Abstract
Iron is an essential micronutrient for a myriad of physiological processes in the body beyond erythropoiesis. Iron deficiency (ID) is a common comorbidity in patients with heart failure (HF), with a prevalence reaching up to 59% even in non-anaemic patients. ID impairs exercise capacity, reduces the quality of life, increases hospitalisation rate and mortality risk regardless of anaemia. Intravenously correcting ID has emerged as a promising treatment in HF as it has been shown to alleviate symptoms, improve quality of life and exercise capacity and reduce hospitalisations. However, the pathophysiology of ID in HF remains poorly characterised. Recognition of ID in HF triggered more research with the aim to explain how correcting ID improves HF status as well as the underlying causes of ID in the first place. In the past few years, significant progress has been made in understanding iron homeostasis by characterising the role of the iron-regulating hormone hepcidin, the effects of ID on skeletal and cardiac myocytes, kidneys and the immune system. In this review, we summarise the current knowledge and recent advances in the pathophysiology of ID in heart failure, the deleterious systemic and cellular consequences of ID.
Highlights
Heart failure (HF) is a complex syndrome in which the heart fails to circulate the required amount of blood and nutrients to meet the body’s demands [1]
That neurohormonal activation leads to MID accompanied by mitochondrial dysfunction by reducing extracellular iron uptake and increasing intracellular iron release [33]. These findings were validated using embryonic rat heart-derived H9c2 cells challenged with norepinephrine and/or angiotensin 2, which led to similar results [33]
In order to understand the consequences of Iron deficiency (ID) in HF patients beyond anaemia, consideration should be directed towards the roles of iron beyond mere erythropoiesis
Summary
Heart failure (HF) is a complex syndrome in which the heart fails to circulate the required amount of blood and nutrients to meet the body’s demands [1]. Despite substantial advances in prevention and treatment strategies of HF, it continues to represent a huge burden on public health worldwide, with an exceptionally high mortality rate reaching up to 75% at 5 years [2]. Iron deficiency (ID) and anaemia are among the most frequently observed comorbidities in HF, and both are independently associated with worse clinical status and outcomes [9,10,11]. Correcting ID was shown to improve quality of life, exercise performance and symptoms regardless of Hb levels [22,23,24,25] These observations underscore the crucial role of iron beyond erythropoiesis [26]. The latest progress in mechanistic studies on the potential role of IV iron supplementation is outlined
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
