High Wall Shear Stress Gradient Research Articles

Hemodynamic factors of spontaneous vertebral artery dissecting aneurysms assessed with numerical and deep learning algorithms: Role of blood pressure and asymmetry

Background and ObjectivesThe pathophysiology of spontaneous vertebral artery dissecting aneurysms (SVADA) is poorly understood. Our goal is to investigate the hemodynamic factors contributing to their formation using computational fluid dynamics (CFD) and deep learning algorithms. MethodsWe have developed software that can use patient imagery as input to recreate the vertebrobasilar arterial system, both with and without SVADA, which we used in a series of three patients. To obtain the kinematic blood flow data before and after the aneurysm forms, we utilized numerical methods to solve the complex Navier-Stokes partial differential equations. This was accomplished through the application of a finite volume solver (OpenFoam/Helyx OS). Additionally, we trained a neural ordinary differential equation (NODE) to learn and replicate the dynamical streamlines obtained from the computational fluid dynamics (CFD) simulations. ResultsIn all three cases, we observed that the equilibrium of blood pressure distributions across the VAs, at a specific vertical level, accurately predicted the future SVADA location. In the two cases where there was a dominant VA, the dissection occurred on the dominant artery where blood pressure was lower compared to the contralateral side. The SVADA sac was characterized by reduced wall shear stress (WSS) and decreased velocity magnitude related to increased turbulence. The presence of a high WSS gradient at the boundary of the SVADA may explain its extension. Streamlines generated by CFD were learned with a neural ordinary differential equation (NODE) capable of capturing the system’s dynamics to output meaningful predictions of the flow vector field upon aneurysm formation. ConclusionIn our series, asymmetry in the vertebrobasilar blood pressure distributions at and proximal to the site of the future SVADA accurately predicted its location in all patients. Deep learning algorithms can be trained to model blood flow patterns within biological systems, offering an alternative to the computationally intensive CFD. This technology has the potential to find practical applications in clinical settings.

Computational hemodynamics study of anterior communicating artery aneurysm associated with fenestration: A case report

Association of intracranial aneurysms with fenestration is of great clinical interest. Hemodynamic characteristics of an intracranial aneurysm associated with fenestration have been rarely reported. We performed a computational hemodynamics analysis of an anterior communicating artery (ACoA) aneurysm associated with fenestration to understand the influence of fenestration on aneurysmal hemodynamics.A patient-specific 3-dimensional geometry of an ACoA aneurysm associated with fenestration was created from the computed tomography (CT) angiography images of a 52-year-old male patient who suffered a sudden loss of consciousness. Computational hemodynamic analysis was performed and some interesting hemodynamic characteristics were found. Fenestration behaved like a flow divider, which led to highly complex blood flow patterns in aneurysm. A pressure elevation and non-uniform wall shear stress (WSS) distribution on aneurysm sac were found. High WSS gradient on the fenestration surface was observed for the first time.Fenestration may significantly influence the hemodynamic characteristics of aneurysms.

Wall shear stress at the initiation site of cerebral aneurysms.

Hemodynamics are believed to play an important role in the initiation of cerebral aneurysms. In particular, studies have focused on wall shear stress (WSS), which is a key regulator of vascular biology and pathology. In line with the observation that aneurysms predominantly occur at regions of high WSS, such as bifurcation apices or outer walls of vascular bends, correlations have been found between the aneurysm initiation site and high WSS. The aim of our study was to analyze the WSS field at an aneurysm initiation site that was neither a bifurcation apex nor the outer wall of a vascular bend. Ten cases with aneurysms on the A1 segment of the anterior cerebral artery were analyzed and compared with ten controls. Aneurysms were virtually removed from the vascular models of the cases to mimic the pre-aneurysm geometry. Computational fluid dynamics (CFD) simulations were created to assess the magnitude, gradient, multidirectionality, and pulsatility of the WSS. To aid the inter-subject comparison of hemodynamic variables, we mapped the branch surfaces onto a two-dimensional parametric space. This approach made it possible to view the whole branch at once for qualitative evaluation. It also allowed us to empirically define a patch for quantitative analysis, which was consistent among subjects and encapsulated the aneurysm initiation sites in our dataset. To test the sensitivity of our results, CFD simulations were repeated with a second independent observer virtually removing the aneurysms and with a 20% higher flow rate at the inlet. We found that branches harboring aneurysms were characterized by high WSS and high WSS gradients. Among all assessed variables, the aneurysm initiation site most consistently coincided with peaks of temporal variation in the WSS magnitude.

