Aneurysm wall thickness varies throughout the sac. The thickness is greatest at the neck and least at the fundus. Compared to small aneurysms, calcification and atheromas are more commonly seen in large aneurysms. Macrophages, present in all stages of atherosclerosis, secrete lytic enzymes (e.g., elastases, collagenases, metalloproteases), lead to the destruction of connective tissue and erosion of the arterial wall. Smooth muscle cell apoptosis and elastin/collagen fiber reconstruction mechanisms contribute to vessel wall weakening [20]. The weakening of aneurysm walls has been demonstrated in histological studies that found degeneration of endothelial cells and internal elastic lamina and thinning of the medial layer [21]. Aneurysm wall tensions and stressors have been noted to be an important contributor to growth, remodeling and rupture in aneurysms. Focal turbulence and discontinuity of the normal architecture at vessel bifurcations may account for the propensity of saccular aneurysm formation [22].