ABSTRACT
As discussed in Chapter 1, because atherothrombosis is the precipitating event in myocardial infarction (MI), stroke, and critical limb ischemia [1], agents to reduce the risk of these events are desirable. The active components of a thrombus are platelets and fibrin, and, while often present, red and white blood cells may be described as minor participants, although erythrocytes can enhance platelet aggregation by releasing adenosine diphosphate (ADP). It follows that effective antithrombotic therapy should be directed towards both platelets and the coagulation pathway that concludes with fibrin formation. Aspirin, heparin, and warfarin have been, and remain, the most commonly used drugs for reducing both the short-term and long-term risk of thrombosis, be it arterial or venous. However, despite commonality of final clinical effect, these drugs have radically different modes of action.
