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Research Papers

Mass Transport of Low Density Lipoprotein in Reconstructed Hemodynamic Environments of Human Carotid Arteries: The Role of Volume and Solute Flux Through the Endothelium

[+] Author and Article Information
Sungho Kim

Wallace H. Coulter Department of
Biomedical Engineering,
Georgia Institute of Technology and Emory University,
Atlanta, GA 30332
e-mail: sunghokim@gatech.edu

Don P. Giddens

Dean Emeritus
Wallace H. Coulter Department of
Biomedical Engineering,
Georgia Institute of Technology and Emory University,
Atlanta, GA 30332
e-mail: don.giddens@bme.gatech.edu

Manuscript received July 11, 2014; final manuscript received October 27, 2014; published online February 11, 2015. Assoc. Editor: Tim David.

J Biomech Eng 137(4), 041007 (Apr 01, 2015) (11 pages) Paper No: BIO-14-1324; doi: 10.1115/1.4028969 History: Received July 11, 2014; Revised October 27, 2014; Online February 11, 2015

The accumulation of low density lipoprotein (LDL) in the arterial intima is a critical step in the initiation and progression of atheromatous lesions. In this study we examine subject-specific LDL transport into the intima of carotid bifurcations in three human subjects using a three-pore model for LDL mass transfer. Subject-specific carotid artery computational models were derived using magnetic resonance imaging (MRI) to obtain the geometry and phase-contract MRI (PC-MRI) to acquire pulsatile inflow and outflow boundary conditions for each subject. The subjects were selected to represent a wide range of anatomical configurations and different stages of atherosclerotic development from mild to moderate intimal thickening. A fluid–solid interaction (FSI) model was implemented in the computational fluid dynamics (CFD) approach in order to consider the effects of a compliant vessel on wall shear stress (WSS). The WSS-dependent response of the endothelium to LDL mass transfer was modeled by multiple pathways to include the contributions of leaky junctions, normal junctions, and transcytosis to LDL solute and plasma volume flux from the lumen into the intima. Time averaged WSS (TAWSS) over the cardiac cycle was computed to represent the spatial WSS distribution, and wall thickness (WTH) was determined from black blood MRI (BBMRI) so as to visualize intimal thickening patterns in the bifurcations. The regions which are exposed to low TAWSS correspond to elevated WTH and higher mass and volume flux via the leaky junctions. In all subjects, the maximum LDL solute flux was observed to be immediately downstream of the stenosis, supporting observations that existing atherosclerotic lesions tend to progress in the downstream direction of the stenosis.

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References

Figures

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Fig. 6

WTH in subjects. (a) Subject 1, (b) subject 2, and (c) subject 3 (units (m)).

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Fig. 5

(a) Streamlines and velocity distributions at four cross sections in subject 3 carotid artery at the middle of diastole. (b) TAWSS in anterior and posterior views (units (Pa)).

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Fig. 4

(a) Streamlines and velocity distributions at four cross sections in subject 2 carotid artery at the middle of diastole. (b) TAWSS in anterior and posterior views (units (Pa)).

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Fig. 3

(a) Streamlines and velocity distributions at four cross sections in subject 1 carotid artery at the middle of diastole (red dot in CCA flow rate profile). (b) TAWSS in anterior and posterior views (units (Pa)).

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Fig. 2

(a) Flow rate profiles of CCA, ICA/ECA for subject 2 in a cardiac period from PCMRI. (b) Generic pressure curve at CCA inlet for FSI simulation.

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Fig. 1

(a) Reconstructed carotid artery from BBMRI. (b) BBMRI of subject 2 at CCA. (c) PCMR image at cross section taken 10 mm inferior from bifurcation apex (units (m/s)) and velocity distribution from FSI with rescaled method at the same location (units (m/s)) at peak acceleration in diastole (red circle in middle CCA flow rate profile).

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Fig. 7

The volume and mass flux for subject 1. (a) The distribution of volume flux via leaky junctions (Jv,Lj) from anterior (left) and posterior view (right) and (b) the volume flux via normal junctions (Jv,Nj) (C) Total mass flux of LDL (Js).

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Fig. 8

The volume and mass flux of subject 2. (a) The distribution of volume flux via leaky junctions (Jv,Lj) from anterior (left) and posterior view (right) and (b) the volume flux via normal junctions (Jv,Nj) (C) Total mass flux of LDL (Js).

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Fig. 9

The volume and mass flux of subject 3. (a) The distribution of volume flux via leaky junctions (Jv,Lj) from anterior (left) and posterior view (right), (b) the volume flux via normal junctions (Jv,Nj), and (c) total mass flux of LDL (Js).

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