Reversed Correlations Between Atherosclerotic Carotid Plaque Progression and Flow Shear Stress/Plaque Wall Stress Based on Past and Current Scan Data: In Vivo MRI-Based 3D FSI Studies

2010 ◽  
Author(s):  
Chun Yang ◽  
Gador Canton ◽  
Chun Yuan ◽  
Thomas Hatsukami ◽  
Dalin Tang
Keyword(s):  
Shear Stress ◽  
Wall Stress ◽  
Significant Negative Correlation ◽  
Shear Stresses ◽  
Plaque Progression ◽  
Flow Shear ◽  
Carotid Plaques ◽  
Flow Shear Stress ◽  
The Difference

It has been well accepted that low and oscillating blood flow shear stresses (LFSS) correlate positively with intimal thickening and atherosclerosis initiation [1,2]. However, the LFSS hypothesis cannot explain why advanced plaques continue to grow under elevated high flow shear stress conditions [3]. For patient tracking studies, plaque progression is often measured by the difference of plaque geometries between two scans (“past” and “current” scans) when medical imaging is used. Mechanical flow shear stress (FSS) and plaque wall stress (PWS) conditions from the two scans may have different correlations with plaque progression. Using 2D structure models based on in vivo magnetic resonance imaging (MRI) human carotid plaques, Tang et al. showed that 18 out of 21 patients had significant negative correlation between plaque progression measured by wall thickness increase (WTI) and plaque wall stress from current scan [3]. The correlation was reversed when plaque wall stress from past scan was used. In this paper, 3D fluid-structure interactions (FSI) models for 32 matched “past-current” scan pairs of human atherosclerotic carotid plaques based on in vivo MRI data were solved and plaque wall stress (PWS) and flow shear stress (FSS) data were obtained to quantify their correlations with plaque progression measured by WTI.

Predicting Human Carotid Plaque Site of Rupture Using 3D Critical Plaque Wall Stress and Flow Shear Stress: A 3D Multi-Patient FSI Study Based on In Vivo MRI of Plaques With and Without Prior Rupture

2010 ◽  
Author(s):  
Zhongzhao Teng ◽  
Gador Canton ◽  
Chun Yuan ◽  
Marina Ferguson ◽  
Chun Yang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Critical Stress ◽  
Plaque Rupture ◽  
Wall Stress ◽  
Global Maximum ◽  
Flow Shear ◽  
Carotid Plaques ◽  
Flow Shear Stress ◽  
Human Carotid

Atherosclerotic plaque rupture is the primary cause of cardiovascular clinical events such as heart attack and stroke. Image-based computational models of vulnerable plaques have been introduced seeking critical mechanical indicators which may be used to identify potential sites of rupture [1–5]. Models derived from 2D ex vivo and in vivo magnetic resonance images (MRI) have shown that 2D local critical stress values rather than global maximum stress values correlated better with plaque vulnerability, as defined by histopathological and morphological analyses [5]. A recent study by Tang et al. [4] using in vivo MRI-based 3D fluid-structure interaction (FSI) models for ruptured human carotid plaques, reported that mean plaque wall stress (PWS) values from ulcer nodes were 86% higher than mean PWS values from all non-ulcer nodes (p<0.0001). This study extends the “critical stress” concept to 3D and uses 3D FSI models based on in vivo MRI data of human atherosclerotic carotid plaques with and without prior rupture to identify 3D critical plaque wall stress (CPWS), critical flow shear stress (CFSS), and to investigate their associations with plaque rupture.

scholarly journals 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

2010 ◽  
Vol 43 (13) ◽  
pp. 2530-2538 ◽  
Author(s):  
Chun Yang ◽  
Gador Canton ◽  
Chun Yuan ◽  
Marina Ferguson ◽  
Thomas S. Hatsukami ◽  
...  
Keyword(s):  
Shear Stress ◽  
Carotid Plaque ◽  
Plaque Progression ◽  
Flow Shear ◽  
Flow Shear Stress ◽  
Scan Data ◽  
Human Carotid

A New Hypothesis for Human Atherosclerotic Plaque Progression Based on Serial In Vivo MRI and Computational Modeling Method

