Numerical modelling of the fluid-structure interaction in complex vascular geometries

A complex network of vessels is responsible for the transportation of blood throughout the body and back to the heart. Fluid mechanics and solid mechanics play a fundamental role in this transport phenomenon and are particularly suited for computer simulations. The latter may contribute to a better comprehension of the physiological processes and mechanisms leading to cardiovascular diseases, which are currently the leading cause of death in the western world. In case these computational models include patient-specific geometries and/or the interaction between the blood flow and the arterial wall, they become challenging to develop and to solve, increasing both the operator time and the computational time. This is especially true when the domain of interest involves vascular pathologies such as a local narrowing (stenosis) or a local dilatation (aneurysm) of the arterial wall. To overcome these issues of high operator times and high computational times when addressing the bio(fluid)mechanics of complex geometries, this PhD thesis focuses on the development of computational strategies which improve the generation and the accuracy of image-based, fluid-structure interaction (FSI) models. First, a robust procedure is introduced for the generation of hexahedral grids, which allows for local grid refinements and automation. Secondly, a straightforward algorithm is developed to obtain the prestress which is implicitly present in the arterial wall of a – by the blood pressure – loaded geometry at the moment of medical image acquisition. Both techniques are validated, applied to relevant cases, and finally integrated into a fluid-structure interaction model of an abdominal mouse aorta, based on in vivo measurements

Numerical analysis of the fluid-structure interaction in a membrane pump

In this research, the fluid-structure interaction in a recently developed membrane pump is analysed. The governing equations for the laminar flow and for the deformation of the membrane are solved with two separate codes, which are coupled with the quasi-Newton technique with an approximation for the inverse of the Jacobian from a least-squares model. After the description of the model and the solution techniques, a detailed analysis of the flow field, the deformation of the structure and the stress in the membrane is presented. An energetic analysis of the pump is performed, and the pump's efficiency is calculated

Inverse modelling of image-based patient-specific blood vessels : zero-pressure geometry and in vivo stress incorporation

In vivo visualization of cardiovascular structures is possible using medical images. However, one has to realize that the resulting 3D geometries correspond to in vivo conditions. This entails an internal stress state to be present in the in vivo measured geometry of e.g. a blood vessel due to the presence of the blood pressure. In order to correct for this in vivo stress, this paper presents an inverse method to restore the original zero-pressure geometry of a structure, and to recover the in vivo stress field of the final, loaded structure. The proposed backward displacement method is able to solve the inverse problem iteratively using fixed point iterations, but can be significantly accelerated by a quasi-Newton technique in which a least-squares model is used to approximate the inverse of the Jacobian. The here proposed backward displacement method allows for a straightforward implementation of the algorithm in combination with existing structural solvers, even if the structural solver is a black box, as only an update of the coordinates of the mesh needs to be performed

An animal-specific FSI model of the abdominal aorta in anesthetized mice

Recent research has revealed that angiotensin II-induced abdominal aortic aneurysm in mice can be related to medial ruptures occurring in the vicinity of abdominal side branches. Nevertheless a thorough understanding of the biomechanics near abdominal side branches in mice is lacking. In the current work we present a mouse-specific fluid-structure interaction (FSI) model of the abdominal aorta in ApoE(-/-) mice that incorporates in vivo stresses. The aortic geometry was based on contrast-enhanced in vivo micro-CT images, while aortic flow boundary conditions and material model parameters were based on in vivo high-frequency ultrasound. Flow waveforms predicted by FSI simulations corresponded better to in vivo measurements than those from CFD simulations. Peak-systolic principal stresses at the inner and outer aortic wall were locally increased caudal to the celiac and left lateral to the celiac and mesenteric arteries. Interestingly, these were also the locations at which a tear in the tunica media had been observed in previous work on angiotensin II-infused mice. Our preliminary results therefore suggest that local biomechanics play an important role in the pathophysiology of branch-related ruptures in angiotensin-II infused mice. More elaborate follow-up research is needed to demonstrate the role of biomechanics and mechanobiology in a longitudinal setting

Differential impact of local stiffening and narrowing on hemodynamics in repaired aortic coarctation: an FSI study

Even after successful treatment of aortic coarctation, a high risk of cardiovascular morbidity and mortality remains. Uncertainty exists on the factors contributing to this increased risk among which are the presence of (1) a residual narrowing leading to an additional resistance and (2) a less distensible zone disturbing the buffer function of the aorta. As the many interfering factors and adaptive physiological mechanisms present in vivo prohibit the study of the isolated impact of these individual factors, a numerical fluid-structure interaction model is developed to predict central hemodynamics in coarctation treatment. The overall impact of a stiffening on the hemodynamics is limited, with a small increase in systolic pressure (up to 8 mmHg) proximal to the stiffening which is amplified with increasing stiffening and length. A residual narrowing, on the other hand, affects the hemodynamics significantly. For a short segment (10 mm), the combination of a stiffening and narrowing (coarctation index 0.5) causes an increase in systolic pressure of 58 mmHg, with 31 mmHg due to narrowing and an additional 27 mmHg due to stiffening. For a longer segment (25 mm), an increase in systolic pressure of 50 mmHg is found, of which only 9 mmHg is due to stiffening