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Journal o f Biomechanics 2006, Vol. 39 (Suppl 1)
Methods: A finite element modeling software developed at IMI for the analysis of large deformations of soft materials was used to solve angioplasty mechanics (Laroche 2003, Delorme 2004). The model computes the device/artery interaction and large deformations that occur during device insertion and deployment into the diseased artery. It predicts the resulting artery lumen patency, the stress distribution and the friction work distribution in the arterial wall. The angioplasty balloon is modeled with membrane elements and the artery with incompressible solid elements, both with a hyperelastic constitutive model. An important contribution of this work is the development of a multi-body contact algorithm that is rapid and robust enough for handling complex contact and friction behavior between the balloon and the artery. The proposed algorithm performs implicit contact detection between virtual surfaces. Results and Conclusion: A proof-of-concept test was performed using IVUS images of one patient who underwent balloon angioplasty. A 3-D model of a 68 mm LAD artery segment was produced from IVUS images. The deployment of a 3.5 by 28 mm balloon was simulated by applying a 12 atm pressure. The proposed model is capable of predicting the effect of intervention strategy on the artery deformation. References Delorme, S. et al. (2004). Annual Technical Conference (ANTEC) of the Society of Plastic Engineers, Chicago, IL. Laroche, D. et al. (2003). ASM Materials & Processes for Medical Devices Conference, Anaheim, CA. 5899 Tu, 16:15-16:30 (P25) An analysis o f stresses in peripheral arteries following stenting using the finite element method M. Early, D.J. Kelly. Trinity Centre for Bioengineering, Department of Mechanical Engineering, Trinity College, Dublin, Ireland Atherosclerosis is a form of cardiovascular disease (CVD) that is characterised by a hardening and thickening of the arteries that results in a reduction in the lumen area. This can lead to heart attacks or strokes, and accounts for up to three quarters of CVD related deaths [1]. Peripheral arterial disease is similar to CVD, but occurs in peripheral arteries, usually the popliteal, femoral and iliac arteries. Rates of restenosis in peripheral arteries following stenting are high, typically up to 30% after 1 year. This compares unfavourably with coronary stents, which have restenosis rates of about 15% or lower after the same period. The main difference between coronary and peripheral stents is size. Coronary stents are between 1.5 and 4 mm in diameter, while peripheral stents range between 4 and 10mm. In addition, Kr6ger et al. [2] have hypothesised that muscle forces create an extreme mechanical stress state in peripheral arteries. For example, knee joint flexion can cause bending of stents in the popliteal and femoropopliteal arteries, reducing patency rates. This study uses a three dimensional finite element model to simulate the expansion of a peripheral stent within an artery. The plasticity model for the stent material is obtained from stress-strain curves for 316L stainless steel. A second order Mooney-Rivlin constitutive equation is used to model the arterial wall. The application of muscle forces is predicted to influence the stresses in the vessel wall. As damage to the arterial wall following stent expansion has been shown to influence restensosis [3], this may provide an explanation for the high rates of restenosis observed after deployment of peripheral stents. References [1] American Heart Association. Heart Disease and Stroke Statistics- 2005 update. [2] Kr6ger K, Santosa F., Goyen M. Biomechanical incompatibility of popliteal stent placement. Journal of Endovascular Therapy 2004; 11 : 686~94. [3] Schwartz R., Holmes D.R. Pigs, dogs, baboons and man; lessons in stenting from animal studies. Journal of Interventional Cardiology 1994; 7: 355-68. 5706 Tu, 16:30-16:45 (P25) Pressure induced restenosis of femoral artery bypass grafts T. Campbell, R. Cole, M. Davies. Stokes Research Institute, University of Limerick, Ireland Arteriosclerosis is a prevalent killer in the western world. It is both an acute and chronic inflammatory disease, resulting from hyperlipidemia and a complex interplay of many environmental, metabolic and genetic risk factors. The principal explanation for the pathogenesis of atherosclerosis is the 'response to injury' hypothesis in which repeated mechanical, haemodynamic, and/or immunological injury to mural and focal regions of the endothelium is the initiating event to vascular dysfunction. The response is characterised by the adhesion of platelets and macrophages at the site of injury, the development of lipid and cell-rich lesions or plaques on the intimal surfaces of the arterial wall and the migration of smooth muscle cells into the intima. The primary cause of plaque proliferation is as of yet unidentified, although much research has been based on wall shear stresses being a contributing factor. However the hypothesis of this work is that an increase in vessel mechanical stress due to increased blood pressure can cause changes in
