scholarly journals Identification of the haemodynamic environment permissive for plaque erosion

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Michael McElroy ◽  
Yongcheol Kim ◽  
Giampaolo Niccoli ◽  
Rocco Vergallo ◽  
Alexander Langford-Smith ◽  
...  

AbstractEndothelial erosion of atherosclerotic plaques is the underlying cause of approximately 30% of acute coronary syndromes (ACS). As the vascular endothelium is profoundly affected by the haemodynamic environment to which it is exposed, we employed computational fluid dynamic (CFD) analysis of the luminal geometry from 17 patients with optical coherence tomography (OCT)-defined plaque erosion, to determine the flow environment permissive for plaque erosion. Our results demonstrate that 15 of the 17 cases analysed occurred on stenotic plaques with median 31% diameter stenosis (interquartile range 28–52%), where all but one of the adherent thrombi located proximal to, or within the region of maximum stenosis. Consequently, all flow metrics related to elevated flow were significantly increased (time averaged wall shear stress, maximum wall shear stress, time averaged wall shear stress gradient) with a reduction in relative residence time, compared to a non-diseased reference segment. We also identified two cases that did not exhibit an elevation of flow, but occurred in a region exposed to elevated oscillatory flow. Our study demonstrates that the majority of OCT-defined erosions occur where the endothelium is exposed to elevated flow, a haemodynamic environment known to evoke a distinctive phenotypic response in endothelial cells.

2015 ◽  
Vol 15 (01) ◽  
pp. 1550008 ◽  
Author(s):  
YULIN FU ◽  
AIKE QIAO ◽  
LONG JIN

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.


Neurosurgery ◽  
2007 ◽  
Vol 61 (4) ◽  
pp. 853-864 ◽  
Author(s):  
Clemens M. Schirmer ◽  
Adel M. Malek

Abstract OBJECTIVE The endothelium is functionally regulated by the magnitude and spatiotemporal gradients of wall shear stress (WSS). Although flow separation and reversal occur beyond high-grade stenoses, little is known of the WSS pattern within clinically relevant mild to moderate stenoses. METHODS An axisymmetric geometry with 25, 50, and 75% stenosis criteria (quantified in accordance with the North American Symptomatic Carotid Endarterectomy Trial) was used to generate a high-resolution, hybrid, tetrahedral-hexahedral computational mesh with boundary-layer enrichment to improve near-wall shear stress gradient (WSSG) computation. Time-dependent computational fluid dynamic analysis was performed using a non-Newtonian Carreau-Yasuda model of blood to yield the shear-dependent viscosity. RESULTS Transition to secondary flow patterns was demonstrated in stenoses of 25, 50, and 75%. A focal region with near-wall flow reversal and retrograde WSS was identified within the stenosis itself and was found to migrate cyclically during the cardiac pulse. A zone of zero WSS and divergent WSSG that shifts in toward the throat with increasing stenotic severity was identified. Focal zones of high WSSG with converging and/or diverging direction were uncovered within the stenosis itself, as were expected changes in the distal poststenotic region. These zones of divergent WSSG shift over a substantial length of the stenosis during the course of the cardiac cycle. CONCLUSION Luminal WSS demonstrates dynamic direction reversal and high spatial gradients within the distal stenosis throat of even clinically moderate lesions. These findings shed light on the complex vessel wall hemodynamics within clinical stenoses and reveal a mechanical microenvironment that is conducive to perpetual endothelial functional dysregulation and stenosis progression.


2019 ◽  
Vol 131 (2) ◽  
pp. 442-452 ◽  
Author(s):  
Alexandra Lauric ◽  
James E. Hippelheuser ◽  
Adel M. Malek

OBJECTIVEEndothelium adapts to wall shear stress (WSS) and is functionally sensitive to positive (aneurysmogenic) and negative (protective) spatial WSS gradients (WSSG) in regions of accelerating and decelerating flow, respectively. Positive WSSG causes endothelial migration, apoptosis, and aneurysmal extracellular remodeling. Given the association of wide branching angles with aneurysm presence, the authors evaluated the effect of bifurcation geometry on local apical hemodynamics.METHODSComputational fluid dynamics simulations were performed on parametric bifurcation models with increasing angles having: 1) symmetrical geometry (bifurcation angle 60°–180°), 2) asymmetrical geometry (daughter angles 30°/60° and 30°/90°), and 3) curved parent vessel (bifurcation angles 60°–120°), all at baseline and double flow rate. Time-dependent and time-averaged apical WSS and WSSG were analyzed. Results were validated on patient-derived models.RESULTSNarrow symmetrical bifurcations are characterized by protective negative apical WSSG, with a switch to aneurysmogenic WSSG occurring at angles ≥ 85°. Asymmetrical bifurcations develop positive WSSG on the more obtuse daughter branch. A curved parent vessel leads to positive apical WSSG on the side corresponding to the outer curve. All simulations revealed wider apical area coverage by higher WSS and positive WSSG magnitudes, with increased bifurcation angle and higher flow rate. Flow rate did not affect the angle threshold of 85°, past which positive WSSG occurs. In curved models, high flow displaced the impingement area away from the apex, in a dynamic fashion and in an angle-dependent manner.CONCLUSIONSApical shear forces and spatial gradients are highly dependent on bifurcation and inflow vessel geometry. The development of aneurysmogenic positive WSSG as a function of angular geometry provides a mechanotransductive link for the association of wide bifurcations and aneurysm development. These results suggest therapeutic strategies aimed at altering underlying unfavorable geometry and deciphering the molecular endothelial response to shear gradients in a bid to disrupt the associated aneurysmal degeneration.


