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The wall motion of atherosclerotic plaque was analyzed using a computational method, and the effects of tissue viscoelasticity, fibrosis thickness, and lipid-core stiffness on wall displacement waveforms were examined. The viscoelasticity of plaque tissues was modeled using a time Prony series with four Maxwell elements. Computational simulation of tissue indentation tests showed the validity of the proposed viscoelastic constitutive models. Decreasing the relative moduli of the viscoelastic model reduced their viscous characteristics while enhancing the stiffness of the wall, which corresponded with the effects of decreased smooth muscle cells content. A finite-element analysis was conducted for atherosclerotic wall models and wall displacement waveforms were computed. The phase difference between the first harmonics of pressure and displacement waves was selected to represent the time delay of the wall motion. As the relative modulus decreased, the wall displacement and phase lag decreased. A thinner wall and softer lipid core corresponded to a greater wall displacement and smaller phase lag. Because the phase lag of the arterial-wall motion was smaller for the plaque with a thinner cap, lower smooth muscle cells content, and softer lipid core (all features of plaques with high rupture risk), first harmonics of pressure and displacement waves can be used as an index to assess plaque vulnerability.

To investigate the effect of longitudinal variations of cap thickness and tissue properties on wall stresses and strains along the atherosclerotic stenosis, stenotic plaque models (uniformly thick, distally thickened, homogenous, and distally stiffened) were constructed and subjected to computational stress analyses with due consideration of fluid-structure interactions (FSI). The analysis considered three different cap thicknesses-45, 65, and 200 μm-and tissue properties-soft, fibrous, and hard. The maximum peak cap stress (PCS) and strain were observed in the upstream throat section and demonstrated increases of the order of 345 and 190%, respectively, as the cap thickness was reduced from 200 to 45 μm in uniformly thick models. Distal stiffening increased PCS in the downstream region; however, the overall effect of this increase was rather small. Distal thickening did not affect maximum PCS and strain values for cap thicknesses exceeding 65 μm; however, a noticeable increase in maximum PCS and corresponding longitudinal variation (or spatial gradient) in stress was observed in the very thin (45-μm-thick) cap. It was, therefore, inferred that existence of a rather thin upstream cap demonstrating distal cap thickening indicates an increased risk of plaque progression and rupture. Graphical Abstract ᅟ.

Effects of longitudinal asymmetric distribution of a lipid core on plaque wall stress IntroductionAtherosclerotic plaque rupture contributes to acute coronary syndrome, one of the leading causes of death in the world. It is composed of lipid rich necrotic cores and calcium deposits enclosed by a protective fibrous cap, which is a thin fibrous tissue between the lumen of the blood vessel and the lipid core. If the fibrous cap is disrupted, a cascade of events that include thrombosis, coronary occlusion, and subsequent myocardial infarction could occur (Libby, 2013). Studies have shown that the mechanical stress and structural integrity of the wall tissues of the plaque determine its susceptibility to disruption.Two different types of stresses act on the plaque tissues: circumferential tensile wall stress, which is caused by pulsating blood pressure, and luminal wall shear stress, which is caused by blood flow. Because tensional wall stress is several orders of magnitude higher than wall shear stress exerted by blood flow (Salger et al., 2005), plaque rupture has been attributed to circumferential wall stress (Ohayon et al., 2005), which is influenced by the morphology and mechanical properties of the plaque. It has been shown that atherosclerotic plaques with large plaque burdens (defined as the plaque area over the vessel area at the cross section) and thin cap thicknesses (less than 65 μm) are more vulnerable (Burke et al. 1997). Computational stress analysis has been performed in order to estimate the plaque wall stress using the idealized plaque models (Ohayon et al. 2008, Akyildiz et al., 2011, Zareh et al., 2015. Recently, three dimensional patient specific plaque models have been reconstructed from diagnostic medical images such as ultrasound, OCT, and MRI images for stress analysis (Nieuwstadt et al., 2013, Kelly-Arnold et al., 2013, Wang et al., 2015 and computational analysis has been performed. They provide a more realistic geometry for wall stress and flow analyses, but they are not ideally suited for obtaining accurate plaque wall morphology due to limitations that include Pengsrorn CHHAI*, Jin Hyun LEE* and Kyehan RHEE* *Department of Mechanical Engineering, Myongji University 38-2 Namdong, Cheoin-gu, Yongin, Gyeonggi-do 449-728, Republic of Korea E-mail: khanrhee@mju.ac.kr AbstractThe rupture of the atherosclerotic plaque is related to the mechanical stress and structural integrity of plaque wall tissues. In order to investigate the longitudinal asymmetry across the stenosis of the arterial plaque wall, asymmetric plaque wall models were constructed by skewing the lipid core distribution in the upstream direction. Wall stress and blood flow in the coronary artery models were computationally analyzed considering fluid and structure interaction. The values of maximum cap stress increased, and its location moved toward the proximal cap as asymmetry increased. Hemodynamic wall shear stress (WSS) did not change much owing to negligible changes in luminal geometry, but the maximum WSS and the spatial gra...

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