 It is currently believed that the principle cause of the clinical symptoms characterizing ACS results from the transient thrombotic occlusion of one or more coronary vessels. Coronary thrombosis is initiated by the exposure of the protein tissue factor TF, which can be found in the sub-endothelial layer of the blood vessel and is a major component of atherosclerotic gruel. The exposure of TF following vascular damage or rupture of a coronary atherosclerotic plaque, results in the rapid formation of the enzymatic complex composed of TF and the serine protease factor VIIa fVIIaTF. The fVIIaTF complex initiates an amplified cascade of proteolytic activation steps resulting in the formation of the serine protease thrombin. The highly amplified generation of thrombin localized to the site of vascular damage or plaque rupture, coupled with the high-shear rheological environment of the coronary vessel, results in the activation and subsequent aggregation of platelets and the formation of an insoluble matrix of fibrin resulting in a platelet-rich thrombus. 