vorapaxar and Angina--Unstable

Platelet activation and thrombin formation play significant roles in the pathophysiology of acute coronary syndrome. To overcome this pathophysiology, antiplatelet agents are utilized to decrease platelet aggregation and anticoagulants to decrease thrombin formation. Current antiplatelet agents are designed to inhibit various mediators of platelet activation, such as thromboxane A2 and adenosine diphosphate, and platelet-surface receptors (e.g., glycoprotein IIb/IIIa receptors). The rationale for upstream versus deferred administration of antiplatelet therapy in patients scheduled for percutaneous intervention and the current ACC/AHA guidelines for the management of patients with unstable angina/non-ST-segment myocardial infarction are discussed. The next-generation antiplatelet drugs are in various stages of clinical development, with unique differentiating mechanistic and pharmacokinetic properties. The newer P2Y12 thienopyridine receptor antagonists and protease receptor inhibitor are also examined, in addition to the rationale of various outcome studies evaluating the efficacy and safety of the different agents.

Topics: Acute Coronary Syndrome; Adenosine Monophosphate; Angina, Unstable; Aspirin; Blood Platelets; Cardiac Catheterization; Fibrinolytic Agents; Humans; Lactones; Myocardial Infarction; Platelet Activation; Platelet Aggregation Inhibitors; Practice Guidelines as Topic; Pyridines; Treatment Outcome