Improving Outcomes in Cardiovascular Diseases- A Review on V
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Antiplatelet agents are the standard of practice in the management of atherosclerosis and acute coronary syndrome (ACS). In contrast to the available antiplatelet agents, vorapaxar represents a novel mechanism of action.

It is an antagonist of the platelet protease-activated receptor-1 (PAR-1) and inhibits thrombin-induced and thrombin receptor agonist peptide (TRAP)- induced platelet aggregation. The TRA2 P-TIMI 50 trial led to the approval of vorapaxar by the Food and Drug Administration and European Medicines Agency for the reduction of thrombotic cardiovascular events in patients with a history of myocardial infarction (MI) or peripheral arterial disease.

TRA2 P-TIMI 50 trial showed that the use of vorapaxar (2.5 mg once/daily) in addition to standard dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 receptor inhibitor, was effective in the secondary prevention of recurrent thrombotic events among patients with previous atherothrombosis, particularly in patients with prior MI; at the expense of an increase in major bleeding.

Another recently published VORA-PRATIC (Vorapaxar in Patients with Prior Myocardial Infarction Treated with prasugrel and ticagrelor) study showed that among post-MI patients treated with potent P2Y12 inhibitors (prasugrel or ticagrelor), vorapaxar reduced platelet-driven global thrombogenicity, an effect that persisted, albeit attenuated, in the absence of aspirin.

The current review summarizes an up to date literature on pharmacokinetics, pharmacodynamics, and clinical efficacy of vorapaxar and proposes future directions of research.

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