Chronic heart failure (HF) is often accompanied by systemic iron deficiency (ID). However, effects of ID on cardiac iron status and progression of HF are unknown. To investigate these effects rats underwent LAD ligation to induce post-myocardial infarction HF or sham operation. After 3 weeks the animals from both groups were randomized into three subgroups: control, moderate ID and severe ID+anemia (IDA) by a combination of phlebotomy and low iron diet for 5 weeks. Serum and hepatic iron content were reduced by 55% and 70% (ID) and by 80% and 77% (IDA), respectively, while cardiac iron content was unchanged in HF rats. Changes in expression of all cardiomyocyte iron handling proteins indicating preserved cardiomyocytes iron status in HF and ID/IDA. Contractile function of LV cardiomyocytes, Ca²⁺ transient amplitude, sarcoplasmic reticulum Ca²⁺ release and SERCA2a function was augmented by ID and IDA and it was accompanied by an increase in serum catecholamines. Neither ID nor IDA affected left ventricular (LV) systolic or diastolic function or dimensions. To sum up, systemic ID does not result in cardiac ID and does not affect progression of HF and even improves contractile function and Ca²⁺ handling of isolated LV cardiomyocytes, however, at the cost of increased catecholamine level. This suggests that intravenous iron therapy should be considered as an additional therapeutic option in HF, preventing the increase of catecholaminergic drive with its well-known long-term adverse effects.

慢性心力衰竭 (HF) 通常伴有全身性缺铁 (ID)。然而，ID 对心脏铁状态和 HF 进展的影响尚不清楚。为了研究这些影响，大鼠接受 LAD 结扎以诱导心肌梗死后 HF 或假手术。3 周后，将两组动物随机分为三个亚组：对照组、中度 ID 和重度 ID + 贫血 (IDA)，通过静脉切开术和低铁饮食相结合，持续 5 周。HF 大鼠的血清和肝脏铁含量分别降低了 55% 和 70% (ID) 以及 80% 和 77% (IDA)，而心脏铁含量没有变化。所有心肌细胞铁处理蛋白的表达变化表明在 HF 和 ID/IDA 中心肌细胞铁状态保持不变。LV心肌细胞的收缩功能，Ca ²⁺ID和IDA增强了瞬时振幅、肌质网Ca ²⁺释放和SERCA2a功能，并伴有血清儿茶酚胺的增加。ID 和 IDA 均不影响左心室 (LV) 收缩或舒张功能或尺寸。综上所述，全身性 ID 不会导致心脏 ID，也不会影响 HF 的进展，甚至可以改善分离的 LV 心肌细胞的收缩功能和 Ca ²⁺处理，但是以增加儿茶酚胺水平为代价。这表明静脉铁剂治疗应被视为 HF 的额外治疗选择，以防止儿茶酚胺能驱动的增加及其众所周知的长期不良反应。