Cynthia M. Westerhout, MSc1,2 and Eric Boersma, PhD1
From the 1Department of Cardiology, Erasmus Medical Centre, Rotterdam, The Netherlands and the 2University of Alberta, Edmonton, AB.
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.
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