{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T06:09:40Z","timestamp":1777529380330,"version":"3.51.4"},"reference-count":30,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2011,5,18]],"date-time":"2011-05-18T00:00:00Z","timestamp":1305676800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cardiovasc Pharmacol Ther"],"published-print":{"date-parts":[[2012,3]]},"abstract":"<jats:p>Iron-induced cardiovascular disease is the leading cause of death in iron-overloaded patients. Deferasirox is a novel tridentate oral chelator that exhibits a half-life suitable for once-daily dosing; however, little is known regarding the effectiveness of this agent in preventing iron-induced cardiovascular disease. Adult male Mongolian gerbils were randomly divided into 3 groups: control, iron overload, and iron overload followed by deferasirox treatment. Iron-overloaded animals received iron dextran 100 mg\/kg intraperitoneally (ip)\/5 days for 10 weeks, while deferasirox was given 100 mg\/kg per d orally (po) for 9 months post iron loading. Cardiac and aortic iron levels were determined by inductively coupled plasma atomic emission spectrometry. Gerbil electro- and echocardiograms were obtained in anesthetized animals at regular intervals. Compared to control animals, iron concentration was 3.3- and 2.4-fold higher in iron-overloaded heart and aorta, respectively ( P &lt; .05). Deferasirox treatment reduced cardiac and aortic iron levels by 32% and 35%, respectively ( P &lt; .05). These results were consistent with the decrease in cellular iron deposition observed with Prussian Blue iron staining. Iron-overloaded gerbils were found to exhibit frequent arrhythmias including premature ventricular contractions, supraventricular tachycardia, and recurrent ventricular tachycardia. In addition, echocardiographic assessment demonstrated iron overload-associated increase in left ventricular dimensions including left ventricular posterior wall dimension (LVPWd: 49%), left ventricular internal dimension (LVIDd: 26%), and left ventricular septum thickness (LVSd: 42%). These parameters were significantly reduced with deferasirox treatment (LVPWd: 23%, LVIDd: 24%, and LVSd: 27%). Iron overload was also associated with reduced ejection fraction (EF: by 30%) and fractional shortening (FS: by 23%) in comparison with controls ( P &lt; .05). With deferasirox treatment, these values were higher (EF: by 30%, FS: by 28%) compared to iron-overloaded group. These findings suggest that deferasirox may be useful for attenuating iron-induced changes in cardiac structure and function.<\/jats:p>","DOI":"10.1177\/1074248411407635","type":"journal-article","created":{"date-parts":[[2011,5,19]],"date-time":"2011-05-19T00:50:38Z","timestamp":1305766238000},"page":"117-125","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":10,"title":["Long-Term Efficacy of Deferasirox in Preventing Cardiovascular Complications in the Iron-Overloaded Gerbil"],"prefix":"10.1177","volume":"17","author":[{"given":"Rabaa M.","family":"Al-Rousan","sequence":"first","affiliation":[{"name":"Department of Pharmaceutical and Administrative Sciences, School of Pharmacy, University of Charleston, Charleston, WV, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kamran","family":"Manzoor","sequence":"additional","affiliation":[{"name":"Charleston Area Medical Center, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Satyanarayana","family":"Paturi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Physiology and Toxicology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ravi Kumar","family":"Arvapalli","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Physiology and Toxicology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joseph P.","family":"Laurino","sequence":"additional","affiliation":[{"name":"Department of Chemistry, University of Tampa, Tampa, FL, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucy","family":"Darnon","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Cabell Huntington Hospital, Huntington, WV, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ernest M.","family":"Walker","sequence":"additional","affiliation":[{"name":"Department of Pathology, Marshall University, Huntington, WV, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eric R.","family":"Blough","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Physiology and Toxicology, Joan C. 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