Numerical Study of Fully Coupled Fluid-Structure Interaction of Stented Ureter by Varying the Stent Side-Holes

Ureteral stents are a measure used for many medical issues involving urology, such as kidney stones or kidney transplants. The purpose of applying stents is to help relieve the urine flow while the ureter is either blocked or trying to close itself, which creates blockages. These ureteral stents, while necessary, cause pain and discomfort to patients due to them being a solid that moves around inside the patients’ body. The ureter normally moves urine to the bladder through peristaltic forces. Due to the ureter being a hyperelastic material, these peristaltic forces cause the ureter to deform easily, making it necessary for the stent to properly move the urine that flows through it for the patient not to face further medical complications. In this study, we seek to find a relation between the amount of stent side holes and the overall flow rate inside the stent with the ureter contracting due to peristalsis. A fully coupled fluid-structure interaction (FSI) model is developed to visualize how the ureter deforms due to peristalsis and the subsequent effect on the urine flow due to the ureter’s deformation. Numerical simulations using COMSOL Multiphysics, a commercial finite-element based solver, were used to study the fluid-structure interaction, and determine whether the stent performs more properly as the amount of stent side holes increases. The results showed that the stent model with a 10 mm distance between side hole pairs provided the highest outlet flow rate, which indicates a proper stent design that allows for maximized urine discharge. We hope this study can help improve the stent design in kidney transplant procedures to further ease the inconvenience on the patients

Coronary plaque composition influences biomechanical stress and predicts plaque rupture in a morpho-mechanic OCT analysis

Plaque rupture occurs if stress within coronary lesions exceeds the protection exerted by the fibrous cap overlying the necrotic lipid core. However, very little is known about the biomechanical stress exerting this disrupting force. Employing optical coherence tomography (OCT), we generated plaque models and performed finite-element analysis to simulate stress distributions within the vessel wall in 10 ruptured and 10 non-ruptured lesions. In ruptured lesions, maximal stress within fibrous cap (peak cap stress [PCS]: 174 ± 67 vs. 52 ± 42 kPa, p<0.001) and vessel wall (maximal plaque stress [MPS]: 399 ± 233 vs. 90 ± 95 kPa, p=0.001) were significantly higher compared to non-ruptured plaques. Ruptures arose in the immediate proximity of maximal stress concentrations (angular distances: 21.8 ± 30.3° for PCS vs. 20.7 ± 23.7° for MPS); stress concentrations excellently predicted plaque rupture (area under the curve: 0.940 for PCS, 0.950 for MPS). This prediction of plaque rupture was superior to established vulnerability features such as fibrous cap thickness or macrophage infiltration. In conclusion, OCT-based finite-element analysis effectively assesses plaque biomechanics, which in turn predicts plaque rupture in patients. This highlights the importance of morpho-mechanic analysis assessing the disrupting effects of plaque stress

Considering the influence of coronary motion on artery-specific biomechanics using fluid-structure interaction simulation

The endothelium in the coronary arteries is subject to wall shear stress and vessel wall strain, which influences the biology of the arterial wall. This study presents vessel-specific fluid-structure interaction (FSI) models of three coronary arteries, using directly measured experimental geometries and boundary conditions. FSI models are used to provide a more physiologically complete representation of vessel biomechanics, and have been extended to include coronary bending to investigate its effect on shear and strain. FSI both without- and with-bending resulted in significant changes in all computed shear stress metrics compared to CFD (p = 0.0001). Inclusion of bending within the FSI model produced highly significant changes in Time Averaged Wall Shear Stress (TAWSS) + 9.8% LAD, + 8.8% LCx, - 2.0% RCA; Oscillatory Shear Index (OSI) + 208% LAD, 0% LCx, + 2600% RCA; and transverse wall Shear Stress (tSS) + 180% LAD, + 150% LCx and + 200% RCA (all p < 0.0001). Vessel wall strain was homogenous in all directions without-bending but became highly anisotropic under bending. Changes in median cyclic strain magnitude were seen for all three vessels in every direction. Changes shown in the magnitude and distribution of shear stress and wall strain suggest that bending should be considered on a vessel-specific basis in analyses of coronary artery biomechanics

