Abstract
Hypercoagulability seems to be intimately correlated to atherosclerosis in terms of its pathogenesis and complications. When the aorta of the rabbit was desquamated by catheterization of polyethylene tube, many platelets adheared to the denudated area, where intimal thickening with proliferation of smooth muscle cells subsequently occured. Immunofluorescence and electron microscopy revealed extensive insudation of fibrinogen and lipoproteins, which seemed to lead to formation of atheroma. Our experiments also revealed that fibrin activated mesenchymal proliferation. Therefore, thrombosis may lead to atherosclerosis in the aorta, even when the level of serum cholesterol remains low. Hypercoagulability following rupture of the atheroma is seen with keen interest. Occulusive thrombosis due to rupture of the atheroma of coronary artery is a major cause of myocardial infarction. It may be caused by the release of thromboplastin from ruptured intima and inhibitory action of LDL to plasminogen tissue activator.
