ABSTRACT

The majority of acute coronary events are related to disruption of a ‘Vulnerable’ atherosclerotic plaque, leading to the exposure of subintimal contents and the formation of a platelet-rich thrombus. The importance of platelet activation in the events leading to vessel occlusion in acute coronary syndromes is supported by the clear clinical benefit of treatment with aspirin for both primary and secondary prevention strategies.1 This process, however, is complex and influenced by a wide variety of cellular and plasmaderived mediators that determine the balance between occlusive and non-occlusive thrombosis. In this chapter, the events that contribute to the process of thrombo sis in the setting of the atherosclerotic plaque will be reviewed.