Considering the Influence of Coronary Motion on Artery‑Specific Biomechanics Using Fluid–Structure Interaction Simulation

The endothelium in the coronary arteries is subject to wall shear stress and vessel wall strain, which influences the biology of the arterial wall. This study presents vessel-specific fluid–structure interaction (FSI) models of three coronary arteries, using directly measured experimental geometries and boundary conditions. FSI models are used to provide a more physiologically complete representation of vessel biomechanics, and have been extended to include coronary bending to investigate its effect on shear and strain. FSI both without- and with-bending resulted in significant changes in all computed shear stress metrics compared to CFD (p = 0.0001). Inclusion of bending within the FSI model produced highly significant changes in Time Averaged Wall Shear Stress (TAWSS) + 9.8% LAD, + 8.8% LCx, − 2.0% RCA; Oscillatory Shear Index (OSI) + 208% LAD, 0% LCx, + 2600% RCA; and transverse wall Shear Stress (tSS) + 180% LAD, + 150% LCx and + 200% RCA (all p \u3c 0.0001). Vessel wall strain was homogenous in all directions without-bending but became highly anisotropic under bending. Changes in median cyclic strain magnitude were seen for all three vessels in every direction. Changes shown in the magnitude and distribution of shear stress and wall strain suggest that bending should be considered on a vessel-specific basis in analyses of coronary artery biomechanics

Role of biomechanical forces in the natural history of coronary atherosclerosis.

Atherosclerosis remains a major cause of morbidity and mortality worldwide, and a thorough understanding of the underlying pathophysiological mechanisms is crucial for the development of new therapeutic strategies. Although atherosclerosis is a systemic inflammatory disease, coronary atherosclerotic plaques are not uniformly distributed in the vascular tree. Experimental and clinical data highlight that biomechanical forces, including wall shear stress (WSS) and plaque structural stress (PSS), have an important role in the natural history of coronary atherosclerosis. Endothelial cell function is heavily influenced by changes in WSS, and longitudinal animal and human studies have shown that coronary regions with low WSS undergo increased plaque growth compared with high WSS regions. Local alterations in WSS might also promote transformation of stable to unstable plaque subtypes. Plaque rupture is determined by the balance between PSS and material strength, with plaque composition having a profound effect on PSS. Prospective clinical studies are required to ascertain whether integrating mechanical parameters with medical imaging can improve our ability to identify patients at highest risk of rapid disease progression or sudden cardiac events.This work was supported by the British Heart Foundation (FS/13/33/30168), Heart Research UK (RG2638/14/16), the Cambridge NIHR Biomedical Research Centre, and the BHF Cambridge Centre for Research Excellence.This is the author accepted manuscript. The final version is available from Nature Publishing Group at http://dx.doi.org/10.1038/nrcardio.2015.203

Evolution and rupture of vulnerable plaques: a review of mechanical effects

Atherosclerosis occurs as a result of the buildup and infiltration of lipid streaks in artery walls, leading to plaques. Understanding the development of atherosclerosis and plaque vulnerability is of critical importance, since plaque rupture can result in heart attack or stroke. Plaques can be divided into two distinct types: those that rupture (vulnerable) and those that are less likely to rupture (stable). In the last few decades, researchers have been interested in studying the influence of the mechanical effects (blood shear stress, pressure forces, and structural stress) on the plaque formation and rupture processes. In the literature, physiological experimental studies are limited by the complexity of in vivo experiments to study such effects, whereas the numerical approach often uses simplified models compared with realistic conditions, so that no general agreement of the mechanisms responsible for plaque formation has yet been reached. In addition, in a large number of cases, the presence of plaques in arteries is asymptomatic. The prediction of plaque rupture remains a complex question to elucidate, not only because of the interaction of numerous phenomena involved in this process (biological, chemical, and mechanical) but also because of the large time scale on which plaques develop. The purpose of the present article is to review the current mechanical models used to describe the blood flow in arteries in the presence of plaques, as well as reviewing the literature treating the influence of mechanical effects on plaque formation, development, and rupture. Finally, some directions of research, including those being undertaken by the authors, are described

