Department of Pharmaceutical and Administrative Sciences, School of Pharmacy, University of Charleston, Charleston, WV, USA.
J Cardiovasc Pharmacol Ther. 2012 Mar;17(1):117-25. doi: 10.1177/1074248411407635. Epub 2011 May 18.
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 < .05). Deferasirox treatment reduced cardiac and aortic iron levels by 32% and 35%, respectively (P < .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 < .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.
铁诱导的心血管疾病是铁过载患者的主要死亡原因。地拉罗司是一种新型三齿口服螯合剂,其半衰期适合每日一次给药;然而,关于该药物在预防铁诱导的心血管疾病方面的有效性知之甚少。成年雄性蒙古沙鼠随机分为 3 组:对照组、铁过载组和铁过载后地拉罗司治疗组。铁过载动物接受铁葡聚糖 100 mg/kg 腹腔内(ip)/5 天,共 10 周,而地拉罗司在铁负荷后 9 个月内每天口服 100 mg/kg。通过电感耦合等离子体原子发射光谱法测定心脏和主动脉铁含量。在麻醉动物中定期获得沙鼠心电图和超声心动图。与对照组动物相比,铁过载心脏和主动脉的铁浓度分别高 3.3 倍和 2.4 倍(P <.05)。地拉罗司治疗使心脏和主动脉铁水平分别降低 32%和 35%(P <.05)。这些结果与普鲁士蓝铁染色观察到的细胞铁沉积减少一致。铁过载沙鼠表现出频繁的心律失常,包括室性早搏、室上性心动过速和反复性室性心动过速。此外,超声心动图评估显示,左心室尺寸包括左心室后壁厚度(LVPWd:49%)、左心室内部直径(LVIDd:26%)和左心室间隔厚度(LVSd:42%)因铁过载而增加。这些参数在用地拉罗司治疗后显著降低(LVPWd:23%,LVIDd:24%,LVSd:27%)。与对照组相比,铁过载还与射血分数(EF:降低 30%)和缩短分数(FS:降低 23%)降低有关(P <.05)。用地拉罗司治疗后,这些值升高(EF:升高 30%,FS:升高 28%)与铁过载组相比。这些发现表明,地拉罗司可能有助于减轻铁诱导的心脏结构和功能变化。