| Summary: | The haemostatic system stops the loss of blood, thereby maintaining the integrity of the circulatory network. Whilst haemostasis is necessary for survival, thrombosis - haemostasis in the wrong place - is the most common cause of mortality in the West. The presence of a thrombus is governed by the triad of endothelial injury, blood constitution and flow. The central protein involved in this process is thrombin which is formed through a reaction network known as the coagulation cascade. Cerebral saccular aneurysms are balloon like dilations of the cerebral vasculature that are estimated to be present in 2-6% of the population. The currently preferred treatment method for such aneurysms is the deliberate initiation of thrombus formation (leading to occlusion) through the placement of platinum coils within the aneurysm. An emerging alternative is the use of a stent which is deployed across the aneurysm neck, reducing the rate at which flow enters the aneurysm, leading again to the controlled formation of a thrombus. A comprehensive model of thrombus formation within cerebral aneurysms should simulate the reduction to flow as the thrombus grows within the aneurysm. The model must capture the spatial and temporal regulators of thrombus formation - incorporating both biological and mechanical factors. This first part of this thesis examines the sensitivity of flow conditions within cerebral aneurysms to changes in boundary conditions (simulated exercise) and geometrical changes (stent placement). The main contribution of this thesis is the development of frameworks which enable examination of thrombus formation. First, an idealised arteriole is used to examine the impact of flow upon two approaches to computational modelling of thrombin generation. The second framework uses the Level Set technique to track the position of a thrombus surface within a patient specific aneurysmal geometry.
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