Vorapaxar in XXXX Management.

@entity1 @entity64 @entity932 @entity583 @entity548 @entity63 @entity3657 @entity1397 @entity117 @entity715 @entity731 @entity8781 @entity65
OBJECTIVE: To review the pharmacology, efficacy, and safety of vorapaxar, a @entity8781 ( @entity8781 ) antagonist, in the management of @entity731 . DATA SOURCES: Peer-reviewed clinical trials and review articles were identified from MEDLINE and Current Content database (both 1966 to December 31, 2014) using the search terms vorapaxar and protease activator receptor antagonist. STUDY SELECTION AND DATA EXTRACTION: A total of 30 clinical studies were identified (16 clinical trials, including subanalyses, 14 related to pharmacology, pharmacokinetics, and pharmacodynamics and drug interactions). DATA SYNTHESIS: Two phase III clinical trials with vorapaxar have been published. In @entity1 with non-ST segment elevation @entity583 ( @entity583 ), vorapaxar failed to significantly reduce the primary efficacy end point (composite of @entity65 , @entity583 , @entity64 , recurrent @entity63 with hospitalization, and urgent coronary revascularization). Conversely, in a study of secondary prevention for @entity1 with @entity65 , the composite end point of @entity65 , @entity583 , or @entity64 was significantly reduced. In both trials, the safety end points of major/minor @entity548 were increased compared with placebo. In the secondary prevention trial, an increased incidence of @entity932 led to the exclusion of @entity1 with a prior history of @entity64 . CONCLUSION: Vorapaxar is approved for use with @entity117 and/or @entity1397 in the secondary prevention of cardiovascular events in stable @entity1 with @entity3657 or a history of @entity583 . However, the addition of vorapaxar to other antiplatelets can significantly increase the risk of @entity548 . It is, therefore, essential to balance the need for further reduction of risk of @entity715 event with @entity1 's individual @entity548 risk.
