Mechanical functional role of non-atherosclerotic intimal thickening
Glagov, S.; Zarins, C.K.; Masawa, N.; Xu, C.P.; Bassiouny, H.; Giddens, D.P.
Frontiers of Medical and Biological Engineering the International Journal of the Japan Society of Medical Electronics and Biological Engineering 5(1): 37-43
1993
ISSN/ISBN: 0921-3775 PMID: 8323881 Document Number: 408573
Arteries adjust to alterations in wall shear stress or tensile stress by changes in diameter, wall thickness, structure and composition. The intima participates in these adaptive reactions, particularly when changes in mechanical stresses are imposed after physiologic stress levels have been established during growth. Decreased wall shear stress due to decreased flow, flow separation or complete flow patterns, or increases in tensile stress due to increases in pressure or radius stimulate non-atherosclerotic intimal proliferation. Intimal fibrocellular hypertrophy (IFH), in the form of compact fibrocellular layers resembling the media, stabilizes when the lumen diameter is reduced sufficiently or wall thickness is increased sufficiently to restore baseline wall shear to tensile stress. Reactive-adaptive intimal proliferation is not necessarily self-limiting and may continue in the form of intimal hyperplasia (IH) which is relatively matrix-free and poorly organized. If mural and intimal changes do not result in restoration of baseline wall shear and tensile stress, IH may proceed to further narrowing and stenosis. Identification of the cellular and molecular mechanisms which underlie the responses which link flow to diameter, diameter and pressure to mural restructuring, and mural restructuring to intimal thickening should provide new insights into the nature of vessel adaptations in the absence or presence of atherogenesis.