A minimally diseased (mean intimal thickness = 56 μm) human aortic bifurcation was replicated in rigid and compliant flow-through casts. Both casts were perfused with physiological flow waves having the same Reynolds and unsteadiness numbers; the pulse pressure in the compliant cast produced radial strains similar to those expected from post-mortem measurements of the compliance of the original tissue. The compliant cast was perfused with a Newtonian fluid and one whose rheology was closer to that of blood. Wall shear rate histories were estimated from near-wall velocities obtained by laser Doppler velocimetry at identical sites in both casts. Intimal thickness was measured at corresponding sites in the original vessel and linear regressions were performed between these thicknesses and several normalized shear rate measures obtained from the histories. The correlations showed a positive slope—that is, the intima was thicker at sites exposed to higher shear rates—consistent with earlier results for relatively healthy vessels, but their significance was often poor. There was no significant effect of either model compliance or fluid rheology on the slopes of the correlations of intimal thickness against any normalized shear rate measure.
Endothelial cells in vivo are believed to adapt to local hemodynamics in regions with largely unidirectional flow [1] and develop a quiescent phenotype. However, the local shear stress is altered occasionally by changes in global hemodynamic variables, such as heart rate and flow rate. These changes are caused by a number of normal physiologic events, such as exercise, smoking, sleep, stress and digestion. The duration of these changes ranges from minutes to hours, and endothelial cells undergo structural remodeling and phenotypic transformation in order to adapt to the altered shear stress. During the adaptive response, the dynamics of endothelial phenotypic change adds a new dimension to the endothelial response to shear stress.
The effects of the outflow of aortic blood through the celiac and renal arteries on the flow field in the external iliac arteries were studied under steady and physiologically realistic pulsatile flow conditions. Laser Doppler velocimetry (LDV) measurements were made close to the lateral, medial, ventral, and dorsal walls of the external iliac branches of a clear, flow-through replica of a porcine aorta and its daughter vessels. The outflow from each branch of the replica was controlled so that the infrarenal aortic flow rate (1000 ml/min) and the flow partition at the aortic trifurcation (3:2:3 through the right iliac, common internal iliac, and left iliac arteries, respectively) were the same for all experiments. LDV measurements were made with flow exiting through both the renal and celiac artery ostia, only the celiac ostium, and neither ostium. The steady flow results indicate that while the outflow through the renal arteries did not have a statistically significant effect on near wall shear rate in the external iliac arteries, the flow through the celiac artery did. However, in pulsatile flow, three indices of near wall velocity in the iliac arteries were unaffected by celiac artery outflow, while a fourth showed a small effect that can be attributed to differences in minimum velocity. These results indicate that reliable simulations of blood flow in the external iliac arteries can be carried out without including the renal and celiac vessels, provided that the correct infrarenal flow wave is used.
The adaptation of vascular endothelial cells to shear stress alteration induced by global hemodynamic changes, such as those accompanying exercise or digestion, is an essential component of normal endothelial physiology in vivo. An understanding of the transient regulation of endothelial phenotype during adaptation to changes in mural shear will advance our understanding of endothelial biology and may yield new insights into the mechanism of atherogenesis. In this study, we characterized the adaptive response of arterial endothelial cells to an acute increase in shear stress magnitude in well-defined in vitro settings. Porcine endothelial cells were preconditioned by a basal level shear stress of 15 ± 15 dyn/cm(2) at 1 Hz for 24 h, after which an acute increase in shear stress to 30 ± 15 dyn/cm(2) was applied. Endothelial permeability nearly doubled after 40-min exposure to the elevated shear stress and then decreased gradually. Transcriptomics studies using microarray techniques identified 86 genes that were sensitive to the elevated shear. The acute increase in shear stress promoted the expression of a group of anti-inflammatory and antioxidative genes. The adaptive response of the global gene expression profile is triphasic, consisting of an induction period, an early adaptive response (ca. 45 min) and a late remodeling response. Our results suggest that endothelial cells exhibit a specific phenotype during the adaptive response to changes in shear stress; this phenotype is different than that of fully adapted endothelial cells.
In this study, we propose a method to estimate arterial wall strain using intravascular ultrasound (IVUS) images. The method is based on a nonrigid image registration algorithm, which represents the displacement field by cubic B-splines, and incorporates smoothness and incompressibility constraints. The 2D displacement field is then used to calculate the local strain tensors. With the 2D strain tensors, both radial and circumferential strain distributions can be obtained, and color-coded for display. The algorithm has been evaluated with synthetic motion IVUS images and phantom IVUS images under two luminal pressures.
The detailed geometry of atherosclerosis-prone vascular segments may influence their susceptibility by mediating local hemodynamics. An appreciation of the role of specific geometric variables is complicated by the considerable correlation among the many parameters that can be used to describe arterial shape and size. Factor analysis is a useful tool for identifying the essential features of such an inter-related data set, as well as for predicting hemodynamic risk in terms of these features and for interpreting the role of specific geometric variables. Here, factor analysis is applied to a set of 14 geometric variables obtained from magnetic resonance images of 50 human carotid bifurcations. Two factors alone were capable of predicting 12 hemodynamic metrics related to shear and near-wall residence time with adjusted squared Pearson’s correlation coefficient as high as 0.54 and P-values less than 0.0001. One factor measures cross-sectional expansion at the bifurcation; the other measures the colinearity of the common and internal carotid artery axes at the bifurcation. The factors explain the apparent lack of an effect of branch angle on hemodynamic risk. The relative risk among the 50 bifurcations, based on time-average wall shear stress, could be predicted with a sensitivity and specificity as high as 0.84. The predictability of the hemodynamic metrics and relative risk is only modestly sensitive to assumptions about flow rates and flow partitions in the bifurcation.
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