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Iron deficiency as therapeutic target in heart failure: a translational approach

Heart Failure Reviews
Constantinos Bakogiannis, Alexandros Briasoulis, Dimitrios Mouselimis, Anastasios Tsarouchas, Nikolaos Papageorgiou, Christodoulos Papadopoulos, Nikolaos Fragakis, Vassilios Vassilikos
Wichtige Hinweise
Constantinos Bakogiannis and Alexandros Briasoulis contributed equally to this work.

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Heart failure (HF) is a potentially debilitating condition, with a prognosis comparable to many forms of cancer. It is often complicated by anemia and iron deficiency (ID), which have been shown to even further harm patients’ functional status and hospitalization risk. Iron is a cellular micronutrient that is essential for oxygen uptake and transportation, as well as mitochondrial energy production. Iron is crucially involved in electrochemical stability, maintenance of structure, and contractility of cardiomyocytes. There is mounting evidence that ID indeed hampers the homeostasis of these properties. Animal model and stem cell research has verified these findings on the cellular level, while clinical trials that treat ID in HF patients have shown promising results in improving real patient outcomes, as electromechanically compromised cardiomyocytes translate to HF exacerbations and arrhythmias in patients. In this article, we review our current knowledge on the role of iron in cardiac muscle cells, the contribution of ID to anemia and HF pathophysiology and the capacity of IV iron therapy to ameliorate the patients’ arrhythmogenic profile, quality of life, and prognosis.

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