Rabbani L E, Loscalzo J
Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Atherosclerosis. 1994 Jan;105(1):1-7. doi: 10.1016/0021-9150(94)90002-7.
Recent evidence suggests that hemostatic determinants play a major role in the evolution of the atherothrombotic plaque. Platelets can serve as cholesterol donors for macrophages, thereby facilitating foam cell formation. Lipoprotein(a) inhibits fibrinolysis and may also contribute to atherogenesis by serving as a ligand for the scavenger receptor. By complexing with fibrin(ogen) in atheromatous lesions, lipoprotein(a) attenuates clearance of this protein, promoting atherogenesis and vascular dysfunction. These observations suggest that thrombotic determinants are critical for the development of the atheromatous plaque, and may guide the appropriate selection of potential therapeutic options in the future.
