Shear-Dependent Thickening of the Human Arterial Intima

Friedman, Morton H.; Deters, O. J.; Bargeron, C. B.; Hutchins, Grover M.; Mark, F.

doi:10.1016/0021-9150(86)90008-0

Cited by 140 publications

(54 citation statements)

References 11 publications

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“…Studies comparing human post-mortem distributions of plaque to in vitro fluid dynamic models have perhaps provided the most direct observational evidence for the relationship between WSS and the focal development of atherosclerotic lesions (1)(2)(3)(4). The mechanisms by which shear stresses alter endothelial function at the cellular, molecular, and genetic level are also now being elucidated (5).…”

mentioning

confidence: 99%

Reconstruction of carotid bifurcation hemodynamics and wall thickness using computational fluid dynamics and MRI

Steinman

Thomas

Ladak

et al. 2001

Magnetic Resonance in Med

225

146

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A thorough understanding of the relationship between local hemodynamics and plaque progression has been hindered by an inability to prospectively monitor these factors in vivo in humans. In this study a novel approach for noninvasively reconstructing artery wall thickness and local hemodynamics at the human carotid bifurcation is presented. Three-dimensional (3D) models of the lumen and wall boundaries, from which wall thickness can be measured, were reconstructed from blackblood magnetic resonance imaging (MRI). Along with time-varying inlet/outlet flow rates measured via phase contrast (PC) MRI, the lumen boundary was used as input for computational fluid dynamic (CFD) simulation of the subject-specific flow patterns and wall shear stresses (WSSs). Results from a 59-yearold subject with early, asymptomatic carotid artery disease show good agreement between simulated and measured velocities, and demonstrate a correspondence between wall thickening and low and oscillating shear at the carotid bulb. High shear at the distal internal carotid artery (ICA) was also colocalized with higher WSS; however, a quantitative general relationship between WSS and wall thickness was not found. Similar results were obtained from a 23-year-old normal subject. Wall shear stress (WSS) is widely believed to play a key role in the development and progression of atherosclerotic plaques. Studies comparing human post-mortem distributions of plaque to in vitro fluid dynamic models have perhaps provided the most direct observational evidence for the relationship between WSS and the focal development of atherosclerotic lesions (1-4). The mechanisms by which shear stresses alter endothelial function at the cellular, molecular, and genetic level are also now being elucidated (5). Despite these advances, however, many questions still remain regarding the role of fluid dynamics in the development and progression of atherosclerosis. One reason for this has been the difficulty of identifying and monitoring the relationships between local fluid dynamic factors and plaque development on a subject-specific basis.In principle, both MR and ultrasound imaging can be used to measure wall thickness (a marker for atherosclerotic burden) and blood velocities (from which WSSs are derived) directly. However, difficulties associated with the quantification of blood velocities in regions of complex flow have in the past limited the application of such an "imaging-only" approach to relatively straight sections of the abdominal aorta (6), femoral artery (7), and common carotid artery (8 -10). While these studies were able to confirm an inverse relationship between mean or peak shear and intimal or intima-media thickness, it is not yet possible to use imaging techniques alone to map WSS in the regions of complex flow where plaques are known to localize, such as at the carotid bifurcation. Recent work by Stokholm et al. (11) suggests that WSS from individual slices at the carotid bifurcation itself can be quantified in vivo by sophisticated postprocessing of ph...