Hemodynamics in Idealized Stented Coronary Arteries: Important Stent Design Considerations.

Stent induced hemodynamic changes in the coronary arteries are associated with higher risk of adverse clinical outcome. The purpose of this study was to evaluate the impact of stent design on wall shear stress (WSS), time average WSS, and WSS gradient (WSSG), in idealized stent geometries using computational fluid dynamics. Strut spacing, thickness, luminal protrusion, and malapposition were systematically investigated and a comparison made between two commercially available stents (Omega and Biomatrix). Narrower strut spacing led to larger areas of adverse low WSS and high WSSG but these effects were mitigated when strut size was reduced, particularly for WSSG. Local hemodynamics worsened with luminal protrusion of the stent and with stent malapposition, adverse high WSS and WSSG were identified around peak flow and throughout the cardiac cycle respectively. For the Biomatrix stent, the adverse effect of thicker struts was mitigated by greater strut spacing, radial cell offset and flow-aligned struts. In conclusion, adverse hemodynamic effects of specific design features (such as strut size and narrow spacing) can be mitigated when combined with other hemodynamically beneficial design features but increased luminal protrusion can worsen the stent’s hemodynamic profile significantly.

THE INFLUENCE OF HEMODYNAMICS ON THE ULCERATION PLAQUES OF CAROTID ARTERY STENOSIS

The further rupture of atherosclerotic ulceration plaque is one of the main triggers of the carotid ischemic stroke. However, the abnormal hemodynamics is not well addressed yet. A lesion-based computational fluid dynamic (CFD) analysis is proposed to investigate the complex hemodynamic change of the ulceration plaque that prevails in patients. The 3D models including eight groups of ulcerations (six groups with single ulceration and two groups with two consecutive ulcerations), were reconstructed based on the computer tomography (CT) images, and the tetrahedral grid was taken to mesh the models with the appropriate numbers. After setting the boundary conditions, numerical simulation was carried out to analyze the pulsatile blood flow in the models. The complex flow in the vicinity of the ulcerations directly leads to a significant effect on the distribution of the wall shear stress (WSS). WSS is respectively from 3.29 to 35.41 Pa at the upstream, from 11.90 to 41.85 Pa at the downstream ulceration, and 18.60 and 30.60 Pa in the area between the two consecutive ulcerations. The rupture from these regions could cause the further rupture of ulceration plaques, particularly at the downstream ulceration and the area between the two consecutive ulcerations. The twisting and the curling of the flow at the ulcerations can lead to thrombosis which may break free later and go through the downstream stenosis by the effect of the flow. The different degrees of WSS in downstream and upstream ulcerations will damage the ulceration on the plaque because of pulling and stretching forces at the ulcerations. Furthermore, high wall shear stress gradient (WSSG) also increases the risk of the further rupture. Our study gives a better understanding in the further rupture mechanism of ulceration plaques and provides the information of the location of thrombosis after aggravated rupturing, which can be referred by surgeons to improve the surgical planning.

E-016 A Comparative Review of the Hemodynamics and Pathogenesis of Cerebral and Abdominal Aortic Aneurysms: Lessons to Learn From Each Other

Introduction/purposeCerebral aneurysms (CAs) and abdominal aortic aneurysms (AAAs) are both degenerative vascular pathologies that manifest as an abnormal dilation of the arterial wall. They arise with different morphologies in different...

