PATHOPHYSIOLOGY OF IRON DEFICIENCY IN HEART FAILURE

Abstract

Iron deficiency (ID) is a prevalent and clinically significant comorbidity in patients with heart failure (HF), affecting up to 50% of stable HF patients and up to 80% in acute HF settings. This review explores the pathophysiology of ID in HF, highlighting both absolute iron deficiency (AID) and functional iron deficiency (FID). The primary mechanisms of ID in HF involve systemic inflammation, which leads to elevated hepcidin levels, impaired iron absorption, and iron sequestration in macrophages, resulting in reduced availability of iron for critical cellular processes. Furthermore, gastrointestinal congestion and the use of medications such as proton pump inhibitors exacerbate iron absorption issues. The deficiency impairs mitochondrial function and energy production, contributing to reduced exercise capacity, muscle fatigue, and poorer quality of life. Additionally, ID increases the risk of hospitalization and mortality, independent of anemia. Treatment approaches such as intravenous iron supplementation, particularly with ferric carboxymaltose (FCM), have demonstrated significant improvements in symptoms, exercise capacity, and overall patient outcomes. Addressing iron deficiency in HF has become a vital therapeutic target to improve both clinical outcomes and patient quality of life.