Circulating thrombomodulin in ischemic heart disease: correlation with the extent and severity of coronary atherosclerosis

Abnormal endothelial physiology has been implicated both in early atherogenesis and, later, in the control of dynamic plaque behavior. The biologic link between endothelial damage and atherosclerosis may be related to decreased arterial bioavailability of nitric oxide (NO), which may predispose to leucocyte and platelet adhesion, vasoconstriction and smooth muscle cell proliferation. Substances released by the endothelium include prostacyclin, NO, endothelin, von Willebrand factor and thrombomodulin (TM), and so on. TM is an integral membrane glycoprotein that can change the function of thrombin, to an anticoagulant through activation of protein C – which, in the presence of protein S, inactivates factor VIIIa and factor Va, and thereby inhibits further formation of thrombin. Soluble TM is thought to indicate endothelial-cell damage. A positive relation between the concentration of soluble thrombomodulin and the risk of atherosclerotic disease is widely assumed.