2007 ◽  
Author(s):  
Sayan Mondal ◽  
Chun Yang ◽  
Joseph D. Petruccelli ◽  
Chun Yuan ◽  
Fei Liu ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Thickness ◽  
Computational Models ◽  
Ex Vivo ◽  
Maximum Principal Stress ◽  
Magnetic Resonance Images ◽  
Shear Stresses ◽  
Flow Shear ◽  
Flow Shear Stress

It has been well-accepted that atherosclerosis initiation and progression correlate positively with low and oscillating flow wall shear stresses. However, this shear stress mechanism cannot fully explain why advanced plaques continue to grow under elevated flow shear stress conditions. Our previous investigations using 3D computational models with fluid-structure interactions (FSI) based on in vivo/ex vivo magnetic resonance images (MRI) of human carotid atherosclerotic plaques indicated that there is a negative correlation between advanced plaque wall thickness and structural maximum principal stress (Stress-P1) in the plaque and a positive correlation between plaque wall thickness and flow shear stress [3].

Advanced Human Coronary Plaque Wall Thickness Correlates Positively With Flow Shear Stress and Negatively With Plaque Wall Stress: An IVUS-Based FSI Study

2013 ◽  
Author(s):  
Dalin Tang ◽  
Chun Yang ◽  
Joseph D. Petruccelli ◽  
Jie Zheng ◽  
Richard Bach ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Thickness ◽  
Wall Stress ◽  
Coronary Plaque ◽  
Stress Conditions ◽  
Patient Specific ◽  
Plaque Progression ◽  
Flow Shear ◽  
Flow Shear Stress

Atherosclerotic plaque progression is believed to be associated with low and oscillating flow shear stress conditions [1–3]. In vivo image-based coronary plaque modeling papers are relatively rare because clinical recognition of vulnerable coronary plaques has remained challenging [3–4]. Samady et al. [3] published their seminal patient follow-up coronary plaque progression study and indicated that flow shear stress (FSS) was associated with plaque progression and remodeling. We have published results based on follow-up studies showing that advanced carotid plaque had positive correlation with flow shear stress and negative correlation with plaque wall stress (PWS) [4]. In this paper, patient-specific intravascular ultrasound (IVUS)-based coronary plaque models with fluid-structure interaction (FSI), on-site pressure and ex vivo biaxial mechanical testing of human coronary plaque material properties were constructed to obtain flow shear stress and plaque wall stress data from six patients to investigate possible associations between vessel wall thickness and both flow shear stress and plaque wall stress conditions.

scholarly journals 3D Critical Plaque Wall Stress Is a Better Predictor of Carotid Plaque Rupture Sites Than Flow Shear Stress: An In Vivo MRI-Based 3D FSI Study

2010 ◽  
Vol 132 (3) ◽  
Author(s):  
Zhongzhao Teng ◽  
Gador Canton ◽  
Chun Yuan ◽  
Marina Ferguson ◽  
Chun Yang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Plaque Rupture ◽  
Wall Stress ◽  
Flow Shear ◽  
Flow Shear Stress ◽  
The Mean ◽  
Group 2 ◽  
Atherosclerotic Plaque Rupture ◽  
Group 1

Atherosclerotic plaque rupture leading to stroke is the major cause of long-term disability as well as the third most common cause of mortality. Image-based computational models have been introduced seeking critical mechanical indicators, which may be used for plaque vulnerability assessment. This study extends the previous 2D critical stress concept to 3D by using in vivo magnetic resonance image (MRI) data of human atherosclerotic carotid plaques and 3D fluid-structure interaction (FSI) models to: identify 3D critical plaque wall stress (CPWS) and critical flow shear stress (CFSS) and to investigate their associations with plaque rupture. In vivo MRI data of carotid plaques from 18 patients scheduled for endarterectomy were acquired using histologically validated multicontrast protocols. Of the 18 plaques, histology-confirmed that six had prior rupture (group 1) as evidenced by presence of ulceration. The remaining 12 plaques (group 2) contained no rupture. The 3D multicomponent FSI models were constructed for each plaque to obtain 3D plaque wall stress (PWS) and flow shear stress (FSS) distributions. Three-dimensional CPWS and CFSS, defined as maxima of PWS and FSS from all vulnerable sites, were determined for each plaque to investigate their association with plaque rupture. Slice-based critical PWS and FSS were also calculated for all slices for more detailed analysis and comparison. The mean 3D CPWS of group 1 was 263.44 kPa, which was 100% higher than that from group 2 (132.77, p=0.03984). Five of the six ruptured plaques had 3D CPWS sites, matching the histology-confirmed rupture sites with an 83% agreement. Although the mean 3D CFSS (92.94 dyn/cm2) for group 1 was 76% higher than that for group 2 (52.70 dyn/cm2), slice-based CFSS showed no significant difference between the two groups. Only two of the six ruptured plaques had 3D CFSS sites matching the histology-confirmed rupture sites with a 33% agreement. CFSS had a good correlation with plaque stenosis severity (R2=0.40 with an exponential function fitting 3D CFSS data). This in vivo MRI pilot study using plaques with and without rupture demonstrates that 3D critical plaque wall stress values are more closely associated with atherosclerotic plaque rupture then critical flow shear stresses. Critical wall stress values may become indicators of high risk sites of rupture. Future work with a larger population will establish a possible CPWS-based plaque vulnerability classification.