Proximal stenosis may induce initiation of cerebral aneurysms by increasing wall shear stress and wall shear stress gradient

Hemodynamic parameters, such as wall shear stress (WSS), WSS gradient (WSSG), aneurysm formation indicator (AFI), or gradient oscillatory number (GON), have been proposed to be linked to initiation of cerebral aneurysms. However, how such conditions occur in humans is unclear. We encountered a rare and interesting case to address this issue. A patient had a newly formed aneurysm with proximal stenosis, which was confirmed by serial imagings. We made two pre-aneurysm models: one with stenosis and the other without stenosis. We performed computational fluid dynamics simulations for these models. Owing to jet flow caused by the stenosis, the maximum WSS and WSSG on the aneurysm initiation site were approximately doubled and tripled, respectively. However, the oscillatory shear index (OSI), AFI, and GON did not change substantially by the stenosis. Computer simulations using artificial vascular models with different degrees of proximal stenosis at different distances demonstrated that oscillatory shear index, AFI, and GON did not change substantially by the stenosis. These results showed that proximal stenosis caused high WSS and high WSSG at the aneurysm initiation site, possibly leading to aneurysm initiation. Proximal stenosis may be a potential factor to induce initiation of one class of cerebral aneurysms by increasing WSS and WSSG.

A Comparative Review of the Hemodynamics and Pathogenesis of Cerebral and Abdominal Aortic Aneurysms: Lessons to Learn From Each Other

ObjectiveCerebral aneurysms (CAs) and abdominal aortic aneurysms (AAAs) are degenerative vascular pathologies that manifest as abnormal dilations of the arterial wall. They arise with different morphologies in different types of blood vessels under different hemodynamic conditions. Although treated as different pathologies, we examine common pathways in their hemodynamic pathogenesis in order to elucidate mechanisms of formation.Materials and MethodsA systematic review of the literature was performed. Current concepts on pathogenesis and hemodynamics were collected and compared.ResultsCAs arise as saccular dilations on the cerebral arteries of the circle of Willis under high blood flow, high wall shear stress (WSS), and high wall shear stress gradient (WSSG) conditions. AAAs arise as fusiform dilations on the infrarenal aorta under low blood flow, low, oscillating WSS, and high WSSG conditions. While at opposite ends of the WSS spectrum, they share high WSSG, a critical factor in arterial remodeling. This alone may not be enough to initiate aneurysm formation, but may ignite a cascade of downstream events that leads to aneurysm development. Despite differences in morphology and the structure, CAs and AAAs share many histopathological and biomechanical characteristics. Endothelial cell damage, loss of elastin, and smooth muscle cell loss are universal findings in CAs and AAAs. Increased matrix metalloproteinases and other proteinases, reactive oxygen species, and inflammation also contribute to the pathogenesis of both aneurysms.ConclusionOur review revealed similar pathways in seemingly different pathologies. We also highlight the need for cross-disciplinary studies to aid in finding similarities between pathologies.

P-024 Stress distribution after intracranial stent by realistic model

There is no effective treatment for symptomatic intracranial atherosclerotic stenosis, which has an association with a high rate of recurrent stroke. Percutaneous transluminal angioplasty and stenting (PTAS) has been applied...

Image-based modeling of hemodynamics in coronary artery aneurysms caused by Kawasaki disease

Kawasaki Disease (KD) is the leading cause of acquired pediatric heart disease. A subset of KD patients develops aneurysms in the coronary arteries, leading to increased risk of thrombosis and myocardial infarction. Currently, there are limited clinical data to guide the management of these patients, and the hemodynamic effects of these aneurysms are unknown. We applied patient-specific modeling to systematically quantify hemodynamics and wall shear stress in coronary arteries with aneurysms caused by KD. We modeled the hemodynamics in the aneurysms using anatomic data obtained by multi-detector computed tomography (CT) in a 10-year-old male subject who suffered KD at age 3years. The altered hemodynamics were compared to that of a reconstructed normal coronary anatomy using our subject as the model. Computer simulations using a robust finite element framework were used to quantify time-varying shear stresses and particle trajectories in the coronary arteries. We accounted for the cardiac contractility and the microcirculation using physiologic downstream boundary conditions. The presence of aneurysms in the proximal coronary artery leads to flow recirculation, reduced wall shear stress within the aneurysm, and high wall shear stress gradients at the neck of the aneurysm. The wall shear stress in the KD subject (2.95-3.81 dynes/sq cm) was an order of magnitude lower than the normal control model (17.10-27.15 dynes/sq cm). Particle residence times were significantly higher, taking 5 cardiac cycles to fully clear from the aneurysmal regions in the KD subject compared to only 1.3 cardiac cycles from the corresponding regions of the normal model. In this novel quantitative study of hemodynamics in coronary aneurysms caused by KD, we documented markedly abnormal flow patterns that are associated with increased risk of thrombosis. This methodology has the potential to provide further insights into the effects of aneurysms in KD and to help risk stratify patients for appropriate medical and surgical interventions.

