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Research Papers

A Fluid–Structure Interaction Model of the Left Coronary Artery

[+] Author and Article Information
Daphne Meza, David A. Rubenstein

Biomedical Engineering Department,
Stony Brook University,
Stony Brook, NY 11794

Wei Yin

Biomedical Engineering Department,
Stony Brook University,
Room 109,
Stony Brook, NY 11794
e-mail: wei.yin@stonybrook.edu

1Corresponding author.

Manuscript received January 19, 2018; final manuscript received June 12, 2018; published online September 25, 2018. Assoc. Editor: C. Alberto Figueroa.

J Biomech Eng 140(12), 121006 (Sep 25, 2018) (8 pages) Paper No: BIO-18-1037; doi: 10.1115/1.4040776 History: Received January 19, 2018; Revised June 12, 2018

A fluid–structure interaction (FSI) model of a left anterior descending (LAD) coronary artery was developed, incorporating transient blood flow, cyclic bending motion of the artery, and myocardial contraction. The three-dimensional (3D) geometry was constructed based on a patient's computed tomography angiography (CTA) data. To simulate disease conditions, a plaque was placed within the LAD to create a 70% stenosis. The bending motion of the blood vessel was prescribed based on the LAD spatial information. The pressure induced by myocardial contraction was applied to the outside of the blood vessel wall. The fluid domain was solved using the Navier–Stokes equations. The arterial wall was defined as a nonlinear elastic, anisotropic, and incompressible material, and the mechanical behavior was described using the modified hyper-elastic Mooney–Rivlin model. The fluid (blood) and solid (vascular wall) domains were fully coupled. The simulation results demonstrated that besides vessel bending/stretching motion, myocardial contraction had a significant effect on local hemodynamics and vascular wall stress/strain distribution. It not only transiently increased blood flow velocity and fluid wall shear stress, but also changed shear stress patterns. The presence of the plaque significantly reduced vascular wall tensile strain. Compared to the coronary artery models developed previously, the current model had improved physiological relevance.

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Figures

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Fig. 1

Patient-specific LAD segmentation workflow. Myocardium region was isolated from CTA data at diastole and at systole: (a) the LAD was segmented and prepared for mesh generation; (b) diseased condition was simulated by adding a 70% stenosis, 8 mm downstream from the LAD inlet.

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Fig. 2

Input waveforms for the FSI model: (a) cyclic displacement of LAD was computed by tracking centerline locations of the LAD at the end of systole and diastole; (b) LAD wall displacement waveform (of the element with the largest displacement), pressure waveform induced by myocardial contraction, and inlet blood velocity waveform during one cardiac cycle (0.9 s). Displacement of the blood vessel varied between 0.3 mm and 7.5 mm, the maximum pressure induced by myocardial contraction was 25 kPa; inlet blood velocity varied between 0 and 15 cm/s. Values are presented as the ratio to the maximum magnitude.

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Fig. 3

Blood flow velocity within (a) the normal LAD and (b) the stenosed LAD

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Fig. 4

The maximum shear stress along the vascular wall under (a) normal and (b) stenosis conditions within the LAD

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Fig. 5

Vascular wall (a) circumferential and (b) axial strain distribution within the normal and stenosed LAD

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Fig. 6

Wall fluid shear stress and tensile strain as a function of time in normal and stenosed LAD, when myocardial compression was included in the model

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Fig. 7

Wall fluid shear stress and tensile strain as a function of time in normal and stenosed LAD, when myocardial compression was not included in the model

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