A test of the role of flow-dependent dilation in arteriolar responses to occlusion

1997 ◽  
Vol 272 (2) ◽  
pp. H714-H721 ◽  
Author(s):  
E. D. McGahren ◽  
K. A. Dora ◽  
D. N. Damon ◽  
B. R. Duling
Keyword(s):  
Shear Stress ◽  
Baseline Level ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Flow Shear ◽  
Flow Through ◽  
Flow Shear Stress ◽  
Arteriolar Diameter

At an arteriolar bifurcation, occlusion of one of the branch arterioles has been reported to result in an increase in flow, shear stress, and vasodilation in the opposite unoccluded branch. This dilator response in the unoccluded branch, often referred to as the "parallel occlusion response," has been cited as evidence that flow-dependent dilation is a primary regulator of arteriolar diameter in the microcirculation. It has not been previously noted that, during this maneuver, flow through the feed arteriole would be expected to decrease and logically should cause that vessel to constrict. We tested this prediction in vivo by measuring red blood cell (RBC) velocity and diameter changes in response to arteriolar occlusion in the microcirculatory beds of three preparations: the hamster cheek pouch, the hamster cremaster, and the rat cremaster. In all preparations, a vasodilation was observed in the feed arteriole, despite a decrease in both flow and calculated wall shear stress through this vessel. Unexpectedly, we found that dilation occurred in the unoccluded branch arterioles even in those cases in which RBC velocity and shear stress did not increase in the unoccluded branch arterioles. All values returned to the baseline level after the removal of occlusion. The magnitude of the dilation of the feed and branch arterioles varied between species and tissues, but feed and branch arterioles within a given preparation always responded in a similar way to each other. We conclude from our experiments that mechanisms other than flow-dependent dilation are involved in the vasodilation observed in the microcirculation during occlusion of an arteriolar branch.

Plaque Growth Functions Combining Wall Stress, Flow Shear Stress and Morphology May Provide Better Prediction for Atherosclerosis Progression: 3D FSI Studies Based on In Vivo Serial MRI

2011 ◽  
Author(s):  
Chun Yang ◽  
Gador Canton ◽  
Chun Yuan ◽  
Tom Hatsukami ◽  
Dalin Tang
Keyword(s):  
Shear Stress ◽  
Atherosclerotic Plaque ◽  
Maximum Shear Stress ◽  
Patient Specific ◽  
Plaque Morphology ◽  
Shear Stresses ◽  
Plaque Progression ◽  
Growth Functions ◽  
Plaque Growth

Atherosclerotic plaque progression involves biological, structural and mechanical factors. Previous work has shown that initiation and early progression of atherosclerotic plaque correlate negatively with flow wall shear stresses [1–2]. However, plaque growth functions based on patient-specific data to predict future plaque growth are lacking in the current literature. Six plaque growth functions based on fluid-structure-interaction (FSI) models and in vivo serial magnetic resonance image (MRI) data were proposed for progression prediction. This is to test the hypothesis that combining plaque morphology, plaque wall maximum principal stress (WS), strain (WSN) and flow maximum shear stress (FSS) could better predict plaque progression.

scholarly journals Transcription Factor β-Catenin Plays a Key Role in Fluid Flow Shear Stress-Mediated Glomerular Injury in Solitary Kidney