Mis-sizing of stent promotes intimal hyperplasia: impact of endothelial shear and intramural stress

Stent can cause flow disturbances on the endothelium and compliance mismatch and increased stress on the vessel wall. These effects can cause low wall shear stress (WSS), high wall shear stress gradient (WSSG), oscillatory shear index (OSI), and circumferential wall stress (CWS), which may promote neointimal hyperplasia (IH). The hypothesis is that stent-induced abnormal fluid and solid mechanics contribute to IH. To vary the range of WSS, WSSG, OSI, and CWS, we intentionally mismatched the size of stents to that of the vessel lumen. Stents were implanted in coronary arteries of 10 swine. Intravascular ultrasound (IVUS) was used to size the coronary arteries and stents. After 4 wk of stent implantation, IVUS was performed again to determine the extent of IH. In conjunction, computational models of actual stents, the artery, and non-Newtonian blood were created in a computer simulation to yield the distribution of WSS, WSSG, OSI, and CWS in the stented vessel wall. An inverse relation (R(2) = 0.59, P < 0.005) between WSS and IH was found based on a linear regression analysis. Linear relations between WSSG, OSI, and IH were observed (R(2) = 0.48 and 0.50, respectively, P < 0.005). A linear relation (R(2) = 0.58, P < 0.005) between CWS and IH was also found. More statistically significant linear relations between the ratio of CWS to WSS (CWS/WSS), the products CWS × WSSG and CWS × OSI, and IH were observed (R(2) = 0.67, 0.54, and 0.56, respectively, P < 0.005), suggesting that both fluid and solid mechanics influence the extent of IH. Stents create endothelial flow disturbances and intramural wall stress concentrations, which correlate with the extent of IH formation, and these effects were exaggerated with mismatch of stent/vessel size. These findings reveal the importance of reliable vessel and stent sizing to improve the mechanics on the vessel wall and minimize IH.

MOLECULAR ALTERATIONS ASSOCIATED WITH ANEURYSMAL REMODELING ARE LOCALIZED IN THE HIGH HEMODYNAMIC STRESS REGION OF A CREATED CAROTID BIFURCATION

Although elevated hemodynamics has been speculated to play a key role in intracranial aneurysm (IA) initiation, little is known about the specific hemodynamic microenvironment that triggers aneurysmal vascular degradation. We previously demonstrated maladaptive remodeling characteristic of IA initiation occurring in hemodynamic regions of combined high wall shear stress (WSS) and high WSS gradient near the apex of an experimentally created carotid bifurcation. This study examines whether this remodeling recapitulates the molecular changes found in IAs and whether molecular changes also correspond to specific hemodynamic environments. De novo bifurcations were surgically created using both native common carotid arteries in each of 6 dogs. Bifurcations were imaged 2 weeks or 2 months after surgery by high-resolution 3-dimensional angiography, from which flow fields were obtained by computational fluid dynamics simulations. Subsequently, harvested tissues, demonstrating early aneurysmal changes near the apex, were immunostained for interleukin-1beta, endothelial and inducible nitric oxide synthases, nitrotyrosine, and matrix metalloproteinase-2 and -9. Spatial distributions of these molecules were comapped with computational fluid dynamics results. The aneurysmal wall showed decreased endothelial nitric oxide synthase expression compared with surrounding segments, the feeding artery, and native controls, whereas all other markers increased. Anti-CD68 staining indicated the absence of inflammatory cells in the aneurysmal wall. Comapping molecular marker distributions with flow fields revealed confinement of these molecular changes within the hemodynamic region of high WSS and high, positive WSS gradient. Aneurysm-initiating remodeling induced by combined high WSS and high, positive WSS gradient is associated with molecular changes implicated in IAs.

