Iron is pivotal in energy-demanding cells such as cardiomyocytes, supporting its critical functions such as electron transfer and energy production. Systemically, iron is mainly absorbed through the gut or through red blood cell turnover by macrophages. This involves the complex interplay of transporters and regulatory proteins such as transferrin, hepcidin, and ferroportin. Intracellularly, iron is regulated by iron regulatory proteins and mRNA-binding proteins such as tristetraprolin, maintaining iron balance within cardiomyocytes. However, iron dysregulation can manifest as iron deficiency or iron overload, each leading to distinct cardiovascular diseases, particularly heart failure, anthracycline-induced cardiotoxicity, hemochromatosis, and Friedreich’s ataxia. Recent clinical trials have investigated the efficacy of intravenous iron supplementation in patients with heart failure and certain criteria for iron deficiency. These trials have examined the efficacy of these therapies in improving heart failure symptoms, hospitalizations, and mortality. Moreover, emerging biomarkers like soluble transferrin-receptors are showing promise in refining the diagnosis of iron deficiency anemia. Here, we discuss the role of iron dysregulation in cardiovascular diseases, therapeutic strategies in heart failure, and future perspectives.