Division of Molecular and Clinical Medicine, Ninewells Hospital and Medical School, University of Dundee, Dundee, UK.
Department of Cardiology, Portsmouth Hospitals NHS Trust, Portsmouth, UK.
Cardiovasc Ther. 2017 Dec;35(6). doi: 10.1111/1755-5922.12301. Epub 2017 Sep 25.
To discuss the pathophysiology of iron metabolism in chronic heart failure (CHF) and the current knowledge of the efficacy of intravenous (IV) iron therapy in patients with CHF and identify points of controversy as well as highlight areas for future research.
Iron deficiency is a recognized complication of many chronic conditions. Numerous studies have reported that iron deficiency is highly prevalent in patients with CHF and is associated with exercise intolerance, reduced quality of life, and increased risk of hospitalization and mortality. Several small studies have demonstrated IV iron to be associated with improvements in symptoms, exercise capacity, quality of life, renal function, New York Heart Association (NYHA) functional class and left ventricular ejection fraction (LVEF), and reduction in NT-pro-brain natriuretic peptide (NT-proBNP) in patients with CHF and iron deficiency. Two larger-scale trials confirming these results (FAIR-HF and CONFIRM-HF) have led to guideline recommendations that IV iron therapy should be considered in patients with CHF with reduced ejection fraction and iron deficiency (serum ferritin <100 μg/L, or ferritin between 100 and 299 μg/L with transferrin saturation <20%) to provide symptomatic relief and improve exercise capacity and quality of life.
Intravenous iron therapy improves symptoms, exercise capacity, and quality of life, at least in the short-to-intermediate time. However, there are still currently no standardized criteria used to define iron deficiency and the underlying mechanism of iron deficiency in CHF remains incompletely understood. Further work is required to improve the ability to identify iron deficiency in patients with CHF and evaluate the effect of iron repletion on hard endpoints including hospitalization and mortality.
讨论慢性心力衰竭（CHF）中铁代谢的病理生理学以及静脉（IV）铁治疗在 CHF 患者中的疗效的现有知识，并确定争议点以及突出未来研究的领域。
铁缺乏是许多慢性疾病的公认并发症。许多研究报告指出，铁缺乏在 CHF 患者中非常普遍，与运动耐量降低、生活质量下降以及住院和死亡风险增加有关。几项小型研究表明，IV 铁与改善症状、运动能力、生活质量、肾功能、纽约心脏协会（NYHA）功能分级和左心室射血分数（LVEF）以及降低 NT-pro-脑钠肽（NT-proBNP）有关在铁缺乏的 CHF 患者中。两项更大规模的试验（FAIR-HF 和 CONFIRM-HF）证实了这些结果，导致指南建议在射血分数降低和铁缺乏（血清铁蛋白<100μg/L，或铁蛋白在 100 至 299μg/L 之间但转铁蛋白饱和度<20%）的 CHF 患者中应考虑 IV 铁治疗，以提供症状缓解并改善运动能力和生活质量。
静脉铁治疗至少在短期至中期内可改善症状、运动能力和生活质量。然而，目前仍然没有用于定义 CHF 中铁缺乏的标准化标准，铁缺乏的潜在机制仍不完全清楚。需要进一步努力提高在 CHF 患者中识别铁缺乏的能力，并评估铁补充对包括住院和死亡在内的硬终点的影响。
