Global and regional mechanics of the cardiac ventricles were investigated using an anatomicallyaccurate computational model formulated from concise mathematical descriptions ofthe left and right ventricular wall geometries and the non-homogeneous laminar microstructureof cardiac muscle. The finite element method for finite deformation elasticity was developedfor the analysis and included specialised coordinate systems, interpolation schemesand parallel processing techniques for greater computational efficiency.The ventricular mechanics model incorporated the fully orthotropic pole-zero constitutivelaw, based on the three-dimensional architecture of myocardium, to account for the nonlinearmaterial response of resting cardiac muscle, relative to the three anatomically relevant axes.A fibre distribution model was introduced to reconcile some of the pole-zero constitutiveparameters with direct mechanical properties of the tissue (such as the limiting strainsestimated from detailed physiological observations of the collagen helices that surroundmyofibres), whilst other parameters were estimated from in-vitro biaxial tension tests onthin sections of myocardium. A non-invasive approach to in-vivo myocardial materialparameter estimation was also developed, based on a magnetic resonance imaging techniqueto effectively tag ventricular wall tissue.The spatially non-homogeneous distribution of myocardial residual strain was accounted forin the ventricular mechanics model using a specialised growth tensor. A simple model of fluidshift was formulated to account for the changes in local tissue volume due to movement ofintramyocardial blood. Contractile properties of ventricular myofibres were approximatedusing a quasi-static relationship between the fibre extension ratio, intracellular calciumconcentration and active fibre stress, and the framework has been developed to include amore realistic model of active myocardial mechanics, which could be coupled to a realisticdescription of the time-varying spread of electrical excitation throughout the ventricularwalls. Simple volumetric cavity models were incorporated to investigate the effects of arterialimpedance on systolic wall mechanics.Ventricular mechanics model predictions of the cavity pressure versus volume relationships,longitudinal dimension changes, torsional wall deformations and regional distributions ofmyocardial strain during the diastolic filling, isovolumic contraction and ejection phasesof the cardiac cycle showed good overall agreement with reported observations derivedfrom experimental studies of isolated and in-vivo canine hearts. Predictions of the spatialdistributions of mechanical stress at end-diastole and end-systole are illustrated.

Global and regional mechanics of the cardiac ventricles were investigated using an anatomicallyaccurate computational model formulated from concise mathematical descriptions ofthe left and right ventricular wall geometries and the non-homogeneous laminar microstructureof cardiac muscle. The finite element method for finite deformation elasticity was developedfor the analysis and included specialised coordinate systems, interpolation schemesand parallel processing techniques for greater computational efficiency.The ventricular mechanics model incorporated the fully orthotropic pole-zero constitutivelaw, based on the three-dimensional architecture of myocardium, to account for the nonlinearmaterial response of resting cardiac muscle, relative to the three anatomically relevant axes.A fibre distribution model was introduced to reconcile some of the pole-zero constitutiveparameters with direct mechanical properties of the tissue (such as the limiting strainsestimated from detailed physiological observations of the collagen helices that surroundmyofibres), whilst other parameters were estimated from in-vitro biaxial tension tests onthin sections of myocardium. A non-invasive approach to in-vivo myocardial materialparameter estimation was also developed, based on a magnetic resonance imaging techniqueto effectively tag ventricular wall tissue.The spatially non-homogeneous distribution of myocardial residual strain was accounted forin the ventricular mechanics model using a specialised growth tensor. A simple model of fluidshift was formulated to account for the changes in local tissue volume due to movement ofintramyocardial blood. Contractile properties of ventricular myofibres were approximatedusing a quasi-static relationship between the fibre extension ratio, intracellular calciumconcentration and active fibre stress, and the framework has been developed to include amore realistic model of active myocardial mechanics, which could be coupled to a realisticdescription of the time-varying spread of electrical excitation throughout the ventricularwalls. Simple volumetric cavity models were incorporated to investigate the effects of arterialimpedance on systolic wall mechanics.Ventricular mechanics model predictions of the cavity pressure versus volume relationships,longitudinal dimension changes, torsional wall deformations and regional distributions ofmyocardial strain during the diastolic filling, isovolumic contraction and ejection phasesof the cardiac cycle showed good overall agreement with reported observations derivedfrom experimental studies of isolated and in-vivo canine hearts. Predictions of the spatialdistributions of mechanical stress at end-diastole and end-systole are illustrated.

