The management of the acute coronary syndrome has changed dramatically in the past decade as a direct consequence of our enhanced understanding of the pathophysiology of coronary plaque instability and the role of the thrombotic response to rupture or erosion of a diseased coronary arterial plaque.Exposure of free flowing blood to the intensely procoagulant environment of the unstable plaque leads to platelet adhesion, activation and aggregation.Therapeutic agents such as aspirin, thienopyridines, and 2b3a inhibitors inhibit and/or compete for receptors on the platelet, preventing further platelet aggregation or even disaggregating platelet clots.Newer antiplatelet agents will also be discussed, such as the thrombin receptor antagonist and novel P2Y 12 inhibitors.Simultaneously, activation of soluble coagulation factors lead to factor Xa activation and ultimately thrombin, which cleaves fibrinogen to form fibrin, the component of the protein strands which bind red blood cells and platelet clumbs, ultimately forming intravascular clots.Conventional agents used world wide include heparin, low molecular heparin, and more recently pentasaccharide and direct-acting antithrombins such as bivalirudin.Emerging oral anticoagulants which inhibit thrombin or Xa hold a great deal of promise, and are under active clinical development.