A thorough understanding of the relationship between local hemodynamics and plaque progression has been hindered by an inability to prospectively monitor these factors in vivo in humans. In this study a novel approach for noninvasively reconstructing artery wall thickness and local hemodynamics at the human carotid bifurcation is presented. Three-dimensional (3D) models of the lumen and wall boundaries, from which wall thickness can be measured, were reconstructed from blackblood magnetic resonance imaging (MRI). Along with time-varying inlet/outlet flow rates measured via phase contrast (PC) MRI, the lumen boundary was used as input for computational fluid dynamic (CFD) simulation of the subject-specific flow patterns and wall shear stresses (WSSs). Results from a 59-yearold subject with early, asymptomatic carotid artery disease show good agreement between simulated and measured velocities, and demonstrate a correspondence between wall thickening and low and oscillating shear at the carotid bulb. High shear at the distal internal carotid artery (ICA) was also colocalized with higher WSS; however, a quantitative general relationship between WSS and wall thickness was not found. Similar results were obtained from a 23-year-old normal subject. Wall shear stress (WSS) is widely believed to play a key role in the development and progression of atherosclerotic plaques. Studies comparing human post-mortem distributions of plaque to in vitro fluid dynamic models have perhaps provided the most direct observational evidence for the relationship between WSS and the focal development of atherosclerotic lesions (1-4). The mechanisms by which shear stresses alter endothelial function at the cellular, molecular, and genetic level are also now being elucidated (5). Despite these advances, however, many questions still remain regarding the role of fluid dynamics in the development and progression of atherosclerosis. One reason for this has been the difficulty of identifying and monitoring the relationships between local fluid dynamic factors and plaque development on a subject-specific basis.In principle, both MR and ultrasound imaging can be used to measure wall thickness (a marker for atherosclerotic burden) and blood velocities (from which WSSs are derived) directly. However, difficulties associated with the quantification of blood velocities in regions of complex flow have in the past limited the application of such an "imaging-only" approach to relatively straight sections of the abdominal aorta (6), femoral artery (7), and common carotid artery (8 -10). While these studies were able to confirm an inverse relationship between mean or peak shear and intimal or intima-media thickness, it is not yet possible to use imaging techniques alone to map WSS in the regions of complex flow where plaques are known to localize, such as at the carotid bifurcation. Recent work by Stokholm et al. (11) suggests that WSS from individual slices at the carotid bifurcation itself can be quantified in vivo by sophisticated postprocessing of ph...