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Iron Deficiency in Heart Failure: Mechanisms and Pathophysiology.
Ridha I S Alnuwaysir1, Martijn F Hoes1, Dirk J van Veldhuisen1
1Department of Cardiology, University Medical Center Groningen, University of Groningen, P.O. Box 30.001, 9700 RB Groningen, The Netherlands.
Journal of Clinical Medicine
|January 11, 2022
Summary
Iron deficiency (ID) is common in heart failure (HF) and worsens outcomes. Intravenous iron can improve symptoms and reduce hospitalizations, but its exact role in HF pathophysiology requires further study.
Area of Science:
- Cardiology
- Hematology
- Nutritional Science
Background:
- Iron deficiency (ID) affects up to 59% of heart failure (HF) patients, independent of anemia.
- ID in HF negatively impacts exercise capacity, quality of life, hospitalizations, and mortality.
- Intravenous iron repletion shows promise for improving HF patient outcomes.
Purpose of the Study:
- To review current knowledge on the pathophysiology of ID in HF.
- To explore the systemic and cellular consequences of ID in HF.
- To summarize recent advances in understanding iron homeostasis and ID in HF.
Main Methods:
- Literature review of current research on iron deficiency and heart failure.
- Synthesis of findings on iron homeostasis, hepcidin, and cellular effects of ID.
- Analysis of the impact of ID on cardiac and skeletal myocytes, kidneys, and the immune system.
Main Results:
- ID has profound effects beyond erythropoiesis, impacting multiple organ systems in HF.
- Understanding iron homeostasis, particularly hepcidin's role, is crucial for characterizing ID in HF.
- ID contributes to reduced exercise capacity, diminished quality of life, and increased mortality in HF patients.
Conclusions:
- ID is a significant comorbidity in HF with serious consequences.
- Intravenous iron therapy is a potential treatment to alleviate HF symptoms and improve outcomes.
- Further research is needed to fully elucidate the pathophysiology of ID in HF and optimize treatment strategies.
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