This paper proposes that arterial wall shear influences atheroma development by altering diffusional mass transport between the arterial wall and flowing blood. The mechanism is framed especially around cholesterol movement.
First-pass extracted concept
shear-dependent mass transfer mechanism for atherogenesis
Aliases
shear dependent mass transport phenomena
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Early atheroma in humans is spatially coincident with arterial regions where wall shear rate is expected to be relatively low, whereas lesion development is inhibited or retarded in regions where wall shear rate is expected to be relatively high.
Cholesterol accumulates in low shear regions because local diffusional efflux from wall to blood is inhibited by a reduced concentration gradient.
Shear enhances mass transport by steepening the concentration gradient so that diffusion from the arterial wall is promoted when diffused material is swept away rapidly.
Wall shear rate may be a major controlling factor in the development of atheroma, and high shear may retard progression of the process.
The observed correlation between low wall shear and early atheroma is inconsistent with a wall-damage-by-blood-motion explanation and instead suggests a shear-dependent mass transport mechanism.
The influence of shear on diffusion between arterial wall and blood depends on the relative resistances of wall-phase and blood-phase diffusion, and diffusion is not appreciably shear dependent if blood-phase resistance is small compared with wall-phase resistance.
A net flux of cholesterol from blood to wall cannot account for the observed quasi-steady-state distribution of atheromatous lesions because mass transport is inhibited in low shear regions by the thick diffusional boundary layer.
The reported correlations provide no support for platelet involvement in the development of early atheroma.
The proposed theoretical schemes may unify naturally occurring and experimentally induced atheroma.