Targeting Inflammation and Iron Deficiency in Heart Failure: A Focus on Older Adults

Background/Objectives: Heart failure (HF) is a leading cause of morbidity and mortality worldwide, with a higher prevalence among older adults. Iron deficiency (ID), affecting up to 50% of HF patients, is closely linked to chronic inflammation, exacerbating HF outcomes. This review aims to explore the interplay between inflammation, ID, and HF, focusing on older patients, and to identify therapeutic gaps and emerging treatment strategies. Methods: A comprehensive review of the literature was conducted, emphasizing the pathophysiological mechanisms of inflammation and ID in HF, the challenges of current diagnostic criteria, and the limitations of available treatments. Emerging pharmacological and diagnostic approaches were analyzed. Results: Chronic inflammation in HF, particularly in older adults, promotes functional ID through elevated hepcidin levels, impairing iron availability and worsening anemia. Current diagnostic criteria, relying heavily on ferritin, often misclassify ID due to inflammation. Intravenous (IV) iron therapy shows clinical benefits in patients with <50% left ventricular ejection fraction (LVEF), but the evidence is limited in heart failure with preserved ejection fraction (HFpEF). Emerging therapies, such as Sodium-Glucose Cotransporter-2 inhibitors (SGLT2is) and prolyl hydroxylase inhibitors like Roxadustat, offer promising avenues to improve iron metabolism and outcomes. Conclusions: ID and inflammation significantly impact HF progression, particularly inolder adults. Refining diagnostic criteria and exploring innovative therapies are critical to addressing these challenges. Future research should prioritize personalized approaches targeting inflammation and ID, especially in underrepresented populations, such as HFpEF and elderly patients.