Siamak Mishani1, Hanane Belhoul-Fakir2, Chris Lagat1, Shirley Jansen3,4,5,6, Brian Evans1, Michael Lawrence-Brown2. 1. WA School of Mines: MECE, Faculty of Science & Engineering, Curtin University, Kensington, WA, Australia. 2. School of Public Health, Faculty of Health Sciences, Curtin University, Nedlands, WA, Australia. 3. Vascular Surgery Curtin Medical School, Curtin University, Perth, WA, Australia. 4. Department of Vascular and Endovascular Surgery, Sir Charles Gairdner Hospital, Perth, WA, Australia. 5. Heart and Vascular Research Institute, Harry Perkins Institute for Medical Research, Perth, WA, Australia. 6. University of Western Australia, Crawley, WA, Australia.
Abstract
BACKGROUND: There is a correlation between the sites of atheroma development and stress points in the arterial system. Generally, pulse pressure results in stresses acting on the vascular vessel, including longitudinal stress, radial or normal stress, tangential stress or hoop stress and shear stress. This paper explores the relationship between arterial wall shear stress and pulsatile blood pressure with the aim of furthering the understanding of atherogenesis and plaque progression. METHODS: We computed the magnitude of the shear stresses within the carotid bifurcation geometry of a patient and calculated the increase in shear stress levels that would occur when the blood pressure and pulse pressures rise during exertion. We also determined in which layer of the artery wall the maximum shear stress is located, and computed the shear stress at different levels within the media. We used the theory of laminate analysis, (Classical Laminate Plate Theory), to analyse the stress distribution on the carotid artery wall. Computational Fluid Dynamics (CFD) analysis was used on anatomy based on a CT angiogram of the carotid bifurcation of a patient with a 90% stenosis on the right side and 10% on the left. The pulsatile non-Newtonian blood flow with a resting blood pressure of 120/80 mmHg and an exertion pressure of 200/100 mmHg was simulated and the resultant forces were transferred to an ANSYS Composite PrepPost (ACP) model for wall shear stress analysis. A multilayer elastic, anisotropic, and inhomogeneous arterial wall (intima, internal elastic lamina, media, external elastic lamina, and adventitial layers) was modelled and the shear stress magnitudes and change over time between the layers was calculated. RESULTS: Shear stress in the individual composite layers is far greater than that acting on the endothelium (less than 5 Pa). At rest, the maximum variation of shear stress in the arterial wall occurs in the intima (138 Pa) and adventitia (135 Pa). The medial layer has the lowest variation of shear stress. Under severe exertion, the maximum shear stress magnitude in the intimal layer and the adjacent medial layer is near the ultimate stress level. The maximum/minimum shear stress ratios during the cardiac cycle vary most widely in the innermost part of the media, adjacent to the intima, with a four-fold ratio increase. This compares with a less than two-fold increase in all the other layers including the intima and adventitia, making the inner media the most vulnerable layer to mechanical injury. CONCLUSIONS: This study showed that the magnitude of exertion-induced shear stress approaches the ultimate stress limit in the intima and the immediate adjacent medial layer. The variation in stress is maximal in the inner layer of the media. These findings correlate the site of atheroma development with the most vulnerable site for injury in the media and emphasise the impact of pulse pressure. Further biological studies are required to ascertain whether this leads to injury that initiates atheroma that then precipitates an injury/healing cycle. 2021 Quantitative Imaging in Medicine and Surgery. All rights reserved.
BACKGROUND: There is a correlation between the sites of atheroma development and stress points in the arterial system. Generally, pulse pressure results in stresses acting on the vascular vessel, including longitudinal stress, radial or normal stress, tangential stress or hoop stress and shear stress. This paper explores the relationship between arterial wall shear stress and pulsatile blood pressure with the aim of furthering the understanding of atherogenesis and plaque progression. METHODS: We computed the magnitude of the shear stresses within the carotid bifurcation geometry of a patient and calculated the increase in shear stress levels that would occur when the blood pressure and pulse pressures rise during exertion. We also determined in which layer of the artery wall the maximum shear stress is located, and computed the shear stress at different levels within the media. We used the theory of laminate analysis, (Classical Laminate Plate Theory), to analyse the stress distribution on the carotid artery wall. Computational Fluid Dynamics (CFD) analysis was used on anatomy based on a CT angiogram of the carotid bifurcation of a patient with a 90% stenosis on the right side and 10% on the left. The pulsatile non-Newtonian blood flow with a resting blood pressure of 120/80 mmHg and an exertion pressure of 200/100 mmHg was simulated and the resultant forces were transferred to an ANSYS Composite PrepPost (ACP) model for wall shear stress analysis. A multilayer elastic, anisotropic, and inhomogeneous arterial wall (intima, internal elastic lamina, media, external elastic lamina, and adventitial layers) was modelled and the shear stress magnitudes and change over time between the layers was calculated. RESULTS: Shear stress in the individual composite layers is far greater than that acting on the endothelium (less than 5 Pa). At rest, the maximum variation of shear stress in the arterial wall occurs in the intima (138 Pa) and adventitia (135 Pa). The medial layer has the lowest variation of shear stress. Under severe exertion, the maximum shear stress magnitude in the intimal layer and the adjacent medial layer is near the ultimate stress level. The maximum/minimum shear stress ratios during the cardiac cycle vary most widely in the innermost part of the media, adjacent to the intima, with a four-fold ratio increase. This compares with a less than two-fold increase in all the other layers including the intima and adventitia, making the inner media the most vulnerable layer to mechanical injury. CONCLUSIONS: This study showed that the magnitude of exertion-induced shear stress approaches the ultimate stress limit in the intima and the immediate adjacent medial layer. The variation in stress is maximal in the inner layer of the media. These findings correlate the site of atheroma development with the most vulnerable site for injury in the media and emphasise the impact of pulse pressure. Further biological studies are required to ascertain whether this leads to injury that initiates atheroma that then precipitates an injury/healing cycle. 2021 Quantitative Imaging in Medicine and Surgery. All rights reserved.
Authors: Umberto Morbiducci; Diego Gallo; Raffaele Ponzini; Diana Massai; Luca Antiga; Franco M Montevecchi; Alberto Redaelli Journal: Ann Biomed Eng Date: 2010-06-30 Impact factor: 3.934
Authors: Gerhard Sommer; Peter Regitnig; Lukas Költringer; Gerhard A Holzapfel Journal: Am J Physiol Heart Circ Physiol Date: 2009-12-24 Impact factor: 4.733