Some atherosclerosis may be a consequence of the normal adaptive vascular response to shear.

Estimates and measurements of fluid dynamic shear at the arterial wall suggest the presence of mechanisms to regulate this quantity. Arterial wall thickening prompted by chronic reductions in wall shear is one mechanism by which that regulation might be accomplished. Reduced wall shears that are a direct consequence of arterial geometry would be less susceptible to this mechanism, leading to exaggerated and focal intimal thickening, possibly leading to atherosclerosis, at affected sites. Thus some foci of vascular disease can be a natural, if undesirable, consequence of fluid shear regulation.