Key result
Fluid-structure interaction simulations revealed that hypertension promoted LDL uptake in the coronary arterial wall, whereas a thickened arterial wall decreased this process.
Why the study?
To compare the effect of different physical factors on low-density lipoprotein accumulation from flowing blood into the arterial wall of the left coronary arteries.
Computational fluid-structure interaction modeling demonstrates that hypertension promotes LDL uptake in the coronary arterial wall, while high wall elasticity and thickened walls alter local flow dynamics and LDL accumulation.
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Patient-specific FSI models link low WSS regions to LDL uptake; leaves open whether hemodynamic targeting alters atherosclerosis risk.
The purpose of this study is to compare the effect of the different physical factors on low-density lipoproteins (LDL) accumulation from flowing blood to the arterial wall of the left coronary arteries. The three-dimensional (3D) computational model of the left coronary arterial tree is reconstructed from a patient-specific computed tomography angiography (CTA) image. The endothelium of the coronary artery is represented by a shear stress dependent three-pore model. Fluid-structure interaction ([Formula: see text]) based numerical method is used to study the LDL transport from vascular lumen into the arterial wall. The results show that the high elastic property of the arterial wall decreases the complexity of the local flow field in the coronary bifurcation system. The places of high levels of LDL uptake coincide with the regions of low wall shear stress. In addition, hypertension promotes LDL uptake from flowing blood in the arterial wall, while the thickened arterial wall decreases this process. The present computer strategy combining the methods of coronary CTA image 3D reconstruction, [Formula: see text] simulation, and three-pore modeling was illustrated to be effective on the simulation of the distribution and the uptake of LDL. This may have great potential for the early prediction of the local atherosclerosis lesion in the human left coronary artery.
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Chen et al. (2021) studied Coronary atherosclerosis (n=1). Physical factors (hypertension, wall thickness, elasticity, viscosity) vs. Normal physiological conditions was evaluated on LDL mass flux and fluid volume flux through the endothelium. Fluid-structure interaction simulations revealed that hypertension promoted LDL uptake in the coronary arterial wall, whereas a thickened arterial wall decreased this process.
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