TF protein was overexpressed by macrophages and smooth muscle cells and deposited in the extracellular matrix of atheroclerotic intimas. TF activity was also enhanced in the atherosclerotic intima, probably resulting in either thrombus formation or intimal fibrin deposition after the exposure of flowing blood and imbibed fibrinogen to TF in atherosclerotic lesions. These findings further support the hypothesis that the coagulation and fibrinolysis systems can play an essential role in the initiation and progression of atherosclerosis, and the clinical implications of this phenomenon may thus contribute to future investigations in the prevention and treatment of atherosclerotic diseases.