4.2 Article

The Story of Wall Shear Stress in Coronary Artery Atherosclerosis: Biochemical Transport and Mechanotransduction

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ASME
DOI: 10.1115/1.4049026

关键词

Coronary artery disease; biochemical transport; Lagrangian coherent structures; mechanotransduction; endothelial cells; hemodynamics

资金

  1. American Heart Association [19AIREA34430058]
  2. Northern Arizona University Presidential Fellowship

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This study explores the impact of wall shear stress on coronary artery atherosclerosis, highlighting how high shear stress can inhibit the development of atherosclerosis while low shear stress can contribute to its formation. Additionally, the role of wall shear stress on different biochemicals is complex, potentially promoting or preventing atherosclerosis.
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.

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