Giving iron directly into the bloodstream might help heart failure patients who are low on iron (even if they don't have anemia) by fixing the iron deficiency in their heart cells.
Scientific Claim
Intravenous iron supplementation may benefit heart failure patients with iron deficiency, even without anemia, by correcting cardiomyocyte iron deficiency.
Original Statement
“Given the high prevalence of iron deficiency in patients with CHF, ranging between 30–50%, the European Society of Cardiology recently recommended the assessment of iron deficiency as a comorbidity in CHF. Furthermore, several clinical trials have now established the benefits of intravenous iron supplementation in CHF patients, with or without anaemia. The mechanisms underlying the anaemia-independent effects of iron deficiency and the benefits of intravenous iron in CHF patients are not fully understood. In light of the direct effect of cardiomyocyte iron deficiency on heart function, demonstrated in this and other studies, it would interesting to explore whether systemic iron deficiency in CHF patients is accompanied by cardiomyocyte iron deficiency, and whether correction of the later underlies the benefits of intravenous iron supplementation in non-anaemic patients.”
Evidence Quality Assessment
Claim Status
overstated
Study Design Support
Design cannot support claim
Appropriate Language Strength
association
Can only show association/correlation
Assessment Explanation
The study is an animal study with no human data, so it cannot support claims about benefits in human patients. 'May benefit' is appropriate but should be framed as a hypothesis based on animal data.
More Accurate Statement
“Based on mouse model findings, intravenous iron supplementation may be associated with benefits for heart failure patients with iron deficiency, even without anemia, by potentially correcting cardiomyocyte iron deficiency, though this requires further investigation in humans.”
Evidence from Studies
Supporting (1)
An essential cell-autonomous role for hepcidin in cardiac iron homeostasis