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Atherosclerosis is an ubiquitous disease effecting degenerative, proliferative and atrophic changes in the vessel wall. Preoccupation with intramural lipid accumulation has been at the expense of studies concerning other aspects of atherosclerosis including the complications. The current view of the lipid hypothesis fails to explain the localization or the complications. They can be accounted for by the thesis that atherosclerosis is due to hemodynamically-induced engineering fatigue. In animal models, in which gross disturbances of flow occur, the disease morphologically similar to atherosclerosis in man, together with the complications, can be reproduced at an accelerated rate, thus substantiating the fatigue hypothesis. Moreover, hemodynamics appears to govern dietary-induced lipid accumulation, but these two factors acting in concert will not reproduce atherosclerosis as it occurs in man.
W.E. Stehbens (Thu,) studied this question.