Impact of Iron Deficiency on Arrhythmic Events and Resting ECG Abnormalities in Patients Hospitalized With Heart Failure

Overview

The relationship between iron deficiency (with or without anemia) and arrhythmic risk or ECG abnormalities in hospitalized HF patients remains poorly characterized. This is particularly relevant in settings where advanced iron therapies (e.g., intravenous iron supplementation) may not be readily available, and where simple clinical and electrocardiographic markers could help identify high-risk patients by evaluating the impact of iron deficiency (with and without anemia) arrhythmic events and resting ECG changes among patients admitted with heart failure. Understanding these associations may offer insights into the arrhythmogenic potential of iron deficiency and support the integration of iron status assessment into routine risk stratification and management of HF patients.

Heart failure (HF) is a major global health problem, associated with high morbidity, mortality, and frequent hospitalizations. Beyond impaired cardiac function, HF is recognized as a systemic syndrome involving a wide range of metabolic, inflammatory, and hematologic disturbances that contribute to disease progression and adverse outcomes. Iron deficiency has emerged as a prevalent and clinically relevant comorbidity, affecting up to 55% of chronic HF patients and in up to 80% of those with AHF, even in the absence of overt anemia. Iron plays a central role in cellular energy metabolism, oxidative phosphorylation, and mitochondrial function, processes that are especially critical in the metabolically demanding environment of the myocardium. In patients with HF, anemia and iron deficiency has been associated with reduced exercise capacity, impaired quality of life, and increased risk of hospitalization, cardiovascular and all-cause mortality. While the impact of iron deficiency on functional status and survival has been widely investigated, its potential influence on cardiac electrical activity remains less well studied. Emerging evidence suggests that iron deficiency may contribute to electrophysiological instability by promoting oxidative stress, altering repolarization, and impairing myocardial conduction. This could create a potential substrate for arrhythmias, which are a major cause of morbidity in patients with HF. Moreover, subtle resting electrocardiographic (ECG) abnormalities, such as QT prolongation, T-wave changes, or conduction delays, may reflect early electrical remodeling in the context of iron deficiency-even in the absence of clinically apparent arrhythmias