Department of Cardiovascular, Neural and Metabolic Sciences, Istituto Auxologico Italiano IRCCS, Ospedale San Luca, Milan, Italy.
Department of Management, Information and Production Engineering, University of Bergamo, Dalmine, Italy.
Eur J Heart Fail. 2022 Oct;24(10):1940-1949. doi: 10.1002/ejhf.2628. Epub 2022 Aug 8.
Intravenous iron therapy can improve symptoms in patients with heart failure, anaemia and iron deficiency. The mechanisms underlying such an improvement might involve chemoreflex sensing and nocturnal breathing patterns.
Patients with heart failure, reduced left ventricular ejection fraction, anaemia (haemoglobin <13 g/dl in men; <12 g/dl in women) and iron deficiency (ferritin <100 or 100-299 μg/L with transferrin saturation <20%) were 2:1 randomized to patient-tailored intravenous ferric carboxymaltose dose or placebo. Chemoreflex sensitivity cardiorespiratory sleep study, symptom assessment and cardiopulmonary exercise test were performed before and 2 weeks after the last treatment dose. Fifty-eight patients (38 active arm/20 placebo arm) completed the study. Intravenous iron was associated with less severe symptoms, higher haemoglobin (12.5 ± 1.4 vs. 11.7 ± 1.0 mg/dl, p < 0.05) and improved haematinic parameters. Ferric carboxymaltose improved the central hypercapnic ventilatory response (-25.8%, p < 0.05 vs. placebo), without changes in peripheral chemosensitivity. In particular, the central hypercapnic ventilatory responses passed from 4.6 ± 6.5 to 2.9 ± 2.9 L/min/mmHg after ferric carboxymaltose and from 4.4 ± 4.6 to 4.6 ± 3.9 L/min/mmHg after placebo (p = 0.046). In patients presenting with sleep-related breathing disorder, apnoea-hypopnoea index was reduced with active treatment as compared to placebo (12 ± 11 vs. 19 ± 13 events/h, p < 0.05). After ferric carboxymaltose, but not after placebo, both peak oxygen uptake (VO ) increased (Δ1.1 ± 2.0 ml/kg/min, p < 0.05) and VO /workload slope was steeper (Δ0.67 ± 1.7 L/min/W, p < 0.01).
Intravenous ferric carboxymaltose improves the hypercapnic ventilatory response and sleep-related breathing disorders in patients with heart failure, anaemia and iron deficiency. These newly described findings, along with improved oxygen delivery to exercising muscles, likely contribute to the favourable effects of ferric carboxymaltose in anaemic patients with heart failure.
静脉铁治疗可改善心力衰竭、贫血和缺铁患者的症状。这种改善的机制可能涉及化学感受器感应和夜间呼吸模式。
心力衰竭、左心室射血分数降低、贫血（男性血红蛋白<13g/dl；女性血红蛋白<12g/dl）和缺铁（铁蛋白<100 或 100-299μg/L，转铁蛋白饱和度<20%）的患者按 2:1 随机分为个体化静脉羧基麦芽糖铁剂量或安慰剂组。在最后一次治疗剂量前后进行化学感受器敏感性心肺睡眠研究、症状评估和心肺运动试验。58 例患者（主动组 38 例，安慰剂组 20 例）完成了研究。静脉铁治疗后，患者症状明显减轻，血红蛋白水平升高（12.5±1.4 比 11.7±1.0mg/dl，p<0.05），血液学参数得到改善。羧基麦芽糖铁改善了中枢性高碳酸血症通气反应（-25.8%，p<0.05 比安慰剂），外周化学感受器敏感性无变化。特别是，羧基麦芽糖铁治疗后，中枢性高碳酸血症通气反应从 4.6±6.5 降至 2.9±2.9L/min/mmHg，而安慰剂组从 4.4±4.6 降至 4.6±3.9L/min/mmHg（p=0.046）。在存在睡眠相关呼吸障碍的患者中，与安慰剂相比，活性治疗可降低睡眠呼吸暂停低通气指数（12±11 比 19±13 次/小时，p<0.05）。羧基麦芽糖铁治疗后，峰值摄氧量（VO ）增加（Δ1.1±2.0ml/kg/min，p<0.05），VO /工作量斜率变陡（Δ0.67±1.7L/min/W，p<0.01），而安慰剂治疗后则无变化。
静脉羧基麦芽糖铁可改善心力衰竭、贫血和缺铁患者的高碳酸血症通气反应和睡眠相关呼吸障碍。这些新发现的发现，以及向运动肌肉输送氧的增加，可能有助于羧基麦芽糖铁对心力衰竭贫血患者的有利影响。
