Modeling of atherosclerotic plaque growth using fluid-structure interaction.

Blood flow through a narrow arterial tube has been a classical mathematical problem dating back to the 1840's, after the pioneer experimental work conducted by Jean Louis Marie Poiseuille, Observations of blood flow, published in Ann. Sci. Naturelles in 1836. However, numerical simulations on atherosclerosis only started to thrive in the 1990's, due to rapid advancement in computer technology. The transportation of low density lipoprotein (LDL) enables lipids like cholesterol and triglycerides to be carried within the water-based bloodstream. Numerous research papers have shown that LDL particles would adhere on the artery wall at the locations where the local wall shear stress (WSS) is too low to move them further, resulting in localised regions with high LDL concentrations. Atherosclerosis tends to develop at regions where LDL accumulation is high and consistent. It is well known in the medical community that high level of LDL is closely related to myocardial infarction and/or stroke due to rupture of atherosclerotic plaques. Some rupture would release highly concentrated lipids and thrombogenic material into the bloodstream, leading to lethal blood clots that result in sudden cardiovascular casualties. In order to explore the dominant phenomenological mechanism, the thesis hypothesizes that LDL accumulation has the sole influence on plaque growth. By applying the hypothesis as the rule of growth, the thesis investigates how LDL accumulation affects the plaque morphology during its growth, aiming to provide a better understanding of atherosclerosis development. In this research the advanced two-way fluid-structural interaction (FSI) method is applied to model the growth of three-dimensional atherosclerotic plaques. The mild 45% axis-asymmetric stenosis model with the bi-elliptical cross-sectional plaque morphology is used as the base model, and then the plaque morphology is updated to the non-elliptical arbitrarily shaped profile across the centre of the plaque in the direction of the flow and elliptical profiles at various cross-sections of the plaque that are perpendicular to the flow direction. The updated plaque morphology is determined according to the simulation results of WSS distribution in the vicinity of the previous plaque and the relationship between the WSS and LDL accumulation derived from the literature. The growth-updated model is then used as the new geometry for the next round of simulation. This process repeats until the stenosis severity is increased to or beyond 79%, which is 1% greater than the critical stenosis as reported in literature. The numerical results of these growth-updated models presented and discussed in the thesis are extensive, providing valuable insight into the plaque development.<br><br><br>