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A computational fluid-structure interaction model for plaque vulnerability assessment in atherosclerotic human coronary arteries
76
Citations
54
References
2014
Year
EngineeringFluid MechanicsMechanical EngineeringBiomedical EngineeringComputational MechanicsCoronary Artery DiseaseBlood FlowRheologyBiostatisticsBiofluid DynamicAtherosclerosisBiophysicsCardiovascular ImagingVascular AdaptationVascular BiologyBiomedical ModelingBiomedical FlowCardiovascular DiseaseFluid-structure InteractionPlaque Vulnerability AssessmentMedicineCoronary ArteryMultiscale Modeling
Coronary artery disease is responsible for a third of global deaths worldwide. Computational simulations of blood flow can be used to understand the interactions of artery/plaque and blood in coronary artery disease and to better predict the rupture of atherosclerotic plaques. So far, the mechanical properties of animals' coronary artery have been mostly used for hemodynamic simulation of atherosclerotic arteries. The mechanical properties of animals' coronary arteries are often not accurate enough and can be only used for an approximate estimation and comparative assessment of the cognate parameters in human. In this study, a three-dimensional (3D) computational fluid-structure interactions model with three different plaque types is presented to perform a more accurate plaque vulnerability assessment for human atherosclerotic plaques. The coronary arteries of twenty-two male individuals were removed during autopsy and subjected to uniaxial tensile loading. The hyperelastic material coefficients of coronary arteries were calculated and implemented to the computational model. The fully coupled fluid and structure models were solved using the explicit dynamics finite element code LS-DYNA. The normal and shear stresses induced within the plaques were significantly affected by different plaque types. The highest von Mises (153 KPa) and shear (57 KPa) stresses were observed for hypocellular plaques, while the lowest von Mises (70 KPa) and shear (39 KPa) stresses were observed on the stiffer calcified plaques. The results suggest that the risk of plaque rupture due to blood flow is lower for cellular and hypocellular plaques, while higher for calcified plaques with low fracture stresses.
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