Zpřesnění existujících biomechanických modelů pro určování napětí ve stěně výdutě břišní aorty

Abstract

Cardiovascular diseases, such as atherosclerosis and aneurysms, are the leading causes of death in the Western world and major contributors to disability. Understanding the causes, progression, and terminal stages of these cardiovascular diseases is the focus of many research teams across disciplines. One of these disciplines is biomechanics, which explains the onset, progression, and terminal stages of these diseases based on physical quantities, including those that describe the behavior of the arterial wall structure and blood hemodynamics. To grasp the complexity of these diseases, an isolated approach—whether structural, hemodynamic, or pathological—is insufficient. A multiphysical perspective is required, allowing for the interaction between the solid domain and the flowing blood, complemented by pathophysiological knowledge. Since it remains unclear whether the physical changes are the cause or the consequence of biological processes leading to development, progression, and rupture of the aneurysm in the chronic phase. In my dissertation thesis, I present a comprehensive analysis of aneurysms, particularly those affecting the abdominal region of the aorta, where gradual dilatation is a characteristic feature that, in the terminal stage, results in the patient’s death. The theoretical part provides a deeper understanding of the disease in terms of pathophysiology, while the practical section explores possible risk factors, such as stenosis of the iliac arteries, which may increase the predisposition to developing the disease. I investigate the influence of risk factors, including stenosis and bifurcation angle, on hemodynamics and wall stress through parametric FSI (fluid-structure interaction) analysis. This analysis allows the interaction between the compliant arterial wall and pulsatile blood flow. To enhance the impact and relevance of these results, an experimental stand was constructed to reflect the numerical simulations, and the experimental results confirmed the effect of stenosis on increased abdominal aortic pressure. When numerical results cannot be verified through experimental measurements, considerable care must be taken in setting up numerical analyses, as the uncertainty of the results is directly related to the uncertainty of their inputs. I address this issue, i.e. the problem of input uncertainties, by creating a simple experimental device that enables the determination of the unloaded thickness of soft tissue independently of the operator and I also address the previously accepted assumption regarding the incompressibility of aortic samples. The terminal stage of aneurysm itself, i.e., rupture, is analyzed in terms of the numerically determined risk of aneurysm rupture probability, with part of this analysis focusing on the modification of this criterion to increase its specificity. Finally, I examine the potential for using biomechanical criteria for determining rupture risk in clinical practice, particularly as a crisis tool for prioritizing patients for surgeries during the period of hospital overcrowding following the end of the state of emergency during the COVID-19 pandemic.