Wall shear stress and early atherosclerotic lesions in the abdominal aorta in young adults

Shear stress may be the most crucial local factor affecting atherogenesis. Enhanced External Counterpulsation (EECP) has been documented to increase arterial wall shear stress in vivo. We hypothesize that chronic exposure to increased pulsatile shear stress by EECP arrests the progression of atherosclerosis due to hypercholesterolemia. Forty-eight pigs were randomized to usual diet (n = 7), high-cholesterol diet (n = 18), and high-cholesterol diet plus EECP (34±2 hours, n = 23). At week 15, the left anterior descending coronary arteries (LAD) were collected for HE staining, transmission electron microscopy examination, immunohistochemical analysis of AKT, caspase- 3 and TUNEL assay. Expression and localization of NK- κB was assessed by immunofluorescence and confocal laser scanning microscope. The aortas were isolated for Sudan staining and Western-blot analysis. Blood lipids, viscosity, Doppler ultrasound flow examination was performed. Statistical analysis was by Kruskal-Wallis and Mann-Whitney tests. During EECP, the peak diastolic arterial wall shear stress in the right brachial artery increased significantly compared with baseline (53.18±3.81 dynes/cm 2 versus 23.92±2.02 dynes/cm 2 , p<0.001), as well as the mean arterial wall shear stress (27.46±2.22 dynes/cm 2 versus 20.43±1.87 dynes/cm 2 , p < 0.001). High-cholesterol diet induced remarkable atherosclerotic lesions with excessive cellular proliferation and apoptosis. In comparison, hypercholesterolemic animals receiving EECP showed ameliorated atherosclerotic lesions in LADs ( lesion/medial area ratio: 19.71±3.79 % versus 7.32±1.59 %, p = 0.001) and aortas (percentage of plaque area: 9.95±1.81 % versus 5.16±1.08 %, p = 0.011), coupled with decreased TUNEL positive staining (64±2.08 % versus 49±2.27 %, p < 0.001), reduced caspase- 3 protein expression, AKT and NF- κB activity. This study demonstrates that EECP administration leads to reduced atherosclerotic lesions, coupled with dual inhibitory effects on vascular cellular proliferation and apoptosis. Its mechanisms are related to chronic increased shear stress by EECP suppressing the over-activation of the AKT/NF-κB signaling pathway.

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Effect of Reynolds number and flow division on patterns of haemodynamic wall shear stress near branch points in the descending thoracic aorta

Journal of The Royal Society Interface ◽

10.1098/rsif.2008.0323 ◽

2008 ◽

Vol 6 (35) ◽

pp. 539-548 ◽

Cited By ~ 15

Author(s):

A. Kazakidi ◽

S.J. Sherwin ◽

P.D. Weinberg

Keyword(s):

Reynolds Number ◽

Shear Stress ◽

Wall Shear Stress ◽

Thoracic Aorta ◽

Flow Region ◽

Side Branch ◽

Branch Points ◽

Atherosclerotic Lesions ◽

Wall Shear ◽

Flow Division

Atherosclerotic lesions are non-uniformly distributed at arterial bends and branch sites, suggesting an important role for haemodynamic factors, particularly wall shear stress (WSS), in their development. The pattern of lesions at aortic branch sites depends on age and species. Using computational flow simulations in an idealized model of an intercostal artery emerging perpendicularly from the thoracic aorta, we studied the effects of Reynolds number and flow division under steady conditions. Patterns of flow and WSS were strikingly dependent on these haemodynamic parameters. With increasing Reynolds number, WSS, normalized by the fully developed aortic value, was lowered at the sides of the ostium and increased upstream and downstream of it. Increasing flow into the side branch exacerbated these patterns and gave rise to a reversing flow region downstream of the ostium. Incorporation of more realistic geometric features had only minor effects and patterns of mean WSS under pulsatile conditions were similar to the steady flow results. Aspects of the observed WSS patterns correlate with, and may explain, some but not all of the lesion patterns in human, rabbit and mouse aortas.

