{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T18:48:16Z","timestamp":1791571696077,"version":"4.3.4"},"reference-count":27,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2008,3]]},"abstract":"<jats:p>\n            <jats:bold>\n              <jats:italic>Objective\u2014<\/jats:italic>\n            <\/jats:bold>\n            The clinical use of venous stents is increasing dramatically. Although antiplatelet agents are required for arterial stent patency, optimal thrombo-prophylaxis after venous stenting remains undefined. To address this issue, PD0348292, a direct Factor Xa inhibitor, was compared with antiplatelet therapy in a porcine venous stent model.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Methods and Results\u2014<\/jats:italic>\n            <\/jats:bold>\n            Four hours before stent deployment, pigs (n=5 to 6 per group) received oral PD0348292 at 0.4, 0.9, 4.3 mg\/kg, or 0.4 mg\/kg plus aspirin (325 mg). Aspirin, clopidogrel (75 mg), aspirin plus clopidogrel, or vehicle (n=10) were administered daily for 2 days before the procedure. Two hours after stent placement, thrombi were quantified by autologous\n            <jats:sup>111<\/jats:sup>\n            In-platelet content and weights. Thrombus weight and platelet deposition were significantly reduced by PD0348292 at 0.4 (49\u00b179 mg and 110\u00b1145\u00d710\n            <jats:sup>6<\/jats:sup>\n            \/cm\n            <jats:sup>2<\/jats:sup>\n            ), 0.9 (5\u00b16 mg and 107\u00b1128\u00d710\n            <jats:sup>6<\/jats:sup>\n            \/cm\n            <jats:sup>2<\/jats:sup>\n            ), 4.3 mg\/kg (0\u00b10 mg and 87\u00b1125\u00d710\n            <jats:sup>6<\/jats:sup>\n            \/cm\n            <jats:sup>2<\/jats:sup>\n            ), and PD348292 plus aspirin (20\u00b140 mg and 157\u00b170\u00d710\n            <jats:sup>6<\/jats:sup>\n            \/cm\n            <jats:sup>2<\/jats:sup>\n            ) compared with vehicle (402\u00b1226 mg; 584\u00b1454\u00d710\n            <jats:sup>6<\/jats:sup>\n            \/cm\n            <jats:sup>2<\/jats:sup>\n            ). Despite prolonging bleeding times and inhibiting platelet aggregation, neither aspirin (567\u00b1683 mg and 533\u00b1622\u00d710\n            <jats:sup>6<\/jats:sup>\n            \/cm\n            <jats:sup>2<\/jats:sup>\n            ), clopidogrel (404\u00b1349 mg and 178\u00b1101\u00d710\n            <jats:sup>6<\/jats:sup>\n            \/cm\n            <jats:sup>2<\/jats:sup>\n            ), nor aspirin plus clopidogrel (247\u00b1261 mg and 231\u00b1266\u00d710\n            <jats:sup>6<\/jats:sup>\n            \/cm\n            <jats:sup>2<\/jats:sup>\n            ) significantly decreased stent thrombosis.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Conclusions\u2014<\/jats:italic>\n            <\/jats:bold>\n            PD0348292 completely inhibited thrombosis after venous stenting. Platelet accretion in these venous thrombi appear to involve pathways distinct from arachidonate metabolism or ADP P\n            <jats:sub>2<\/jats:sub>\n            Y\n            <jats:sub>12<\/jats:sub>\n            receptor activation.\n          <\/jats:p>","DOI":"10.1161\/atvbaha.107.158691","type":"journal-article","created":{"date-parts":[[2007,12,21]],"date-time":"2007-12-21T02:07:07Z","timestamp":1198202827000},"page":"413-418","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":24,"title":["Iliac Venous Stenting"],"prefix":"10.1161","volume":"28","author":[{"suffix":"II","given":"Robert D.","family":"McBane","sequence":"first","affiliation":[{"name":"From the Section of Hematology Research (R.D.M., K.K., W.W.), Mayo Clinic, Rochester, Minn; Cardiovascular, Metabolic, and Endocrine Diseases Biology (R.J.L., S.M.B.), Pfizer Global Research and Development, Ann Arbor, Mich; and the Division of Cardiology (R.D.M., W.W.), Mayo Clinic, Rochester, Minn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr","given":"Robert J.","family":"Leadley","sequence":"additional","affiliation":[{"name":"From the Section of Hematology Research (R.D.M., K.K., W.W.), Mayo Clinic, Rochester, Minn; Cardiovascular, Metabolic, and Endocrine Diseases Biology (R.J.L., S.M.B.), Pfizer Global Research and Development, Ann Arbor, Mich; and the Division of Cardiology (R.D.M., W.W.), Mayo Clinic, Rochester, Minn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sangita M.","family":"Baxi","sequence":"additional","affiliation":[{"name":"From the Section of Hematology Research (R.D.M., K.K., W.W.), Mayo Clinic, Rochester, Minn; Cardiovascular, Metabolic, and Endocrine Diseases Biology (R.J.L., S.M.B.), Pfizer Global Research and Development, Ann Arbor, Mich; and the Division of Cardiology (R.D.M., W.W.), Mayo Clinic, Rochester, Minn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Krzysztof","family":"Karnicki","sequence":"additional","affiliation":[{"name":"From the Section of Hematology Research (R.D.M., K.K., W.W.), Mayo Clinic, Rochester, Minn; Cardiovascular, Metabolic, and Endocrine Diseases Biology (R.J.L., S.M.B.), Pfizer Global Research and Development, Ann Arbor, Mich; and the Division of Cardiology (R.D.M., W.W.), Mayo Clinic, Rochester, Minn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Waldemar","family":"Wysokinski","sequence":"additional","affiliation":[{"name":"From the Section of Hematology Research (R.D.M., K.K., W.W.), Mayo Clinic, Rochester, Minn; Cardiovascular, Metabolic, and Endocrine Diseases Biology (R.J.L., S.M.B.), Pfizer Global Research and Development, Ann Arbor, Mich; and the Division of Cardiology (R.D.M., W.W.), Mayo Clinic, Rochester, Minn."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1148\/radiology.211.1.r99ap4739"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000133277.88655.00"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.33"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0741-5214(99)70277-6"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1051-0443(07)61652-2"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0003-4975(98)00952-7"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1097\/01.RVI.0000149904.26242.54"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0741-5214(95)70271-7"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1136\/jcp.27.7.517"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1160\/TH06-07-0364"},{"key":"e_1_3_3_11_2","unstructured":"Wysokinski WE Karnicki KK McBane RD. 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