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Patient-specific three-dimensional simulation of LDL accumulation in a human left coronary artery in its healthy and atherosclerotic states


Olgac, U; Poulikakos, D; Saur, S C; Alkadhi, H; Kurtcuoglu, V (2009). Patient-specific three-dimensional simulation of LDL accumulation in a human left coronary artery in its healthy and atherosclerotic states. American Journal of Physiology. Heart and Circulatory Physiology, 296(6):H1969-H1982.

Abstract

We calculate low-density lipoprotein (LDL) transport from blood into arterial walls in a three-dimensional patient-specific model of a human left coronary artery. The in-vivo anatomy data are obtained from computed tomography (CT) images of a patient with coronary artery disease. Models of the artery anatomy in its healthy and diseased states are derived after segmentation of the vessel lumen with and without the detected plaque, respectively. Spatial shear stress distribution at the endothelium is determined through the reconstruction of the arterial blood flow field using computational fluid dynamics (CFD). The arterial endothelium is represented by a shear-stress dependent three-pore model taking into account blood plasma and LDL passage through normal junctions, leaky junctions and the vesicular pathway. 70 mmHg and 120 mmHg of intraluminal pressures are employed as the normal and hypertensive operating pressures. By applying our model to both the healthy and diseased states, we show that the location of the plaque in the diseased state corresponds to one of the two sites with predicted high LDL concentration in the healthy state. We further show that in the diseased state, the site with high LDL concentration has shifted distal to the plaque, which is in agreement with the clinical observation that plaques generally grow in the downstream direction. We also demonstrate that hypertension leads to increased number of regions with high LDL concentration, elucidating one of the ways in which hypertension may promote atherosclerosis. Key words: LDL transport, Lipid Accumulation, Patient-Specific Simulations, Atherosclerosis.

Abstract

We calculate low-density lipoprotein (LDL) transport from blood into arterial walls in a three-dimensional patient-specific model of a human left coronary artery. The in-vivo anatomy data are obtained from computed tomography (CT) images of a patient with coronary artery disease. Models of the artery anatomy in its healthy and diseased states are derived after segmentation of the vessel lumen with and without the detected plaque, respectively. Spatial shear stress distribution at the endothelium is determined through the reconstruction of the arterial blood flow field using computational fluid dynamics (CFD). The arterial endothelium is represented by a shear-stress dependent three-pore model taking into account blood plasma and LDL passage through normal junctions, leaky junctions and the vesicular pathway. 70 mmHg and 120 mmHg of intraluminal pressures are employed as the normal and hypertensive operating pressures. By applying our model to both the healthy and diseased states, we show that the location of the plaque in the diseased state corresponds to one of the two sites with predicted high LDL concentration in the healthy state. We further show that in the diseased state, the site with high LDL concentration has shifted distal to the plaque, which is in agreement with the clinical observation that plaques generally grow in the downstream direction. We also demonstrate that hypertension leads to increased number of regions with high LDL concentration, elucidating one of the ways in which hypertension may promote atherosclerosis. Key words: LDL transport, Lipid Accumulation, Patient-Specific Simulations, Atherosclerosis.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Diagnostic and Interventional Radiology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:June 2009
Deposited On:09 Apr 2009 11:48
Last Modified:05 Oct 2016 07:01
Publisher:American Physiological Society
ISSN:0363-6135
Publisher DOI:https://doi.org/10.1152/ajpheart.01182.2008
PubMed ID:19329764

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