Endothelial Cell Layer Subjected to Impinging Flow Mimicking the Apex of an Arterial Bifurcation

Little is known about endothelial responses to the impinging flow hemodynamics that occur at arterial bifurcation apices, where intracranial aneurysms usually form. Such hemodynamic environments are characterized by high wall shear stress (WSS >40 dynes/cm(2)) and high wall shear stress gradients (WSSG >300 dynes/cm(3)). In this study, confluent bovine aortic endothelial cells were exposed to impinging flow in a T-shaped chamber designed to mimic a bifurcation. After 24-72 h under flow, cells around the stagnation point maintained polygonal shapes but cell density was reduced, whereas cells in adjacent downstream regions exposed to very high WSS and WSSG were elongated, aligned parallel to flow, and at higher density. Such behavior was not blocked by inhibiting proliferation, indicating that cells migrated downstream from the stagnation point in response to impinging flow. Furthermore, although the area of highest cell density moved downstream and away from the impingement point over time, it never moved beyond the WSS maximum. The accumulation of cells upstream of maximal WSS and downstream of maximal WSSG suggests that positive WSSG is responsible for the observed migration. These results demonstrate a unique endothelial response to aneurysm-promoting flow environments at bifurcation apices.

A MODEL SYSTEM FOR MAPPING VASCULAR RESPONSES TO COMPLEX HEMODYNAMICS AT ARTERIAL BIFURCATIONS IN VIVO

Cerebral aneurysms are preferentially located at arterial bifurcation apices with complex hemodynamics. To understand disease mechanisms associated with aneurysm initiation, we attempted to establish a causal relationship between local hemodynamics and vascular responses. Arterial bifurcations were surgically created from native common carotid arteries in two dogs, angiographically imaged 2 weeks and 2 months later, and then excised. We characterized local morphological changes in response to specifically manipulated hemodynamics. Computational fluid dynamics simulations were performed on the in vivo images and results mapped onto histological images. Local flow conditions, such as high wall shear stress and high wall shear stress gradient, were found to be associated with vascular changes, including an intimal pad in the flow impingement region and a "groove" bearing the characteristics of an early aneurysm. This novel method of histohemodynamic micromapping reveals a direct correlation between an altered hemodynamic microenvironment and vascular responses consistent with aneurysm development.

Are intramural suction-squeezing effects generated by the variations in radial wall stress during each heart beat the motor of atherosclerosis? A new concept

In the early sixties, the existence of predilection sites for atherosclerotic lesions inside the arterial circulation led to the concept that low wall shear stress (WSS) was responsible, together with systemic factors like high blood pressure, hypercholesterolemia, or diabetes, for the genesis and progression of atherosclerosis. It was found later that oscillating WSS and high WSS gradients could also be incriminated. Yet, this concept, which is broadly accepted today, fails to explains several facts, for instance that some arteries (e.g. epicardial coronary arteries) are more prone to become atherosclerotic than other ones exposed to the same systemic factors (e.g. hepatic and brain arteries). In this paper, we present a quite different concept. It is based on the fact that the increase in intravascular pressure and flow that occur in the arteries during systole generates, at the predilection sites of atherosclerotic lesions (bends, bifurcations, and branchings), an increase of radial wall stress in the outer layers of the arterial wall so that this stress becomes momentarily tensile. These cyclic stress increases have a suction effect that is likely to facilitate the diffusion of atherogenic cells and substances inside the wall. Furthermore, since arteries are not primarily structured to resist inversions of radial stress, they may also create damages (e.g. disruptions of cell membranes and elastic lamellae) followed by inflammations and micro-haemorrhages in the wall. This new concept may provide a complementary (or possibly alternative) explanation of atherosclerosis.

Alteration of Reynolds number and flow partition modify wall shear stresses at arterial branches in a way that can explain age- and species-dependent patterns of arterial disease

