Key result
Vorapaxar added to standard dual antiplatelet therapy is effective in the secondary prevention of recurrent thrombotic events among patients with previous atherothrombosis, but increases major bleeding.
Why the study?
To summarize up-to-date literature on the pharmacokinetics, pharmacodynamics, and clinical efficacy of vorapaxar and propose future directions of research.
Does vorapaxar reduce thrombotic cardiovascular events in patients with a history of myocardial infarction or peripheral arterial disease?
Does vorapaxar reduce thrombotic cardiovascular events in patients with a history of myocardial infarction or peripheral arterial disease?
This review highlights that vorapaxar reduces recurrent thrombotic events in patients with prior MI or PAD when added to standard antiplatelet therapy, though it increases major bleeding risk.
Highlights bleeding risk caution with vorapaxar in secondary prevention; supports prior RCT efficacy while extending to newer P2Y12 inhibitors.
Antiplatelet agents are the standard of practice in the management of atherosclerosis and acute coronary syndrome. 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 and inhibits thrombin-induced and thrombin receptor agonist peptide-induced platelet aggregation. The Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events-Thrombolysis in Myocardial Infarction 50 (TRA 2°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. TRA 2°P-TIMI 50 trial showed that the use of vorapaxar (2.5 mg once/daily) in addition to standard dual antiplatelet therapy 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 Vorapaxar Therapy in Patients With Prior Myocardial Infarction Treated With Newer Generation P2Y12 Receptor Inhibitors Prasugrel and Ticagrelor (VORA-PRATIC) 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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Chaudhary et al. (2021) conducted a review in Cardiovascular Diseases. Vorapaxar was evaluated. Vorapaxar added to standard dual antiplatelet therapy is effective in the secondary prevention of recurrent thrombotic events among patients with previous atherothrombosis, but increases major bleeding.
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