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This Article Full Text Full Text (PDF) All Versions of this Article: 296/6/H1969    most recent 01182.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Olgac, U. Articles by Kurtcuoglu, V. PubMed PubMed Citation Articles by Olgac, U. Articles by Kurtcuoglu, V.

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

¹Laboratory of Thermodynamics in Emerging Technologies, Department of Mechanical and Process Engineering, and ²Computer Vision Laboratory, Department of Information Technology and Electrical Engineering, ETH Zurich, and ³Institute of Diagnostic Radiology, University Hospital Zurich, Zurich, Switzerland

Submitted 12 November 2008 ; accepted in final form 24 March 2009

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 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. 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. Intraluminal pressures of 70 and 120 mmHg are employed as the normal and hypertensive operating pressures, respectively. 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.

low-density lipoprotein transport; lipid accumulation; patient-specific simulations; atherosclerosis; leaky junction