Thrombosis within the target vessel is one of the most feared complications
associated with coronary intervention, as it is often associated with seve
re adverse clinical sequelae. This thrombosis is mediated via the activatio
n and aggregation of platelets and therefore considerable effort has been d
irected at ways of inhibiting platelet function. It is now mandatory to con
sider the use of two and often three different antiplatelet agents, particu
larly when intracoronary stents are inserted. Using these regimes, many of
the adverse clinical outcomes associated with platelet activation can be re
duced.