{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T01:23:07Z","timestamp":1789521787885,"version":"build-2803163510"},"reference-count":44,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2018,2,6]]},"abstract":"\n Background<\/jats:title>\n \n We examined the cardiovascular risk of abatacept compared with tumor necrosis factor (\n TNF<\/jats:styled-content>\n ) inhibitors in patients with rheumatoid arthritis with and without diabetes mellitus (\n DM<\/jats:styled-content>\n ).\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n We conducted a cohort study of patients with rheumatoid arthritis who newly started abatacept or\n TNF<\/jats:styled-content>\n inhibitors using claims data from Medicare and MarketScan. The primary outcome was a composite cardiovascular end point of myocardial infarction (\n MI<\/jats:styled-content>\n ), stroke\/transient ischemic attack, and coronary revascularization. To account for >60 baseline characteristics, abatacept initiators were 1:1 propensity score (\n PS<\/jats:styled-content>\n ) matched to\n TNF<\/jats:styled-content>\n initiators in each database. Cox proportional hazards models estimated hazard ratio (\n HR<\/jats:styled-content>\n ) and 95% confidence interval (\n CI<\/jats:styled-content>\n ) in the\n PS<\/jats:styled-content>\n \u2010matched cohort per database. A fixed\u2010effects meta\u2010analysis pooled database\u2010specific\n HR<\/jats:styled-content>\n s. We included a total of 13\u00a0039\n PS<\/jats:styled-content>\n \u2010matched pairs of abatacept and\n TNF<\/jats:styled-content>\n inhibitor initiators (6103 pairs in Medicare and 6936 pairs in MarketScan). A total of 34.7% in Medicare and 19.8% in MarketScan had baseline\n DM<\/jats:styled-content>\n . The\n HR<\/jats:styled-content>\n (95%\n CI<\/jats:styled-content>\n ) for the primary outcome associated with abatacept use versus\n TNF<\/jats:styled-content>\n inhibitor was 0.81 (0.66\u20130.99) in Medicare and 0.95 (0.74\u20131.23) in MarketScan, with a pooled\n HR<\/jats:styled-content>\n of 0.86 (95% CI, 0.73\u20131.01;\n P<\/jats:italic>\n =0.3 for heterogeneity). The risk of the primary outcome was lower in abatacept initiators versus\n TNF<\/jats:styled-content>\n inhibitors in the\n DM<\/jats:styled-content>\n subgroup, with a pooled\n HR<\/jats:styled-content>\n of 0.74 (95% CI, 0.57\u20130.96;\n P<\/jats:italic>\n =0.7 for heterogeneity), but not in the non\u2010\n DM<\/jats:styled-content>\n subgroup, with a pooled\n HR<\/jats:styled-content>\n of 0.94 (95% CI, 0.77\u20131.14;\n P<\/jats:italic>\n =0.4 for heterogeneity).\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n In this large population\u2010based cohort of patients with rheumatoid arthritis, abatacept use appeared to be associated with a modestly reduced cardiovascular risk when compared with\n TNF<\/jats:styled-content>\n inhibitor use, particularly in patients with DM.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.117.007393","type":"journal-article","created":{"date-parts":[[2018,1,25]],"date-time":"2018-01-25T01:10:26Z","timestamp":1516842626000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":64,"title":["Comparative Cardiovascular Risk of Abatacept and Tumor Necrosis Factor Inhibitors in Patients With Rheumatoid Arthritis With and Without Diabetes Mellitus: A Multidatabase Cohort Study"],"prefix":"10.1161","volume":"7","author":[{"given":"Eun Ha","family":"Kang","sequence":"first","affiliation":[{"name":"Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA"},{"name":"Division of Rheumatology, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yinzhu","family":"Jin","sequence":"additional","affiliation":[{"name":"Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory","family":"Brill","sequence":"additional","affiliation":[{"name":"Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer","family":"Lewey","sequence":"additional","affiliation":[{"name":"Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA"},{"name":"Division of Cardiology, University of Pennsylvania, Philadelphia, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisabetta","family":"Patorno","sequence":"additional","affiliation":[{"name":"Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rishi J.","family":"Desai","sequence":"additional","affiliation":[{"name":"Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seoyoung C.","family":"Kim","sequence":"additional","affiliation":[{"name":"Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA"},{"name":"Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard Medical School, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.1780370408"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000054612.26458.B2"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.20853"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.24836"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1002\/1529-0131(200112)44:12<2737::AID-ART460>3.0.CO;2-#"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1136\/ard.2006.059980"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1136\/ard.2009.122226"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1136\/ard.2006.053488"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1186\/ar3442"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2007.01.004"},{"key":"e_1_3_3_12_2","first-page":"2425","article-title":"Metabolic syndrome and subclinical atherosclerosis in rheumatoid arthritis","volume":"33","author":"Dessein PH","year":"2006","unstructured":"Dessein PH, Tobias M, Veller MG. 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