TY - JOUR
T1 - The Story of Wall Shear Stress in Coronary Artery Atherosclerosis
T2 - Biochemical Transport and Mechanotransduction
AU - Mahmoudi, Mostafa
AU - Farghadan, Ali
AU - McConnell, Daniel R.
AU - Barker, Alex J.
AU - Wentzel, Jolanda J.
AU - Budoff, Matthew J.
AU - Arzani, Amirhossein
N1 - Publisher Copyright:
© 2020 Royal Society of Chemistry. All rights reserved.
PY - 2021/4/1
Y1 - 2021/4/1
N2 - Coronary artery atherosclerosis is a local, multifactorial, complex disease, and the leading cause of death in the US. Complex interactions between biochemical transport and biomechanical forces influence disease growth. Wall shear stress (WSS) affects coronary artery atherosclerosis by inducing endothelial cell mechanotransduction and by controlling the near-wall transport processes involved in atherosclerosis. Each of these processes is controlled by WSS differently and therefore has complicated the interpretation of WSS in atherosclerosis. In this paper, we present a comprehensive theory for WSS in atherosclerosis. First, a short review of shear stress-mediated mechanotransduction in atherosclerosis was presented. Next, subject-specific computational fluid dynamics (CFD) simulations were performed in ten coronary artery models of diseased and healthy subjects. Biochemical-specific mass transport models were developed to study low-density lipoprotein, nitric oxide, adenosine triphosphate, oxygen, monocyte chemoattractant protein-1, and monocyte transport. The transport results were compared with WSS vectors and WSS Lagrangian coherent structures (WSS LCS). High WSS magnitude protected against atherosclerosis by increasing the production or flux of atheroprotective biochemicals and decreasing the near-wall localization of atherogenic biochemicals. Low WSS magnitude promoted atherosclerosis by increasing atherogenic biochemical localization. Finally, the attracting WSS LCS's role was more complex where it promoted or prevented atherosclerosis based on different biochemicals. We present a summary of the different pathways by which WSS influences coronary artery atherosclerosis and compare different mechanotransduction and biotransport mechanisms.
AB - Coronary artery atherosclerosis is a local, multifactorial, complex disease, and the leading cause of death in the US. Complex interactions between biochemical transport and biomechanical forces influence disease growth. Wall shear stress (WSS) affects coronary artery atherosclerosis by inducing endothelial cell mechanotransduction and by controlling the near-wall transport processes involved in atherosclerosis. Each of these processes is controlled by WSS differently and therefore has complicated the interpretation of WSS in atherosclerosis. In this paper, we present a comprehensive theory for WSS in atherosclerosis. First, a short review of shear stress-mediated mechanotransduction in atherosclerosis was presented. Next, subject-specific computational fluid dynamics (CFD) simulations were performed in ten coronary artery models of diseased and healthy subjects. Biochemical-specific mass transport models were developed to study low-density lipoprotein, nitric oxide, adenosine triphosphate, oxygen, monocyte chemoattractant protein-1, and monocyte transport. The transport results were compared with WSS vectors and WSS Lagrangian coherent structures (WSS LCS). High WSS magnitude protected against atherosclerosis by increasing the production or flux of atheroprotective biochemicals and decreasing the near-wall localization of atherogenic biochemicals. Low WSS magnitude promoted atherosclerosis by increasing atherogenic biochemical localization. Finally, the attracting WSS LCS's role was more complex where it promoted or prevented atherosclerosis based on different biochemicals. We present a summary of the different pathways by which WSS influences coronary artery atherosclerosis and compare different mechanotransduction and biotransport mechanisms.
KW - Coronary artery disease
KW - Lagrangian coherent structures
KW - biochemical transport
KW - endothelial cells
KW - hemodynamics
KW - mechanotransduction
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U2 - 10.1115/1.4049026
DO - 10.1115/1.4049026
M3 - Article
C2 - 33156343
AN - SCOPUS:85098083021
SN - 0148-0731
VL - 143
JO - Journal of Biomechanical Engineering
JF - Journal of Biomechanical Engineering
IS - 4
M1 - 041002
ER -