Issue title: Proceedings of the Fourth International Congress of Biorheology. Jikei University School of Medicine, Tokyo, Japan, 27 July – 1 August 1981. Dedicated to Alex Silberberg
Affiliations: Department of Pathology, Wellington Clinical School of Medicine and the Wellington Cancer and Medical Research Institute, Wellington 2, New Zealand
Note: [1] Plenary lecture presented at the 4th International Congress of Biorheology, Tokyo, 1981.
Abstract: 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.
