{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T05:32:31Z","timestamp":1777440751142,"version":"3.51.4"},"reference-count":19,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2017,12,18]],"date-time":"2017-12-18T00:00:00Z","timestamp":1513555200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["European Heart Journal: Acute Cardiovascular Care"],"published-print":{"date-parts":[[2019,3]]},"abstract":"<jats:sec><jats:title>Background:<\/jats:title><jats:p> Despite dual antiplatelet therapy, persistent thrombin generation and thrombin-mediated platelet activation account in part for the residual risk of atherothrombotic disease among patients with prior acute coronary syndrome (ACS). Inhibition of thrombin generation among high-risk ACS patients (biomarker-positive ACS) with the factor Xa inhibitor rivaroxaban may limit ongoing thrombus formation and myocardial necrosis and thereby improve clinical outcomes. <\/jats:p><\/jats:sec><jats:sec><jats:title>Objectives and methods:<\/jats:title><jats:p> ATLAS ACS 2-TIMI 51 was a double-blind, placebo-controlled clinical trial that randomized ACS patients to either rivaroxaban 2.5 mg b.i.d., rivaroxaban 5 mg b.i.d., or placebo plus standard-of-care antiplatelet therapy for a mean of 13.1 months and up to 31 months ( N=15,526). This post-hoc analysis evaluates the safety and efficacy of rivaroxaban among biomarker-positive ACS patients with and without a history of prior stroke of transient ischemic attack in the ATLAS ACS 2-TIMI 51 trial. <\/jats:p><\/jats:sec><jats:sec><jats:title>Results:<\/jats:title><jats:p> A total of 12,626 biomarker-positive ACS patients were included in this analysis. Among biomarker-positive patients without a prior history of stroke or transient ischemic attack, rivaroxaban 2.5 b.i.d. was associated with a reduction in the primary efficacy endpoint (composite of cardiovascular death, myocardial infarction, or stroke) as compared with placebo (hazard ratio=0.80, 95% confidence interval (0.68\u20130.94), p=0.007) at the expense of an increase in non-coronary-artery-bypass-graft-related Thrombolysis in Myocardial Infarction major bleeding (1.9% vs. 0.7%, p&lt;0.0001), but not a significant increase in either intracranial hemorrhage (0.4% vs. 0.2%, p=0.11) or fatal bleeding (0.1% vs. 0.3%, p=0.16). <\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion:<\/jats:title><jats:p> Rivaroxaban 2.5 mg b.i.d. was associated with a significant reduction in the composite of cardiovascular death, myocardial infarction, or stroke with no increase in fatal bleeding. Biomarker-positive patients with no prior history of stroke or transient ischemic attack may be a optimal target population to receive \u201cdual pathway\u201d therapy with rivaroxaban plus dual antiplatelet therapy for secondary prevention following ACS. <\/jats:p><\/jats:sec>","DOI":"10.1177\/2048872617745003","type":"journal-article","created":{"date-parts":[[2017,12,18]],"date-time":"2017-12-18T11:32:06Z","timestamp":1513596726000},"page":"186-193","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":12,"title":["Safety and efficacy of rivaroxaban for the secondary prevention following acute coronary syndromes among biomarker-positive patients: Insights from the ATLAS ACS 2-TIMI 51 trial"],"prefix":"10.1093","volume":"8","author":[{"given":"Serge","family":"Korjian","sequence":"first","affiliation":[{"name":"PERFUSE Study Group. Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eugene","family":"Braunwald","sequence":"additional","affiliation":[{"name":"TIMI Study Group, Cardiovascular Division, Department of Medicine, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, MA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yazan","family":"Daaboul","sequence":"additional","affiliation":[{"name":"PERFUSE Study Group. Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Freek","family":"Verheugt","sequence":"additional","affiliation":[{"name":"Radboud University, Nijmegen University Medical Center, Nijmegen, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christoph","family":"Bode","sequence":"additional","affiliation":[{"name":"University Hospital Freiburg, Freiburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michal","family":"Tendera","sequence":"additional","affiliation":[{"name":"Medical University of Silesia, Katowice, Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Purva","family":"Jain","sequence":"additional","affiliation":[{"name":"PERFUSE Study Group. Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexei","family":"Plotnikov","sequence":"additional","affiliation":[{"name":"Johnson & Johnson Pharmaceutical Research and Development, Raritan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul","family":"Burton","sequence":"additional","affiliation":[{"name":"Johnson & Johnson Pharmaceutical Research and Development, Raritan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C Michael","family":"Gibson","sequence":"additional","affiliation":[{"name":"PERFUSE Study Group. 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