Platelet aggregation and thrombus formation represent the basic mechanism for clinical, electrocardiographic, and biomarker changes consistent with acute coronary syndrome. Various oral and intravenous formulations of platelet function inhibitors have been developed to help decrease platelet aggregation due to acute atherosclerotic plaque rupture. In this article, we review the various mechanisms, pharmacokinetics/pharmacodynamics, and the key clinical trials related to the platelet inhibitors that form the basis for current recommendations of their use in the ST elevation myocardial infarction guidelines by the American College of Cardiology/American Heart Association.
- Acute coronary syndrome
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