Oral Presentations tissue structure and mechanical properties. The distal junction of a femoral artery bypass graft has a predilection for failure due to restenosis. Thus the principal objectives in this study are to examine both the stress and strain caused by the intramural pressure in a bypass region and compare it with the strain that exists in a physiological geometry. In addition, it will be determined if the stresses and strains, found in the distal junction region, instigate changes in the protective functionality of endothelial cell layer by completing a number of cell culture studies. 7418 Tu, 16:45-17:00 (P25) Rapid formation model of tissue engineered aritificial vascular graft K. Furukawa 1, N. Matsuura 1, R. Noaki 1, T. Tateishi 1, T. Ushida 1,2. 1Biomedical Engineering Laboratory, Graduate School of Engineering, 2 Center for Disease Biology and Integrative Medicine, School of Medicine, University of Tokyo, Tokyo, Japan Although rapid formation of a smooth inner surface is important in constructing an artificial vascular graft, a conventional model which uses a biodegradable polymer such as poly-glycolic acid, needs long-term culture to form it. In another model which uses collagen gel, it is reported that prompt formation of the smooth inner surface was achieved. But, the mechanical properties were not suitable, resulting in rupture under high pressure at the arterial level. Therefore, we propose a new artificial vascular graft model made of biodegradable polymer, gel and cells. At first we manufactured an artificial vascular graft (i.d.5 mm, o.d.7 mm) constituting of poly L-lactic acid (PLLA) with open pore structures by using gas-forming methods. After mixing human normal aortic smooth muscle cells (SMCs) with type I collagen solution, pores of the PLLA scaffold were filled with the mixture. The collagen mixture was made into gel in the pores of the PLLA scaffold, incubating at 37°C. WET-SEM analysis showed that the prompt formation of a smooth inner surface was achieved in the new model. The ratio of incorporation of SMCs into the artificial vascular graft became approximately 100% by using the cell-collagen mixture, whereas only 40% of SMCs were trapped in the conventional model where SMCs were inoculated as a cell-medium suspension. Therefore, it was suggested that the new artificial vascular graft model was superior in smooth inner surface formation and cell inoculation, compared with conventional models using either biodegradable polymer or gel. Furthermore, we cultured the artificial vascular graft under pulsatile flow conditions, 0.2 Pa, 0.2 Hz, for 1 week. The pulsatile flow loading with culture medium on the vascular graft improved the rupture strength. Quantitative analysis showed enhanced cell proliferation and matrix production by pulsatile flow. Therefore, our rapid formation model of tissue engineered vascular graft may be useful for clinical applications. 6303 Tu, 17:00-17:15 (P25) Mechanical analysis of human common carotid arteries affected by PseudoXanthoma Elasticum E. Diouf 1, I. Masson 1, P. Boutouyrie 2, B. Labat 1, M. Zidi 1. 1Universit6 Paris 12 Val de Marne, Facult~ de M6decine, UMR INSERM 651, Cr6teil, France, 2H6pital Europ#en Georges Pompidou, Service de Pharmacologie, Paris, Fran ce Diseases such as hypertension or arteriosclerosis have been extensively studied by various scientists while genetic diseases have not been the subject of considerable attention. It is the case of the PseudoXanthoma Elasticum (PXE), a rare hereditary disease that leads serious cardiovascular complications and actually therapeutic treatments are non-existent. Note that this disease affects elastin and proteoglycans, and consequently the mechanical properties of the arterial wall. In this study, control human common carotid arteries (CCA) and others affected by the PXE disease were studied. For that, non-invasive measurements of 31 patients were performed by echotracking and tonometry systems to obtain internal diameter, wall thickness and internal pressure of arteries during a cardiac cycle. Furthermore, based on finite elasticity theory, the artery was modeled as a thick-walled cylindrical shell taking into account the non homogeneity and the compressibility of the arterial wall which was often observed in the PXE disease. The proposed strain energy function was expressed by two terms representing respectively the mechanical contribution of the tissue matrix and fibers reinforcement. The non linear equations governing the boundary value problem were solved numerically using Runge-Kutta method for order 4 to obtain pressure and stress distributions during a cardiac cycle. The numerical results show a good agreement in comparison to the experimental data although there is a difficulty to identify all parameters of the kind of model obtained by non invasive measurements. Nevertheless, the proposed approach appears to be a "good candidate" for the investigation of the mechanics of CCA, healthy or affected by PXE.