Iron Deficiency (ID) is increasingly recognized as a prevalent comorbid condition in Heart Failure (HF). Despite this, the pathophysiological mechanisms for progressive ID in either chronic or acute HF are still poorly understood. Beyond the traditional factors for iron deficit in the general population, we ought to review the specificities of such paucity in the HF patient, particularly focusing on the interplay between heightened inflammation, overactivity of the sympathetic nervous system and the so-called cardio-renal-anaemia-ID syndrome.
