The elusive local factor in atherosclerosis

Recent evidence confirms that local haemodynamic stresses account for the initiation, topographical localization and complications of atherosclerosis. These causative stresses are vibratory and associated with pulse pressure and the lesser vibrations of greater frequency generated by blood flow at predilection sites. This bioengineering fatigue hypothesis is further substantiated by analogous effects of repetitive stresses on erythrocytes and in the musculoskeletal system. The mechanism underlying fatigue is cumulative molecular scissions of the mural constituents which ultimately result in failure of the wall as a whole. Free radicals and oxidation products are by-products of this molecular scission in atherogenesis. This theory which explains the progressive inexorable loss of mural cohesion, its pathogenesis and complications is completely substantiated by the iatrogenic and experimental reproduction of the disease by haemodynamic means.