A biologically plausible model of thickening of arterial intima under shear.

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Abstract
A biologically plausible model of the early thickening of the arterial intima has been developed to interpret experimental data relating hemodynamic shear to human intimal morphology. The model included many processes known or commonly believed to take place in the vascular intima, including: smooth muscle cell migration, proliferation, metabolism, and expression of extracellular matrix; lipoprotein kinetics and binding; and monocyte chemotaxis, conversion to macrophage, and foam cell formation. Certain of these processes were allowed to be shear-dependent. The best fit to the data was obtained when smooth muscle cell accumulation was more rapid, and extracellular matrix expression proceeded more slowly where the fluid shear was relatively high and unidirectional. This result is consistent with the earlier inference that competing shear-dependent processes take place in the wall; it is also consistent with the notion that intimal thickening might be part of an adaptive mechanism by which the artery maintains a favorable shear environment.

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