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1253
Author(s):  
Tarak Srivastava ◽  
Daniel P. Heruth ◽  
R. Scott Duncan ◽  
Mohammad H. Rezaiekhaligh ◽  
Robert E. Garola ◽  
...  
Keyword(s):  
Shear Stress ◽  
Transcription Factor ◽  
Fluid Flow ◽  
Immunofluorescence Microscopy ◽  
Solitary Kidney ◽  
Glomerular Injury ◽  
Flow Shear ◽  
Flow Shear Stress ◽  
Fluid Flow Shear Stress

Increased fluid flow shear stress (FFSS) in solitary kidney alters podocyte function in vivo. FFSS-treated cultured podocytes show upregulated AKT-GSK3β-β-catenin signaling. The present study was undertaken to confirm (i) the activation of β-catenin signaling in podocytes in vivo using unilaterally nephrectomized (UNX) TOPGAL mice with the β-galactosidase reporter gene for β-catenin activation, (ii) β-catenin translocation in FFSS-treated mouse podocytes, and (iii) β-catenin signaling using publicly available data from UNX mice. The UNX of TOPGAL mice resulted in glomerular hypertrophy and increased the mesangial matrix consistent with hemodynamic adaptation. Uninephrectomized TOPGAL mice showed an increased β-galactosidase expression at 4 weeks but not at 12 weeks, as assessed using immunofluorescence microscopy (p < 0.001 at 4 weeks; p = 0.16 at 12 weeks) and X-gal staining (p = 0.008 at 4 weeks; p = 0.65 at 12 weeks). Immunofluorescence microscopy showed a significant increase in phospho-β-catenin (Ser552, p = 0.005) at 4 weeks but not at 12 weeks (p = 0.935) following UNX, and the levels of phospho-β-catenin (Ser675) did not change. In vitro FFSS caused a sustained increase in the nuclear translocation of phospho-β-catenin (Ser552) but not phospho-β-catenin (Ser675) in podocytes. The bioinformatic analysis of the GEO dataset, #GSE53996, also identified β-catenin as a key upstream regulator. We conclude that transcription factor β-catenin mediates FFSS-induced podocyte (glomerular) injury in solitary kidney.

Letters to the Editor

1998 ◽  
Vol 274 (1) ◽  
pp. H382-H383 ◽  
Author(s):  
Akos Koller gabor Kaley
Keyword(s):  
Shear Stress ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Letters To The Editor ◽  
Flow Shear ◽  
Flow Through ◽  
Flow Shear Stress ◽  
Arteriolar Diameter

The following is the abstract of the article discussed in the subsequent letter: McGahren, Eugene D., Kim A. Dora, David N. Damon, and Brian R. Duling. A test of the role of flow-dependent dilation in arteriolar responses to occlusion. Am. J. Physiol. 272 ( Heart Circ. Physiol. 41): H714–H721, 1997.—At an arteriolar bifurcation, occlusion of one of the branch arterioles has been reported to result in an increase in flow, shear stress, and vasodilation in the opposite unoccluded branch. This dilator response in the unoccluded branch, often referred to as the “parallel occlusion response,” has been cited as evidence that flow-dependent dilation is a primary regulator of arteriolar diameter in the microcirculation. It has not been previously noted that, during this maneuver, flow through the feed arteriole would be expected to decrease and logically should cause that vessel to constrict. We tested this prediction in vivo by measuring red blood cell (RBC) velocity and diameter changes in response to arteriolar occlusion in the microcirculatory beds of three preparations: the hamster cheek pouch, the hamster cremaster, and the rat cremaster. In all preparations, a vasodilation was observed in the feed arteriole, despite a decrease in both flow and calculated wall shear stress through this vessel. Unexpectedly, we found that dilation occurred in the unoccluded branch arterioles even in those cases in which RBC velocity and shear stress did not increase in the unoccluded branch arterioles. All values returned to the baseline level after the removal of occlusion. The magnitude of the dilation of the feed and branch arterioles varied between species and tissues, but feed and branch arterioles within a given preparation always responded in a similar way to each other. We conclude from our experiments that mechanisms other than flow-dependent dilation are involved in the vasodilation observed in the microcirculation during occlusion of an arteriolar branch.

Sign in / Sign up

Export Citation Format

Share Document