{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T11:41:22Z","timestamp":1790077282394,"version":"4.0.1"},"reference-count":21,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[2017,8]]},"abstract":"<jats:sec>\n            <jats:title>Background and Purpose\u2014<\/jats:title>\n            <jats:p>Limited real-world data exist comparing each non\u2013vitamin K antagonist oral anticoagulant (NOAC) to warfarin in patients with nonvalvular atrial fibrillation who have had a previous ischemic stroke or transient ischemic attack.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods\u2014<\/jats:title>\n            <jats:p>Using MarketScan claims from January 2012 to June 2015, we identified adults newly initiated on oral anticoagulation, with \u22652 diagnosis codes for nonvalvular atrial fibrillation, a history of previous ischemic stroke\/transient ischemic attack, and \u2265180 days of continuous medical and prescription benefits before anticoagulation initiation. Three analyses were performed comparing 1:1 propensity score\u2013matched cohorts of apixaban versus warfarin (n=2514), dabigatran versus warfarin (n=1962), and rivaroxaban versus warfarin (n=5208). Patients were followed until occurrence of a combined end point of ischemic stroke and intracranial hemorrhage (ICH) or major bleed, switch\/discontinuation of index oral anticoagulation, insurance disenrollment, or end of follow-up. Mean follow-up was 0.5 to 0.6 years for all matched cohorts.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results\u2014<\/jats:title>\n            <jats:p>Using Cox regression, neither apixaban nor dabigatran reduced the combined primary end point of ischemic stroke or ICH (hazard ratio [HR], 0.70; 95% confidence interval [CI], 0.33\u20131.48 and HR, 0.53; 95% CI, 0.26\u20131.07) and had nonsignificant effect on hazards of major bleeding (HR, 0.79; 95% CI, 0.38\u20131.64 and HR, 0.58; 95% CI, 0.26\u20131.27) versus warfarin. Rivaroxaban reduced the combined end point of ischemic stroke or ICH (HR, 0.45; 95% CI, 0.29\u20130.72) without an effect on major bleeding (HR, 1.07; 95% CI, 0.71\u20131.61). ICH occurred at rates of 0.16 to 0.61 events per 100 person-years in the 3 NOAC analyses, with no significant difference for any NOAC versus warfarin.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>Results from our study of the 3 NOACs versus warfarin in nonvalvular atrial fibrillation patients with a previous history of stroke\/transient ischemic attack are relatively consistent with their respective phase III trials and previous stroke\/transient ischemic attack subgroup analyses. All NOACs seemed no worse than warfarin in respect to ischemic stroke, ICH, or major bleeding risk.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/strokeaha.117.017474","type":"journal-article","created":{"date-parts":[[2017,6,28]],"date-time":"2017-06-28T00:55:21Z","timestamp":1498611321000},"page":"2142-2149","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":88,"title":["Effectiveness and Safety of Apixaban, Dabigatran, and Rivaroxaban Versus Warfarin in Patients With Nonvalvular Atrial Fibrillation and Previous Stroke or Transient Ischemic Attack"],"prefix":"10.1161","volume":"48","author":[{"given":"Craig I.","family":"Coleman","sequence":"first","affiliation":[{"name":"From the University of Connecticut School of Pharmacy, Storrs (C.I.C.); Department of Emergency Medicine, Baylor College of Medicine, Houston, TX (W.F.P.); Crystal Run Healthcare, Middletown, NY (T.J.B.); Ayer Neuroscience Institute, Hartford HealthCare, CT (M.J.A.); and Department of Neurology, Hartford Hospital, CT (M.J.A.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W. Frank","family":"Peacock","sequence":"additional","affiliation":[{"name":"From the University of Connecticut School of Pharmacy, Storrs (C.I.C.); Department of Emergency Medicine, Baylor College of Medicine, Houston, TX (W.F.P.); Crystal Run Healthcare, Middletown, NY (T.J.B.); Ayer Neuroscience Institute, Hartford HealthCare, CT (M.J.A.); and Department of Neurology, Hartford Hospital, CT (M.J.A.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas J.","family":"Bunz","sequence":"additional","affiliation":[{"name":"From the University of Connecticut School of Pharmacy, Storrs (C.I.C.); Department of Emergency Medicine, Baylor College of Medicine, Houston, TX (W.F.P.); Crystal Run Healthcare, Middletown, NY (T.J.B.); Ayer Neuroscience Institute, Hartford HealthCare, CT (M.J.A.); and Department of Neurology, Hartford Hospital, CT (M.J.A.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark J.","family":"Alberts","sequence":"additional","affiliation":[{"name":"From the University of Connecticut School of Pharmacy, Storrs (C.I.C.); Department of Emergency Medicine, Baylor College of Medicine, Houston, TX (W.F.P.); Crystal Run Healthcare, Middletown, NY (T.J.B.); Ayer Neuroscience Institute, Hartford HealthCare, CT (M.J.A.); and Department of Neurology, Hartford Hospital, CT (M.J.A.)."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0000000000000040"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(12)70092-3"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(10)70274-X"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(12)70042-X"},{"key":"e_1_3_3_6_2","unstructured":"Truven Health Analytics. 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