Cynthia M. Westerhout, MSc^1,2 and Eric Boersma, PhD¹
From the ¹Department of Cardiology, Erasmus Medical Centre, Rotterdam, The Netherlands and the ²University of Alberta, Edmonton, AB.

Introduction
The chain of events leading to acute coronary syndromes (ACS), including unstable angina (UA) and non-ST-segment elevation (NSTE) or ST-segment elevation myocardial infarction (STEMI), is triggered by the disruption of an atherosclerotic plaque, which leads to the formation of a platelet-rich thrombus within a coronary artery.^1,2 The inhibition of platelet aggregation is fundamental to the treatment of these patients; however, standard antiplatelet agents such as aspirin do not completely obstruct this activity. Advances in understanding the pathophysiology of ACS have to the recognition of the activation of the glycoprotein IIb/IIIa (Gp IIb/IIIa) receptors on platelets as the final common pathway leading to platelet aggregation. With this target in mind, pharmacological treatment of ACS has been propelled into a new era with agents that completely inhibit platelet aggregation.