Post-stenotic core flow behavior in pulsatile flow and its effects on wall shear stress

Abstract

Arteries of several species, including man, tend to adjust their diameters such that the mean wall shear stress is in the range of 10–20 dynes cm −2. Additionally, intimal thickening in the human carotid bifurcation correlates well with the reciprocal of wall shear stress as determined in model studies. The correlation indicates that wherever the local mean wall shear stress exceeds approximately 10 dynes cm −2, the artery tends to be spared from intimal thickening. However, it is not known whether mean shear stress, i.e. the time-averaged value, or the instantaneous shear stress is the appropriate correlative variable. Each of these variables suggests different mechanisms for the reaction of the artery wall to its hemodynamic environment. It is therefore important to devise means by which the effects of mean shear and pulsatile shear can be separated in the study of atherogenesis. The present investigation examines the post-stenotic flow field in Plexiglas ™ models under pulsatile conditions approximating those in the aortas of the cynomolgus monkey, an animal often employed in atherogenesis research. Behavior of the core flow and its effects on wall shear stress are studied for stenoses of 75 and 90% area reductions using laser velocimetry. The results show that the post-stenotic field contains regions in which the mean wall shear stress is low, but the pulsatile excursions are large. A preliminary comparison of the present results with data available from a separate animal study suggests that intimal thickening in the neighborhood of a coarctation in the aorta of the cynomolgus monkey correlates better with the reciprocal of the maximum of the absolute value of pulsatile wall shear than with the reciprocal of the mean shear. This suggests that atherosclerotic intimal thickening requires that the wall shear stress must be low throughout the pulsatile cycle, not simply low in the mean sense. The present model studies provide a basis for the design of in vivo experiments which can test hypotheses relating wall shear to atherosclerotic intimal thickening.