ABSTRACT
Arterial thrombus formation occurs on a fissured or ulcerated atherosclerotic plaque upon exposure to flowing blood of its inner components.1 We demonstrated that the thrombogenicity of atherosclerotic lesions is closely related to their tissue factor (TF) content which is highest in the lipid-rich core.2 TF is able to activate the coagulation cascade by binding factors VII/VIIa which activate factors IX and X leading to the generation of thrombin that, in turn, mediates fibrin deposition and platelet recruitment.3 Thrombin is the fastest and most powerful activator of platelets and platelet-rich thrombus formation on severely injured vessel wall (such as that resulting after plaque rupture or percutaneous transluminal coronary angioplasty-PTCA) is highly dependent on local thrombin generation.4-6 Clot-bound thrombin is also responsible for the high thrombogenicity of mural thrombus that may persist after reperfusion by thrombolysis or PTCA7-9 PTCA is associated with severe local vascular damage, which may cause thrombin generation and mural thrombus formation immediately after the procedure.10 Thrombin is also able to mediate the secretion of a series of growth factors at the site of vascular lesion, such as platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-β),13 and to directly stimulate smooth muscle cell migration and proliferation,14 thus playing a crucial role in neointima formation and restenosis.