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Fluid Flow and Plaque Formation in an Aortic Bifurcation

Journal of Biomechanical Engineering ◽

10.1115/1.3168385 ◽

1989 ◽

Vol 111 (4) ◽

pp. 316-324 ◽

Cited By ~ 27

Author(s):

M. Nazemi ◽

C. Kleinstreuer ◽

J. P. Archie ◽

F. Y. Sorrell

Keyword(s):

Shear Stress ◽

Wall Shear Stress ◽

Reverse Flow ◽

Plaque Formation ◽

Surgical Reconstruction ◽

Shear Stresses ◽

Computer Simulation Model ◽

Predictive Tool ◽

Atherosclerotic Lesions ◽

Wall Shear

Considering steady laminar flow in a two-dimensional symmetric branching channel with local occlusions, a finite element model has been developed to study velocity fields including reverse flow regions, pressure profiles and wall shear stress distributions for different Reynolds numbers, bifurcation angles and lumen reductions. The flow analysis has been extended to include a new submodel for the pseudo-transient formation of plaque at sites and deposition rates defined by the physical characteristics of the flow. Specifically, simulating the onset of atherosclerotic lesions, sinusoidal plaque layers have been placed in areas of critically low wall shear stresses, and simulating the growth of particle depositions, plaque layers have been added in a stepwise fashion in regions of critically high and low shear. Thus two somewhat conflicting hypothetical correlations between critical wall shear stress levels and atheroma have been tested and a solution has been postulated. The validated computer simulation model is a predictive tool for analyzing the effects of local changes in wall curvature due to surgical reconstruction and/or atherosclerotic lesions, and for investigating the design of aortic bifurcations which mitigate plaque formation.

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Quantification and comparison of 4D Flow MRI derived wall shear stress and MRE derived wall shear stiffness of abdominal aorta

Journal of Cardiovascular Magnetic Resonance ◽

10.1186/1532-429x-18-s1-p360 ◽

2016 ◽

Vol 18 (S1) ◽

Cited By ~ 1

Author(s):

Venkata Sita Priyanka Illapani ◽

Julio Garcia ◽

Ria Mazumder ◽

Richard D White ◽

Michael Markl ◽

...

Keyword(s):

Shear Stress ◽

Wall Shear Stress ◽

Abdominal Aorta ◽

Shear Stiffness ◽

4D Flow Mri ◽

4D Flow ◽

Flow Mri ◽

Wall Shear

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Abdominal aortic hemodynamics in young healthy adults at rest and during lower limb exercise: quantification using image-based computer modeling

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01301.2005 ◽

2006 ◽

Vol 291 (2) ◽

pp. H668-H676 ◽

Cited By ~ 84

Author(s):

Beverly T. Tang ◽

Christopher P. Cheng ◽

Mary T. Draney ◽

Nathan M. Wilson ◽

Philip S. Tsao ◽

...

Keyword(s):

Shear Stress ◽

Wall Shear Stress ◽

Abdominal Aorta ◽

Infrarenal Aorta ◽

Mechanical Stimuli ◽

Flow Recirculation ◽

Regional Flow ◽

Lower Limb Exercise ◽

Wall Shear ◽

Rest And Exercise

Localization of atherosclerotic lesions in the abdominal aorta has been previously correlated to areas of adverse hemodynamic conditions, such as flow recirculation, low mean wall shear stress, and high temporal oscillations in shear. Along with its many systemic benefits, exercise is also proposed to have local benefits in the vasculature via the alteration of these regional flow patterns. In this work, subject-specific models of the human abdominal aorta were constructed from magnetic resonance angiograms of five young, healthy subjects, and computer simulations were performed under resting and exercise (50% increase in resting heart rate) pulsatile flow conditions. Velocity fields and spatial variations in mean wall shear stress (WSS) and oscillatory shear index (OSI) are presented. When averaged over all subjects, WSS increased from 4.8 ± 0.6 to 31.6 ± 5.7 dyn/cm2 and OSI decreased from 0.22 ± 0.03 to 0.03 ± 0.02 in the infrarenal aorta between rest and exercise. WSS significantly increased, whereas OSI decreased between rest and exercise at the supraceliac, infrarenal, and suprabifurcation levels, and significant differences in WSS were found between anterior and posterior sections. These results support the hypothesis that exercise provides localized benefits to the cardiovascular system through acute mechanical stimuli that trigger longer-term biological processes leading to protection against the development or progression of atherosclerosis.

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