Translating evidence into practice: Managing electrolyte imbalances and iron deficiency in heart failure

Mineral abnormalities are a common complication of heart failure (HF). In particular, dyskalaemia, hyponatraemia, and hypomagnesaemia are prevalent, with hypo- and hyperkalaemia observed in over 40 % of HF patients, hyponatraemia in 18-27 %, hypomagnesaemia in 7-52 %, and phosphate imbalance in 13 %. These abnormalities serve as indicators of the severity of HF and are strongly associated with an increased risk of morbidity and mortality. The neurohumoral activation, including the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system, and vasopressin, HF medications such as diuretics and RAAS inhibitors, amd concomitant diseases such as chronic kidney disease, can disrupt mineral homeostasis. Iron deficiency (ID) is another of the most common mineral abnormalities, affecting up to 60 % of HF patients. ID is significantly associated with adverse clinical outcomes such as reduced quality of life and exercise capacity, HF re-hospitalization, and all-cause mortality. Various pathways contribute to the development of ID in HF, including reduced iron intake due to anorexia, increased hepcidin levels associated with chronic inflammation and hepatic congestion, and occult gastrointestinal bleeding due to the concomitant use of antithrombotic agents. The efficacy of iron replacement therapy has been demonstrated in clinical trials, particularly in heart failure with reduced ejection fraction (HFrEF), whilst more recently, it has also been shown to improve exercise capacity in patients with heart failure with preserved ejection fraction (HFpEF). This review focuses on potassium and phosphate abnormalities, hyponatraemia, hypomagnesaemia, and ID in HF, providing a comprehensive overview of the mechanisms, clinical significance, and intervention strategies with the latest findings.