1995 ◽  
Vol 117 (3) ◽  
pp. 350-357 ◽  
Author(s):  
M. Lei ◽  
C. Kleinstreuer ◽  
G. A. Truskey

Atherosclerosis, a disease of large- and medium-size arteries, is the chief cause of death in the US and most of the western world. It is widely accepted that the focal nature of the disease in arterial bends, junctions, and bifurcations is directly related to locally abnormal hemodynamics, often labeled “disturbed flows.” Employing the aorto-celiac junction of rabbits as a representative atherosclerotic model and considering other branching blood vessels with their distinctive input wave forms, it is suggested that the local wall shear stress gradient (WSSG) is the single best indicator of nonuniform flow fields leading to atherogenesis. Alternative predictors of susceptible sites are briefly evaluated. The results discussed include transient velocity vector fields, wall shear stress gradient distributions, and a new dimensionless parameter for the prediction of the probable sites of stenotic developments in branching blood vessels. Some of the possible underlying biological aspects of atherogenesis due to locally significant |WSSG|-magnitudes are briefly discussed.


1989 ◽  
Vol 111 (1) ◽  
pp. 47-54 ◽  
Author(s):  
R. Yamaguchi

The distributions of mass transfer rate and wall shear stress in sinusoidal laminar pulsating flow through a two-dimensional asymmetric stenosed channel have been studied experimentally and numerically. The distributions are measured by the electrochemical method. The measurement is conducted at a Reynolds number of about 150, a Schmidt number of about 1000, a nondimensional pulsating frequency of 3.40, and a nondimensional flow amplitude of 0.3. It is suggested that the deterioration of an arterial wall distal to stenosis may be greatly enhanced by fluid dynamic effects.


Author(s):  
Arun Ramu ◽  
Guo-Xiang Wang

Intracranial aneurysms are abnormal enlargement in the walls of cerebral arteries. The rupture of aneurysms is the leading cause of subarachnoid hemorrhage (SAH), with a high mortality and morbidity rate. A majority of saccular cerebral aneurysms occur at sites of arterial bifurcations. However, a good percentage of aneurysms are curvature induced and are found along the cavernous arterial segment. The occurrence of such non branching aneurysms, clinically called dorsal aneurysms, can be related to the increased wall shear stress at the curved arteries. The rupture of aneurysms usually occurs at the dome region, which is subjected to reduced wall shear stress (wss) owing to low re-circulating flow. Hence it is important to understand the impact of arterial curvature on the WSS distribution along the dome of aneurysms. Previously, studies have not taken into account the aspect of low WSS along the dome region. In the present 3-d computational fluid dynamic approach, we investigate the impact of varying arterial curvature on spherical dorsal aneurysms. The primary velocity patterns, the WSS distribution along the dome of the aneurysm and the area of increased WSS have been quantified for steady flow conditions.


Author(s):  
Leonie Rouleau ◽  
Monica Farcas ◽  
Jean-Claude Tardif ◽  
Rosaire Mongrain ◽  
Richard Leask

Endothelial cell (EC) dysfunction has been linked to atherosclerosis through their response to hemodynamic forces. Flow in stenotic vessels creates complex spatial gradients in wall shear stress. In vitro studies examining the effect of shear stress on endothelial cells have used unrealistic and simplified models, which cannot reproduce physiological conditions. The objective of this study was to expose endothelial cells to the complex shear shear pattern created by an asymmetric stenosis. Endothelial cells were grown and exposed for different times to physiological steady flow in straight dynamic controls and in idealized asymmetric stenosis models. Cells subjected to 1D flow aligned with flow direction and had a spindle-like shape when compared to static controls. Endothelial cell morphology was noticeable different in the regions with a spatial gradient in wall shear stress, being more randomly oriented and of cobblestone shape. This occurred despite the presence of an increased magnitude in shear stress. No other study to date has described this morphology in the presence of a positive wall shear stress gradient or gradient of significant shear magnitude. This technique provides a more realistic model to study endothelial cell response to spatial and temporal shear stress gradients that are present in vivo and is an important advancement towards a better understanding of the mechanisms involved in coronary artery disease.


2004 ◽  
Vol 286 (5) ◽  
pp. H1916-H1922 ◽  
Author(s):  
Heather A. Himburg ◽  
Deborah M. Grzybowski ◽  
Andrew L. Hazel ◽  
Jeffrey A. LaMack ◽  
Xue-Mei Li ◽  
...  

A better understanding of how hemodynamic factors affect the integrity and function of the vascular endothelium is necessary to appreciate more fully how atherosclerosis is initiated and promoted. A novel technique is presented to assess the relation between fluid dynamic variables and the permeability of the endothelium to macromolecules. Fully anesthetized, domestic swine were intravenously injected with the albumin marker Evans blue dye, which was allowed to circulate for 90 min. After the animals were euthanized, silicone casts were made of the abdominal aorta and its iliac branches. Pulsatile flow calculations were subsequently made in computational regions derived from the casts. The distribution of the calculated time-dependent wall shear stress in the external iliac branches was directly compared on a point-by-point basis with the spatially varying in vivo uptake of Evans blue dye in the same arteries. The results indicate that in vivo endothelial permeability to albumin decreases with increasing time-average shear stress over the normal range. Additionally, endothelial permeability increases slightly with oscillatory shear index.


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