The progression rate in a coronary artery was lower with a higher inlet velocity flow rate and higher with a smaller value of the blood viscosity.