Infrared based visualization of wall shear stress distributions with a high temporal and spatial resolution

2007 ◽  
Vol 10 (1) ◽  
pp. 8-8 ◽  
Author(s):  
I. Rudolph ◽  
M. Reyer ◽  
W. Nitsche
2018 ◽  
Vol 5 (3) ◽  
pp. 171447 ◽  
Author(s):  
R. Xing ◽  
A. M. Moerman ◽  
Y. Ridwan ◽  
M. J. Daemen ◽  
A. F. W. van der Steen ◽  
...  

Wall shear stress (WSS) is involved in atherosclerotic plaque initiation, yet its role in plaque progression remains unclear. We aimed to study (i) the temporal and spatial changes in WSS over a growing plaque and (ii) the correlation between WSS and plaque composition, using animal-specific data in an atherosclerotic mouse model. Tapered casts were placed around the right common carotid arteries (RCCA) of ApoE −/− mice. At 5, 7 and 9 weeks after cast placement, RCCA geometry was reconstructed using contrast-enhanced micro-CT. Lumen narrowing was observed in all mice, indicating the progression of a lumen intruding plaque. Next, we determined the flow rate in the RCCA of each mouse using Doppler Ultrasound and computed WSS at all time points. Over time, as the plaque developed and further intruded into the lumen, absolute WSS significantly decreased. Finally at week 9, plaque composition was histologically characterized. The proximal part of the plaque was small and eccentric, exposed to relatively lower WSS. Close to the cast a larger and concentric plaque was present, exposed to relatively higher WSS. Lower WSS was significantly correlated to the accumulation of macrophages in the eccentric plaque. When pooling data of all animals, correlation between WSS and plaque composition was weak and no longer statistically significant. In conclusion, our data showed that in our mouse model absolute WSS strikingly decreased during disease progression, which was significantly correlated to plaque area and macrophage content. Besides, our study demonstrates the necessity to analyse individual animals and plaques when studying correlations between WSS and plaque composition.


Author(s):  
Kevin R. Johnson ◽  
John N. Oshinski

Low and oscillatory arterial wall shear stress (WSS) have been shown to have an effect on many factors implicated in atherosclerotic lesion development. The majority of studies on the relationship between low or oscillating WSS and sites of intimal thickening and early atherosclerotic lesion development are based on in-vitro model studies of flow and WSS distribution. These models are based on average vessel geometries with average flow conditions and compared to average pathology distribution of lesions that may obscure the true relationship between WSS and lesion distribution[1]. Recent techniques have been developed using coronary MR angiography to create patient-specific 3D models along with velocity measurements of blood flow using phase contrast magnetic resonance (PCMR). However, these models may lack adequate spatial resolution for accurate, localized calculation of WSS[2]. Current, state-of-art multidetector CT scanners offer improvements in spatial resolution over MRI for creation of 3D vessel models.


2015 ◽  
Vol 137 (6) ◽  
Author(s):  
Othmane Oulaid ◽  
Junfeng Zhang

Using a simplified two-dimensional divider-channel setup, we simulate the development process of red blood cell (RBC) flows in the entrance region of microvessels to study the wall shear stress (WSS) behaviors. Significant temporal and spatial variation in WSS is noticed. The maximum WSS magnitude and the strongest variation are observed at the channel inlet due to the close cell-wall contact. From the channel inlet, both the mean WSS and variation magnitude decrease, with a abrupt drop in the close vicinity near the inlet and then a slow relaxation over a relatively long distance; and a relative stable state with approximately constant mean and variation is established when the flow is well developed. The correlations between the WSS variation features and the cell free layer (CFL) structure are explored, and the effects of several hemodynamic parameters on the WSS variation are examined. In spite of the model limitations, the qualitative information revealed in this study could be useful for better understanding relevant processes and phenomena in the microcirculation.


2009 ◽  
Vol 202 (2) ◽  
pp. 483-490 ◽  
Author(s):  
E. Wellnhofer ◽  
L. Goubergrits ◽  
U. Kertzscher ◽  
K. Affeld ◽  
E. Fleck

2005 ◽  
Vol 128 (3) ◽  
pp. 347-359 ◽  
Author(s):  
Divakar Rajamohan ◽  
Rupak K. Banerjee ◽  
Lloyd H. Back ◽  
Ashraf A. Ibrahim ◽  
Milind A. Jog

A major consequence of stent implantation is restenosis that occurs due to neointimal formation. This patho-physiologic process of tissue growth may not be completely eliminated. Recent evidence suggests that there are several factors such as geometry and size of vessel, and stent design that alter hemodynamic parameters, including local wall shear stress distributions, all of which influence the restenosis process. The present three-dimensional analysis of developing pulsatile flow in a deployed coronary stent quantifies hemodynamic parameters and illustrates the changes in local wall shear stress distributions and their impact on restenosis. The present model evaluates the effect of entrance flow, where the stent is placed at the entrance region of a branched coronary artery. Stent geometry showed a complex three-dimensional variation of wall shear stress distributions within the stented region. Higher order of magnitude of wall shear stress of 530dyn∕cm2 is observed on the surface of cross-link intersections at the entrance of the stent. A low positive wall shear stress of 10dyn∕cm2 and a negative wall shear stress of −10dyn∕cm2 are seen at the immediate upstream and downstream regions of strut intersections, respectively. Modified oscillatory shear index is calculated which showed persistent recirculation at the downstream region of each strut intersection. The portions of the vessel where there is low and negative wall shear stress may represent locations of thrombus formation and platelet accumulation. The present results indicate that the immediate downstream regions of strut intersections are areas highly susceptible to restenosis, whereas a high shear stress at the strut intersection may cause platelet activation and free emboli formation.


1992 ◽  
Vol 49 (3) ◽  
pp. 261-270 ◽  
Author(s):  
Henri A. Siller ◽  
Richard J. Perkins ◽  
Gerd Janke

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