Global and regional mechanics of the cardiac ventricles were investigated using an anatomicallyaccurate computational model formulated from concise mathematical descriptions ofthe left and right ventricular wall geometries and the non-homogeneous laminar microstructureof cardiac muscle. The finite element method for finite deformation elasticity was developedfor the analysis and included specialised coordinate systems, interpolation schemesand parallel processing techniques for greater computational efficiency.The ventricular mechanics model incorporated the fully orthotropic pole-zero constitutivelaw, based on the three-dimensional architecture of myocardium, to account for the nonlinearmaterial response of resting cardiac muscle, relative to the three anatomically relevant axes.A fibre distribution model was introduced to reconcile some of the pole-zero constitutiveparameters with direct mechanical properties of the tissue (such as the limiting strainsestimated from detailed physiological observations of the collagen helices that surroundmyofibres), whilst other parameters were estimated from in-vitro biaxial tension tests onthin sections of myocardium. A non-invasive approach to in-vivo myocardial materialparameter estimation was also developed, based on a magnetic resonance imaging techniqueto effectively tag ventricular wall tissue.The spatially non-homogeneous distribution of myocardial residual strain was accounted forin the ventricular mechanics model using a specialised growth tensor. A simple model of fluidshift was formulated to account for the changes in local tissue volume due to movement ofintramyocardial blood. Contractile properties of ventricular myofibres were approximatedusing a quasi-static relationship between the fibre extension ratio, intracellular calciumconcentration and active fibre stress, and the framework has been developed to include amore realistic model of active myocardial mechanics, which could be coupled to a realisticdescription of the time-varying spread of electrical excitation throughout the ventricularwalls. Simple volumetric cavity models were incorporated to investigate the effects of arterialimpedance on systolic wall mechanics.Ventricular mechanics model predictions of the cavity pressure versus volume relationships,longitudinal dimension changes, torsional wall deformations and regional distributions ofmyocardial strain during the diastolic filling, isovolumic contraction and ejection phasesof the cardiac cycle showed good overall agreement with reported observations derivedfrom experimental studies of isolated and in-vivo canine hearts. Predictions of the spatialdistributions of mechanical stress at end-diastole and end-systole are illustrated.

No description available.

Indiana University-Purdue University Indianapolis (IUPUI) / Atherosclerotic lesions of human beings are common diagnosed in regions of arte- rial branching and curvature. The prevalence of atherosclerosis is usually associated with hardening and ballooning of aortic wall surfaces because of narrowing of flow path by the deposition of fatty materials, platelets and influx of plasma through in- timal wall of Aorta. High Wall Shear Stress (WSS) is proved to be the main cause behind all these aortic diseases by physicians and researchers. Due to the fact that the atherosclerotic regions are associated with complex blood flow patterns, it has believed that hemodynamics and fluid-structure interaction play important roles in regulating atherogenesis. As one of the most complex flow situations found in cardio- vascular system due to the strong curvature effects, irregular geometry, tapering and branching, and twisting, theoretical prediction and in vivo quantitative experimental data regarding to the complex blood flow dynamics are substantial paucity. In recent years, computational fluid dynamics (CFD) has emerged as a popular research tool to study the characteristics of aortic flow and aim to enhance the understanding of the underlying physics behind arteriosclerosis. In this research, we study the hemo- dynamics and flow-vessel interaction in patient specific normal (healthy) and dilated (diseased) aortas using Ansys-Fluent and Ansys-Workbench. The computation con- sists of three parts: segmentation of arterial geometry for the CFD simulation from computed tomography (CT) scanning data using MIMICS; finite volume simulation of hemodynamics of steady and pulsatile flow using Ansys-Fluent; an attempt to perform the Fluid Structure Simulation of the normal aorta using Ansys-Workbench. Instead of neglecting the branching or smoothing out the wall for simplification as a lot of similar computation in literature, we use the exact aortic geometry. Segmen- tation from real time CT images from two patients, one young and another old to represent healthy and diseased aorta respectively, is on MIMICS. The MIMICS seg- mentation operation includes: first cropping the required part of aorta from CT dicom data of the whole chest, masking of the aorta from coronal, axial and saggital views of the same to extract the exact 3D geometry of the aorta. Next step was to perform surface improvement using MIMICS 3-matic module to repair for holes, noise shells and overlapping triangles to create a good quality surface of the geometry. A hexahe- dral volume mesh was created in T-Grid. Since T-grid cannot recognize the geometry format created by MIMICS 3-matic; the required step geometry file was created in Pro-Engineer. After the meshing operation is performed, the mesh is exported to Ansys Fluent to perform the required fluid simulation imposing adequate boundary conditions accordingly. Two types of study are performed for hemodynamics. First is a steady flow driven by specified parabolic velocity at inlet. We captured the flow feature such as skewness of velocity around the aortic arch regions and vortices pairs, which are in good agreement with open data in literature. Second is a pulsatile flow. Two pulsatile velocity profiles are imposed at the inlet of healthy and diseased aorta respectively. The pulsatile analysis was accomplished for peak systolic, mid systolic and diastolic phase of the entire cardiac cycle. During peak systole and mid-systole, high WSS was found at the aortic branch roots and arch regions and diastole resulted in flow reversals and low WSS values due to small aortic inflow. In brief, areas of sudden geometry change, i.e. the branch roots and irregular surfaces of the geom- etry experience more WSS. Also it was found that dilated aorta has more sporadic nature of WSS in different regions than normal aorta which displays a more uniform WSS distribution all over the aorta surface. Fluid-Structure Interaction simulation is performed on Ansys-WorkBench through the coupling of fluid dynamics and solid mechanics. Focus is on the maximum displacement and equivalent stress to find out the future failure regions for the peak velocity of the cardiac cycle.