ABSTRACT
Atherothrombosis, the common pathogenesis of myocardial infarction, peripheral artery disease and ischemic stroke, may be defined as atherosclerosis with superimposed thrombotic complications (Blecic, 1998; Gent, 1998a; Libby, 1998; Dormandy, 1998; Fuster et al., 1998; Haberl and Dembowski, 1999; Guillot, 1999; Nenci, 1999). In the pathogenesis of atherohrombosis the involvement of platelet activation is critical (Fuster et al., 1992a and 1992b; Ware and Heistad, 1993; Del Zoppo, 1998; Cimminiello and Toschi, 1999; Prentice, 1999). Many clinical trials of secondary prevention after symptomatic artery disease have evaluated the benefit of long-term use of antiplatelet drugs in reducing the risk of subsequent vascular events (Antiplatelet Trialists’ Collaboration, 1988 and 1994).
