Hemodynamics of human carotid artery bifurcations: computational studies with models reconstructed from magnetic resonance imaging of normal subjects.
PURPOSE: The precise role played by hemodynamics, particularly wall shear stress, in the development and progression of vascular disease remains unclear, in large part because of a lack of in vivo studies with humans. Although technical challenges remain for noninvasively imaging wall shear stresses in humans, vascular anatomy can be imaged with sufficiently high resolution to allow reconstruction of three-dimensional models for computational hemodynamic studies. In this paper we present an entirely noninvasive magnetic resonance imaging (MRI) protocol that provides carotid bifurcation geometry and flow rates from which the in vivo hemodynamics can be computed. Maps of average, oscillatory, and gradients of wall shear stress are presented for two normal human subjects, and their data are compared with those computed for an idealized carotid bifurcation model. METHODS: An MRI protocol was developed to acquire all necessary image data in scan times suitable for patient studies. Three-dimensional models of the carotid bifurcation lumen were reconstructed from serial black blood MR images of two normal volunteers. Common and internal carotid artery flow rate waveforms were determined from MRI phase-contrast velocity imaging in the same subjects and were used to impose fully developed velocity boundary conditions for the computational model. Subject-specific time-resolved velocities and wall shear stresses were then computed with a finite element-based Navier-Stokes equation solver. RESULTS: Models reconstructed from in vivo MRI of two subjects showed obvious differences in branch angle, bulb size and extent, and three-dimensional curvature. Maps of a variety of wall shear stress indices showed obvious qualitative differences in patterns between the in vivo models and between the in vivo models and the idealized model. Secondary, helical flow patterns, induced primarily by the asymmetric and curved in vivo geometries, were found to play a key role in determining the resulting wall shear stress patterns. The use of in vivo flow rate waveforms was found to play a minor but noticeable role in some of the wall shear stress behavior observed. CONCLUSIONS: Conventional "averaged" carotid bifurcation models mask interesting hemodynamic features observed in realistic models derived from noninvasive imaging of normal human subjects. Observation of intersubject variations in the in vivo wall shear stress patterns supports the notion that more conclusive evidence regarding the role of hemodynamics in vascular disease may be derived from such individual studies. The techniques presented here, when combined with subject-specific MRI measurements of carotid artery plaque thickness and composition, provide the tools necessary for entirely noninvasive, prospective, in vivo human studies of hemodynamics and the relationship of hemodynamics to vascular disease.