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dc.contributor.authorRosser, G.
dc.contributor.authorTricoci, P.
dc.contributor.authorMorrow, D.
dc.contributor.authorChristopoulos, C.
dc.contributor.authorNiespialowska-Steuden, M.
dc.contributor.authorKozarski, Robert
dc.contributor.authorWilcox, R.
dc.contributor.authorGorog, Diana
dc.date.accessioned2014-10-07T11:00:45Z
dc.date.available2014-10-07T11:00:45Z
dc.date.issued2014-11
dc.identifier.citationRosser , G , Tricoci , P , Morrow , D , Christopoulos , C , Niespialowska-Steuden , M , Kozarski , R , Wilcox , R & Gorog , D 2014 , ' PAR-1 antagonist vorapaxar favorably improves global thrombotic status in patients with coronary disease ' , Journal of Thrombosis and Thrombolysis , vol. 38 , no. 4 , pp. 423-429 . https://doi.org/10.1007/s11239-014-1075-4
dc.identifier.issn1573-742x
dc.identifier.otherPURE: 2929309
dc.identifier.otherPURE UUID: d07ca9dc-05f5-4b4b-af97-c2d02109ebc0
dc.identifier.otherScopus: 84910108335
dc.identifier.urihttp://hdl.handle.net/2299/14549
dc.description.abstractTo assess the effect of vorapaxar on global thrombotic and thrombolytic status. The propensity for thrombus formation is determined by the balance between prothrombotic factors and endogenous thrombolysis. Impaired thrombolytic status increases cardiovascular risk. Vorapaxar is a novel, oral, protease-activated receptor-1 antagonist that inhibits thrombin-induced platelet activation. In the TRACER and TRA 2°P-TIMI 50 studies, patients with acute coronary syndromes and established atherosclerosis were randomized to vorapaxar 2.5 mg daily or placebo, in addition to standard care. In 57 patients enrolled in a single center, blood was tested with the point-of-care global thrombosis test, on and off treatment. This automated test employs non-anticoagulated blood to assess thrombotic and thrombolytic status, measuring the time required to form a shear-induced thrombus under physiological conditions (occlusion time, OT), and subsequently, the time to achieve endogenous lysis of the thrombus (lysis time, LT). Patients on vorapaxar exhibited longer OT on vs. off treatment [median 561 s (interquartile range 422-654) vs. 372 s(338-454), P = 0.003] and shorter LT on treatment than off [1,158 s(746-1,492) vs. 1,733 s(1,388-2,230), P = 0.016]. Patients on placebo showed no difference in OT [419 s(343-514) vs. 411 s(346-535), P = 0.658] or LT [1,236 s(985-1,594) vs. 1,400 s(1,092-1,686), P = 0.524] on and off treatment. During treatment, OT was longer in patients taking vorapaxar [561 s(422-654) vs. 419 s(343-514), P = 0.009], but LT was similar in vorapaxar and placebo arms [1,158 s(746-1,492) vs. 1,236 s(985-1,594), P = 0.277]. Vorapaxar prolongs OT and shortens LT, with favorable effects on thrombotic and thrombolytic status. In addition to its antiplatelet effect, vorapaxar may enhance endogenous thrombolysis, which is frequently impaired in coronary disease.en
dc.format.extent7
dc.language.isoeng
dc.relation.ispartofJournal of Thrombosis and Thrombolysis
dc.titlePAR-1 antagonist vorapaxar favorably improves global thrombotic status in patients with coronary diseaseen
dc.contributor.institutionDepartment of Psychology
dc.contributor.institutionCentre for Lifespan and Chronic Illness Research
dc.contributor.institutionHealth Services and Medicine
dc.contributor.institutionSchool of Life and Medical Sciences
dc.contributor.institutionHealth & Human Sciences Research Institute
dc.contributor.institutionCentre for Postgraduate Medicine
dc.contributor.institutionPostgraduate Medicine
dc.contributor.institutionPharmacology and Clinical Science Research
dc.description.statusPeer reviewed
dc.relation.schoolSchool of Life and Medical Sciences
dcterms.dateAccepted2014-11
rioxxterms.versionVoR
rioxxterms.versionofrecordhttps://doi.org/10.1007/s11239-014-1075-4
rioxxterms.typeJournal Article/Review
herts.preservation.rarelyaccessedtrue


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