It is assumed that critical hemodynamic factors play an important role in the onset, localization and degree of post-operative complications, for example, thrombosis and restenosis. Of special interest are sudden expansion flows, which may occur in straight artery segments such as the common carotid after endarterectomy or end-to-end anastomoses. Sudden expansion geometries are possible origins of early post-operative emboli and significant myointimal hyperplasia resulting in early or late complications. Transient laminar axisymmetric and fully three-dimensional blood flows were simulated employing a validated finite volume code in conjunction with a Runge–Kutta particle tracking technique. Disturbed flow indicators, which may predict the onset of thrombosis and/or restenosis, were identified and employed to evaluate 90°-step and smooth expansion geometries.Smooth expansion geometries have weaker disturbed flow features than step expansion geometries. Specifically, the regions near the expansion wall and the reattachment point are susceptible to both atherosclerotic lesion and thrombi formations as indicated by non-uniform hemodynamic indicators such as near-zero wall shear stress and elevated wall shear stress gradients as well as blood particle accumulation and deposition. A new parameter, the wall shear stress angle deviation (WSSAD) has been introduced, which indicates areas of abnormal endothelial cell morphology and particle wall deposition. In turn, regions of low wall shear stress and high wall shear stress gradients are recognized as susceptible sites for arterial diseases. Thus, it is interesting to note that high WSSAD surface areas cover low wall shear stress, high wall shear stress gradient locations as well as high wall particle deposition.A gradual change in step expansion geometry provides better results in terms of WSSAD values and hence potentially reducing atherosclerosis as well as thrombi formation.

Hemodynamics analyses of arterial expansions with implications to thrombosis and restenosis

It is assumed that critical hemodynamic factors play an important role in the onset, localization and degree of post-operative complications, for example, thrombosis and restenosis. Of special interest are sudden expansion flows, which may occur in straight artery segments such as the common carotid after endarterectomy or end-to-end anastomoses. Sudden expansion geometries are possible origins of early post-operative emboli and significant myointimal hyperplasia resulting in early or late complications. Transient laminar axisymmetric and fully three-dimensional blood flows were simulated employing a validated finite volume code in conjunction with a Runge–Kutta particle tracking technique. Disturbed flow indicators, which may predict the onset of thrombosis and/or restenosis, were identified and employed to evaluate 90°-step and smooth expansion geometries. Smooth expansion geometries have weaker disturbed flow features than step expansion geometries. Specifically, the regions near the expansion wall and the reattachment point are susceptible to both atherosclerotic lesion and thrombi formations as indicated by non-uniform hemodynamic indicators such as near-zero wall shear stress and elevated wall shear stress gradients as well as blood particle accumulation and deposition. A new parameter, the wall shear stress angle deviation (WSSAD) has been introduced, which indicates areas of abnormal endothelial cell morphology and particle wall deposition. In turn, regions of low wall shear stress and high wall shear stress gradients are recognized as susceptible sites for arterial diseases. Thus, it is interesting to note that high WSSAD surface areas cover low wall shear stress, high wall shear stress gradient locations as well as high wall particle deposition. A gradual change in step expansion geometry provides better results in terms of WSSAD values and hence potentially reducing atherosclerosis as well as thrombi formation.

Computational design of a bypass graft that minimizes wall shear stress gradients in the region of the distal anastomosis.

Recent experimental and theoretic studies show that large wall shear stress gradients characterize disturbed flow patterns associated with the location of myointimal hyperplasia, atheroma, or both. Graft-to-artery anastomoses that minimize wall shear stress gradients may reduce the degree of myointimal development and the propensity for thrombosis. This study analyzes the distribution of distal anastomotic wall shear stress gradients for conventional geometries and for the optimized geometry assuming idealized merging of the graft with the artery. A validated computational fluid dynamics program was used to solve the transient three-dimensional partial differential equations and auxiliary equations that describe laminar incompressible blood flow. Time-averaged wall shear stresses and wall shear stress gradients were calculated for three distal graft-artery anastomoses: a standard end-to-side, a Taylor patch, and an optimized geometry. The latter was obtained iteratively by minimizing the local wall shear stress gradients and was analyzed under resting and exercise inflow waveforms. Both the standard and Taylor patch anastomoses have relatively high wall shear stress gradients in the regions of the toe and heel. For all flow inputs studied nonuniform hemodynamics in the optimized graft design are largely eliminated, and the time-averaged wall shear stress gradients are greatly reduced throughout the anastomotic zone. At resting flow the Taylor patch produces slightly lower wall shear stress gradients in the anastomotic region than the standard end-to-side anastomosis. The optimized design reduces wall shear stress gradients to almost one half of that of the standard and Taylor patch geometries. At exercise flow wall shear stress gradients almost triple in the standard anastomosis and increase approximately 30% in the Taylor patch. In contrast, the geometrically optimized design is basically independent of the type of flow input waveform in terms of time-averaged wall shear stress gradients and disturbed flow patterns. This study demonstrates that it is possible to design a terminal graft geometry for an end-to-side anastomosis that significantly reduces wall shear stress gradients. If the wall shear stress gradient is confirmed to be a major hemodynamic determinant of intimal hyperplasia and restenosis, these results may point to the design of optimal bypass graft geometries.

