{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T03:34:23Z","timestamp":1790048063739,"version":"4.0.1"},"reference-count":43,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circ: Cardiovascular Imaging"],"published-print":{"date-parts":[[2021,3]]},"abstract":"<jats:sec>\n            <jats:title>Background:<\/jats:title>\n            <jats:p>\n              The postthrombotic syndrome is a common, often morbid sequela of venous thrombosis (VT) that arises from thrombus persistence and inflammatory scarring of juxtaposed vein walls and valves. Noninvasive\n              <jats:sup>18<\/jats:sup>\n              F-fluorodeoxyglucose (FDG) positron emission tomography\/computed tomography (PET\/CT) imaging can measure neutrophil inflammation in VT. Here, we hypothesized (1) early fluorodeoxyglucose positron emission tomography\/computed tomography (FDG-PET\/CT) VT inflammation can predict subsequent vein wall scarring (VWS) and (2) statin therapy can reduce FDG-PET VT inflammation and subsequent VWS.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods:<\/jats:title>\n            <jats:p>C57BL\/6J mice (n=75) underwent induction of stasis-induced VT of the inferior vena cava or jugular vein. Inferior vena cava VT mice (n=44) were randomized to daily oral rosuvastatin 5 mg\/kg or saline starting at day \u22121. Subgroups of mice then underwent FDG-PET\/CT 2 days after VT induction. On day 14, a subset of mice was euthanized, and VWS was assessed via histology. In vitro studies were further performed on bone marrow-derived neutrophils.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results:<\/jats:title>\n            <jats:p>\n              Statin therapy reduced early day 2 FDG-PET VT inflammation, thrombus neutrophil influx, and plasma IL (interleukin)-6 levels. At day 14, statin therapy reduced VWS but did not affect day 2 thrombus mass, cholesterol, or white blood counts, nor reduce day 2 glucose transporter 1 or myeloperoxidase expression in thrombus or in isolated neutrophils. In survival studies, the day 2 FDG-PET VT inflammation signal as measured by mean and maximum standardized uptake values predicted the extent of day 14 VWS (area under the receiver operating characteristic curve =0.82) with a strong correlation coefficient (\n              <jats:italic>r<\/jats:italic>\n              ) of\n              <jats:italic>r<\/jats:italic>\n              =0.73 and\n              <jats:italic>r<\/jats:italic>\n              =0.74, respectively. Mediation analyses revealed that 40% of the statin-induced VWS reduction was mediated by reductions in VT inflammation as quantified by FDG-PET.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions:<\/jats:title>\n            <jats:p>Early noninvasive FDG-PET\/CT imaging of VT inflammation predicts the magnitude of subsequent VWS and may provide a new translatable approach to identify individuals at risk for postthrombotic syndrome and to assess anti-inflammatory postthrombotic syndrome therapies, such as statins.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circimaging.120.011898","type":"journal-article","created":{"date-parts":[[2021,3,16]],"date-time":"2021-03-16T09:07:34Z","timestamp":1615885654000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":8,"title":["Fluorodeoxyglucose Positron Emission Tomography\/Computed Tomography Imaging Predicts Vein Wall Scarring and Statin Benefit in Murine Venous Thrombosis"],"prefix":"10.1161","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2711-0069","authenticated-orcid":true,"given":"Chase W.","family":"Kessinger","sequence":"first","affiliation":[{"name":"Cardiology Division, Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA (C.W.K., G.Q., F.A.J.)."},{"name":"Department of Cardiovascular Medicine, Masonic Medical Research Institute, Utica, NY (C.W.K.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guanming","family":"Qi","sequence":"additional","affiliation":[{"name":"Cardiology Division, Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA (C.W.K., G.Q., F.A.J.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Malek Z.O.","family":"Hassan","sequence":"additional","affiliation":[{"name":"Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston (M.Z.O.H., A.T., F.A.J.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter K.","family":"Henke","sequence":"additional","affiliation":[{"name":"Conrad Jobst Vascular Research Laboratory, Section of Vascular Surgery, Departments of Surgery and Medicine, University of Michigan Medical School, Ann Arbor (P.K.H.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahmed","family":"Tawakol","sequence":"additional","affiliation":[{"name":"Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston (M.Z.O.H., A.T., F.A.J.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7980-384X","authenticated-orcid":true,"given":"Farouc A.","family":"Jaffer","sequence":"additional","affiliation":[{"name":"Cardiology Division, Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA (C.W.K., G.Q., F.A.J.)."},{"name":"Cardiology Division, 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