Finite Element Methods to Analyze Helical Stent Expansion

Stent angioplasty or stenting is the standard noninvasive therapy method to address narrowing of the arteries and restore blood flow. Although drug-eluting stents have resolved immediate restenosis (i.e., re-narrowing of the stented arteries), late in-stent restenosis continues to provide challenges for this treatment. One way to address this is through the use of biodegradable stents, such as the helical stent configuration investigated in this work, which may reduce the risk of late in-stent restenosis. The focus of this study was to analyze the mechanical performance and expansion of a polymeric helical stent, applied to a coronary artery. Experimental testing of such a device presents many challenges and is costly. Hence, initial evaluation using numerical methods provides an opportunity to investigate some aspects of the mechanical performance in detail. Existing stent expansion modeling methods originally developed for metallic wire mesh stent simulations were used to investigate the response of a 5 coil polymeric helical stent. The methods include: prescribed displacement, uniform expansion and balloon expansion. It was determined that only the balloon expansion could capture the important aspects of the helical stent expansion such as non-uniform expansion, foreshortening and change in pitch observed in experimental tests, since the expansion mechanism of this stent is different compared to traditional stents. More important, it was found that the helical stent expansion was limited by non-uniform expansion (dog boning) and a unique progressive expansion method was proposed to mitigate this issue. Finally, the stent and progressive balloon expansion models were used to investigate helical stent expansion within an artery containing plaque. The models predicted that interaction with the artery decreased foreshortening compared to free expansion of the stent. An artery with plaque demonstrated higher stresses in the vicinity of the plaque and modest stresses outside of this region, which are desirable in terms of reducing the occurrence of restenosis. The modeling techniques developed in this work have allowed for the evaluation of a novel polymeric biodegradable helical stent and progressive expansion method. The balloon expansion model was found to most accurately predict the geometric effects of expansion and, although this particular stent geometry demonstrated some challenges in terms of non-uniform expansion, the stresses in an artery with plaque were relatively low outside the plaque zone making this a promising approach to address restenosis

Role of Local Renin-Angiotensin System in Potentiating Early Calcific Aortic Valve Disease

Angiotensin-II (Ang-II), a peptide hormone, is a potent vasoconstrictor and cell mitogen. It has been implicated in the development of hypertension as well as atherosclerosis. Recent work has shown that sclerotic aortic valves possess expression of angiotensin type I receptor (AT-1R) and angiotensin converting enzyme (ACE), suggesting altered angiotensin signaling during disease. The role of altered angiotensin signaling on aortic valve mechanics, however, is not clearly understood. We seek to understand the direct effects of the renin angiotensin signaling (RAS) system on the biological and biomechanical properties of aortic valve tissue and develop a finite constitutive model that mimics the effects of RAS on aortic valves. Our results showed that the mechanical properties such as stiffness were altered by RAS mediators. Three phenomenological constitutive models were utilize to characterize the biomechanical changes that occur due to RAS mediators on aortic valves, and the Fung-type model was shown to be the best fit model for the experimental data. Tissue maintained in anisotropy behavior, but the cross-coupling of the fibers was affected. Immunohistochemistry (IHC) showed that RAS affects the phenotypic properties of the cells in the aortic valve tissues. Picrosirius red (PSR) staining suggests that RAS mediators affect the production of collagen fibers, and quantitative polarized light imaging (QPLI) demonstrated that RAS mediators affect the orientation of collagen fibers. We concluded that RAS mediators affected the biological and mechanical functions of the aortic valve leaflet. The activation of VICS and increased production and disorganization of collagen fibers correlated to the stiffness of the tissue. These are all hallmarks of early disease progression, and in the future, we will further investigate the effects of RAS mediators in mechanics of the valve leaflet at the cellular level