(ILT), which complicates AAA progression and risk of rupture. Patient-specific computational fluid dynamics modeling of 10 small human AAA was performed to investigate relations between hemodynamics and ILT progression. The patients were imaged using magnetic resonance twice in a 2-to 3-yr interval. Wall content data were obtained by a planar T1-weighted fast spin echo black-blood scan, which enabled quantification of thrombus thickness at midaneurysm location during baseline and followup. Computational simulations with patient-specific geometry and boundary conditions were performed to quantify the hemodynamic parameters of time-averaged wall shear stress (TAWSS), oscillatory shear index (OSI), and mean exposure time at baseline. Spatially resolved quantifications of the change in ILT thickness were compared with the different hemodynamic parameters. Regions of low OSI had the strongest correlation with ILT growth and demonstrated a statistically significant correlation coefficient. Prominent regions of high OSI (Ϟ0.4) and low TAWSS (Ͻ1 dyn/cm 2 ) did not appear to coincide with locations of thrombus deposition. computational fluid dynamics; hemodynamics; oscillatory shear index; thrombosis; wall shear stress ABDOMINAL AORTIC ANEURYSM (AAA) is a permanent dilation (50% greater than the normal arterial wall diameter) of the abdominal aorta. The disease is progressive and fatal if untreated. Between 11,000 and 17,000 patients die annually in the United States (18a) from AAA rupture following progressive, often asymptomatic, enlargement, and only invasive treatments have proven effective at preventing rupture and premature death (13). Male gender, age, smoking, genetic factors, hypertension, and high cholesterol are among known risk factors (10), and diabetes is a negative risk factor (47). Degradation of the aortic wall, inflammation with immune responses, and biochemical wall stress are mechanisms that promote AAA initiation, influenced by molecular genetics (1). After the irreversible process of aneurysm formation, the dilated vessel creates an environment with complex blood flow and wall shear stress distribution (4,5,9,14,22,37,38), which is thought to perpetuate aneurysm progression.The presence of intraluminal thrombus (ILT) complicates AAA growth. ILT is fibrin structure compound of platelets, blood cells, blood proteins, and cellular debris (20). ILT is more frequent in larger AAA since most patients develop thrombus as the aneurysm progresses. It has been proposed that platelets activate in regions of high shear and are subsequently advected towards the aneurysm wall where they accumulate in regions of low shear and form thrombus (8), with a possible role played by the vortical structures formed inside the aneurysm (9). It has also been shown that the flow field inside AAA may promote ILT formation by increasing residence time and trapping blood particles (7,37,38).The effect of ILT on AAA progression and rupture remains controversial (48). ILT may deprive the aneurysm wall of oxygen, which may exacerba...