Abstract
The blood velocity field and sites of occurrence of early atheroma are considered in arterial bifurcations in man. Evidence is increasing that these lesions occur preferentially where wall shear stress is low. Mechanisms are examined which might account for this correlation and also the influence of wall shear stress on the permeability of the arterial intima to macromolecules. Hypertension seemingly favours the development of atheroma, but the focal occurrence of lesions is not readily explained in terms of the arterial blood pressure. A widely held view is that atheroma results from damage to the endothelium and increased influx of lipoprotein, and interaction of platelets with the damaged wall leading to smooth muscle cell replication and migration. Exposed subendothelium is, however, rarely seen, except over advanced lesions and a theory appears necessary to account for the observed findings in the absence of endothelial damage. Recent studies suggest that the media may offer a barrier to the drainage of material from the subendothelial space to the adventitia and that the transport properties of the media may be influenced by arterial blood pressure and medial smooth muscle tone.
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