{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T16:13:44Z","timestamp":1790525624444,"version":"4.1.0"},"reference-count":30,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2011,2]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>Early recognition of an acute coronary occlusion (ACO) improves clinical outcomes. Soluble fms-like tyrosine kinase-1 (sFLT1) is an endothelium-derived protein induced by hypoxia. We tested whether sFLT1 levels are elevated in ACO.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods and Results\u2014<\/jats:title>\n            <jats:p>\n              Serum sFLT1 levels were measured by enzyme-linked immunosorbent assay in patients with ST-segment elevations and angiographically confirmed ACO, unstable angina\/non ST-segment elevation myocardial infarction, and 2 control groups. To further explore sFLT1 release, a mouse model of ACO and in vitro human coronary artery endothelial cell injury were used. sFLT1 levels were increased in ACO compared with unstable angina\/non-ST-elevation myocardial infarction, catheterized controls, or healthy volunteers (200.7\u00b115.5 versus 70.7\u00b144.0 versus 10.2\u00b14.0 versus 11.7\u00b11.7 pg\/mL respectively,\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001 versus ACO). At presentation, all ACO patients had elevated sFLT1 levels (&gt;15 pg\/mL, 99th percentile in controls), whereas 57% had levels of the MB isoform of creatine kinase levels &gt;10 ng\/mL (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.01) and 85% had ultrasensitive troponin I levels &gt;0.05 ng\/mL (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05). Within 60 minutes after symptom onset, sFLT1 was more sensitive than the MB isoform of creatine kinase or ultrasensitive troponin I for ACO (100% versus 20% versus 20% respectively;\n              <jats:italic>P<\/jats:italic>\n              \u22640.01 for each). Within 60 minutes of ACO in mice, sFLT1 levels were elevated. Hypoxia and thrombin increased sFLT1 levels within 15 minutes in human coronary artery endothelial cells.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion\u2014<\/jats:title>\n            <jats:p>sFLT1 levels may be an early indicator of endothelial hypoxia in ACO.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.110.215897","type":"journal-article","created":{"date-parts":[[2010,11,12]],"date-time":"2010-11-12T04:39:35Z","timestamp":1289536775000},"page":"443-450","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":19,"title":["Elevated Soluble fms-Like Tyrosine Kinase-1 Levels in Acute Coronary Occlusion"],"prefix":"10.1161","volume":"31","author":[{"given":"Navin K.","family":"Kapur","sequence":"first","affiliation":[{"name":"From the Molecular Cardiology Research Institute, Division of Cardiology, Tufts Medical Center, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin S.","family":"Heffernan","sequence":"additional","affiliation":[{"name":"From the Molecular Cardiology Research Institute, Division of Cardiology, Tufts Medical Center, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adil A.","family":"Yunis","sequence":"additional","affiliation":[{"name":"From the Molecular Cardiology Research Institute, Division of Cardiology, Tufts Medical Center, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tuan A.","family":"Nguyen","sequence":"additional","affiliation":[{"name":"From the Molecular Cardiology Research Institute, Division of Cardiology, Tufts Medical Center, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark J.","family":"Aronovitz","sequence":"additional","affiliation":[{"name":"From the Molecular Cardiology Research Institute, Division of Cardiology, Tufts Medical Center, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Parpos","sequence":"additional","affiliation":[{"name":"From the Molecular Cardiology Research Institute, Division of Cardiology, Tufts Medical Center, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Szuhuei","family":"Wilson","sequence":"additional","affiliation":[{"name":"From the Molecular Cardiology Research Institute, Division of Cardiology, Tufts Medical Center, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Corey K.","family":"Baker","sequence":"additional","affiliation":[{"name":"From the Molecular Cardiology Research Institute, Division of Cardiology, Tufts Medical Center, Boston, Mass."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michele L.","family":"Esposito","sequence":"additional","affiliation":[{"name":"From the Molecular Cardiology Research Institute, Division of Cardiology, Tufts Medical 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