Pulsatile Wall Shear Stress Gradient and Aortoseptal Angle: Implications for Subaortic Stenosis † 147

A better understanding of the etiology of discrete subaortic stenosis (SAS) would be useful in identifying patients at risk and in surgical decision making since the onset, progression, and recurrence of SAS are difficult to predict. Previous studies have shown that congenital defects and morphologic abnormalities associated with SAS (such as steepened aortoseptal angle [AoSA]) cause significant, localized elevations in peak wall shear stress and the wall shear stress gradient (WSSG). High WSSG has been associated with cellular changes in the endothelium. Since the magnitude of wall shear stress varies thoughout the cardiac cycle, we addressed the hypothesis that these morphologic abnormalities have similar effects on the time-averaged shear stress and WSSG. Methods: A finite element model of the left ventricular outflow tract was implemented on the Cray C90 at the Pittsburgh Supercomputing Center for typical pulsatile flow conditions. AoSA was varied between 120 and 150 degrees, maximum aortic velocities from 0.5 to 1 m/s, and aortic diameter from 1 to 1.5 cm. Shear stress and WSSG were directly calculated from the velocity field at discrete points in time. The time-averaged wall shear stress and WSSG at the location of the peak was determined. Results: At an aortic velocity of 1 m/s, the peak and time-averaged shear stress increased with steeper AoSA by 52% and 49.5% respectively. WSSG was more sensitive to changes in AoSA with the peak WSSG increasing by 217%, compared to the time-averaged WSSG which increased by 225%. Conclusions: Geometric variables had similar effects on both the peak and mean shear stress and WSSG. Although the progression and recurrence of SAS may be dependent on time-varying exposure to shear stress, this exposure may be quantified using either a peak or a mean value.

Effect of carotid artery geometry on the magnitude and distribution of wall shear stress gradients

Recent information indicates that large, sustained wall shear stress gradients are a dominant hemodynamic parameter associated with the location and severity of atherosclerosis and myointimal hyperplasia. This study computes the spatial values of wall shear stresses and their gradients for three carotid artery bifurcation geometries. A computational fluid dynamics program was used to solve the transient two-dimensional partial differential equations that describe fluid flow. Blood was treated as both a Newtonian and a non-Newtonian incompressible fluid. Solutions for the velocities, wall shear stresses, and wall shear-stress gradients were obtained for three carotid bifurcation geometries: a normal carotid bifurcation (similar to a primarily reconstructed carotid endarterectomy), a patch-reconstructed carotid endarterectomy, and a gradually tapered, low-angle carotid bifurcation (no carotid bulb). Computed velocity profiles closely match published experimental ones. Disturbed flow velocities are largest in the bulb segment of the normal carotid bifurcation. Peak and minimum wall shear stresses and peak shear stress gradients occurred in the lateral internal carotid artery wall. These were binodal in the normal or primarily reconstructed carotid artery, localized at the distal end of the patch-reconstructed carotid bifurcation, and minimal in the smooth, tapered carotid bifurcation. Wall shear stresses and their gradients were slightly higher for non-Newtonian than Newtonian fluids in the normal carotid artery but were similar in the other two geometric configurations. These results indicate that flow disturbances in general and wall shear stress gradients in particular are markedly reduced in carotid artery bifurcations that are smooth and gradually tapered and do not have a bulb. Abrupt geometric wall changes such as those occurring in the normal carotid bulb and at the distal end of a patch-reconstruction after carotid endarterectomy are harbingers of disturbed flow and high wall shear stress gradients. These results suggest that carotid endarterectomy reconstruction geometry characterized by a gradually tapered internal carotid artery may minimize the hemodynamically induced component of early myointimal hyperplasia and thrombosis and late atherosclerotic restenosis.