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mentioning

confidence: 99%

Reconstruction of carotid bifurcation hemodynamics and wall thickness using computational fluid dynamics and MRI

Steinman

Thomas

Ladak

et al. 2001

Magnetic Resonance in Med

225

146

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“…This change in the sign of the slope of the thickness-shear rate relationship was seen in the original experimental data. 1 The behavior shown in Figure 5 offers an explanation of what has sometimes been called the "high shear-low shear" controversy: some investigators have found that sites associated with high shear have thicker intimas, whereas other experimenters have reported the opposite. Figure 5 shows that either of these results can be obtained, depending on the extent to which the thickening process has progressed at the time of the measurements.…”

Section: Role Of Hemodynamics: the High Shear-low Shear Controversymentioning

confidence: 99%

“…The gathering of these data is described by Friedman et al 1 In most of the simulations, the hemodynamic variable on which the parameters in Table 2 were allowed to depend was normalized maximum shear rate, s™,, defined as the maximum instantaneous shear rate at a site divided by the average of the maximum shear rates at all the sites examined in that cast. At a site exposed to this average maximum shear rate, s^ would be equal to unity.…”

Section: Correlation Of Datamentioning

confidence: 99%

“…An equivalent result was found for the earlier model. 1 This also suggests that the process (or processes) with the stronger shear dependence may be the dominant one(s) in the long term; certainly, the presence of large amounts of ECM is one of the characteristics of substantially thickened intima.…”

Section: Plausibility Of the Modelmentioning

confidence: 99%

“…n earlier work, 1 we presented the correlations between intimal thickness and wall shear rates measured in flow-through casts of 10 human aortic bifurcations. These correlations suggested that the intima initially thickens more rapidly where shear is high or unidirectional, but ultimately reaches greater thicknesses where the shear is relatively low and oscillatory.…”

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confidence: 99%

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A biologically plausible model of thickening of arterial intima under shear.

Friedman

1989

Arteriosclerosis

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A biologically plausible model of the early thickening of the arterial Intima has been developed to interpret experimental data relating hemodynamlc shear to human Intimal morphology. The model Included many processes known or commonly believed to take place In the vascular Intima, including: smooth muscle cell migration, proliferation, metabolism, and expression of extracellular matrix; llpoproteln kinetics and binding; and monocyte chemotaxls, conversion to macrophage, and foam cell formation. Certain of these processes were allowed to be shear-dependent. The best fit to the data was obtained when smooth muscle cell accumulation was more rapid, and extracellular matrix expression proceeded more slowly where the fluid shear was relatively high and unidirectional. This result Is consistent with the earlier Inference that competing shear-dependent processes take place in the wall; It is also consistent with the notion that Intimal thickening might be part of an adaptive mechanism by which the artery maintains a favorable shear environment. (Arteriosclerosis 9:511-522, July/August 1989) I n earlier work, 1 we presented the correlations between intimal thickness and wall shear rates measured in flow-through casts of 10 human aortic bifurcations. These correlations suggested that the intima initially thickens more rapidly where shear is high or unidirectional, but ultimately reaches greater thicknesses where the shear is relatively low and oscillatory. It was shown that this behavior, more complex than had earlier been supposed, could reflect the influence of competing shear-dependent processes.A simple mathematical model of intimal thickening was developed to demonstrate that competing processes could be responsible for the experimental results; in it, intimal thickness was determined by a balance between the shear-dependent uptake and shear-dependent removal of an unspecified blood-borne substance. Here, we extend this demonstration by using a more realistic model that better reflects current understanding of the biological processes that take place in the arterial wall during the early stages of intimal thickening.This paper begins with a description of the baseline model and certain optional processes. Following a welldefined protocol, a more complex model Is then constructed by adding to the baseline model two optional processes whose inclusion significantly improves the fit of the model to the intimal thickness and hemodynamic data obtained earlier.

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Numerical study of blood flow in an anatomically realistic aorto-iliac bifurcation generated from MRI data

Long

Bourne

et al. 2000

Magn. Reson. Med.

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Shear-Dependent Thickening of the Human Arterial Intima

Cited by 140 publications

References 11 publications

Reconstruction of carotid bifurcation hemodynamics and wall thickness using computational fluid dynamics and MRI

Reconstruction of carotid bifurcation hemodynamics and wall thickness using computational fluid dynamics and MRI

A biologically plausible model of thickening of arterial intima under shear.

Numerical study of blood flow in an anatomically realistic aorto-iliac bifurcation generated from MRI data

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