Usefulness and safety of vorapaxar in patients with non-ST-segment elevation
acute coronary syndrome undergoing percutaneous coronary intervention (from the
TRACER Trial).
Author(s): Valgimigli M(1), Tricoci P(2), Huang Z(2), Aylward PE(3), Armstrong PW(4), Van de
Werf F(5), Leonardi S(6), White HD(7), Widimsky P(8), Harrington RA(9), Cequier
A(10), Chen E(11), Lokhnygina Y(2), Wallentin L(12), Strony J(13), Mahaffey
KW(9), Moliterno DJ(14).
Affiliation(s): Author information:
(1)Thoraxcenter, Erasmus MC, Rotterdam, The Netherlands. Electronic address:
m.valgimigli@erasmusmc.nl.
(2)Duke Clinical Research Institute, Durham, North Carolina.
(3)Flinders University and Medical Centre, Bedford Park, Adelaide, Australia.
(4)Division of Cardiology, University of Alberta, Edmonton, Canada.
(5)Department of Cardiology, University of Leuven, Leuven, Belgium.
(6)Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.
(7)Green Lane Cardiovascular Service, Auckland, New Zealand.
(8)University Hospital Kralovske Vinohrady, Charles University, Prague, Czech
Republic.
(9)Department of Medicine, Stanford University, Stanford, California.
(10)Hospital Universitari de Bellvitge, Universitat de Barcelona, Barcelona, Spain.
(11)Bayer HealthCare Pharmaceuticals Inc., Whippany, New Jersey.
(12)Department of Medical Sciences, Uppsala Clinical Research Center, Uppsala,
Sweden.
(13)Merck & Co., Whitehouse Station, New Jersey.
(14)Division of Cardiovascular Medicine, Gill Heart Institute, University of
Kentucky, Lexington, Kentucky.
Publication date & source: 2014, Am J Cardiol. , 114(5):665-73
The therapeutic potential of vorapaxar in patients with non-ST-segment elevation
acute coronary syndrome undergoing percutaneous coronary intervention (PCI) is
unknown. This prespecified analysis of a postrandomization subgroup evaluated the
effects of vorapaxar compared with placebo among Thrombin Receptor Antagonist for
Clinical Event Reduction in Acute Coronary Syndrome (TRACER) participants
undergoing PCI, focusing on the implanted stent type (drug-eluting stent [DES] vs
bare-metal stent [BMS]). Among 12,944 recruited patients, 7,479 (57.8%) underwent
PCI during index hospitalization, and 3,060 (40.9%) of those patients received
exclusively BMS, whereas 4,015 (53.7%) received DES. The median (twenty-fifth,
seventy-fifth percentiles) duration of thienopyridine therapy was 133 days (47,
246) with BMS and 221 days (88, 341) with DES. At 2 years among patients
undergoing PCI, the primary (cardiovascular death, myocardial infarction, stroke,
recurrent ischemia with rehospitalization, or urgent coronary revascularization)
and secondary (cardiovascular death, myocardial infarction, or stroke) end points
did not differ between vorapaxar and placebo groups, which was consistent with
the treatment effect observed in the overall study population (p value for
interaction = 0.540). However, the treatment effect trended greater (p value for
interaction = 0.069) and the risk for bleeding in patients taking vorapaxar
versus placebo appeared attenuated in BMS-only recipients. After adjustment for
confounders, the interaction was no longer significant (p value = 0.301). The
covariate that mostly explained the stent-type-by-treatment interaction was the
duration of clopidogrel therapy. In conclusion, among patients with PCI, the
effect of vorapaxar is consistent with the overall TRACER results. Patients who
received a BMS underwent shorter courses of clopidogrel therapy and displayed
trends toward greater ischemic benefit from vorapaxar and lesser bleeding risk,
compared with patients who received a DES.
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