Vitamin D Supplementation in Heart Failure—Confusion Without a Cause?

Heart failure (HF) remains a global health burden with high morbidity and mortality, despite significant pharmacological advances. Vitamin D deficiency (VDD) is commonly observed in HF patients and may exacerbate disease progression through various pathophysiological mechanisms, including activation of the renin-angiotensin-aldosterone system, inflammation, oxidative stress, and impaired calcium homeostasis. While vitamin D (VD) supplementation may positively influence surrogate markers in selected patient groups-particularly those with reduced ejection fraction or severe vitamin D deficiency-its effect on primary endpoints such as mortality or HF-related hospitalization varies significantly across studies and patient populations. As a result, while VD supplementation may benefit VD-deficient HF patients, current evidence does not support routine administration across the whole HF population. It is still a matter of debate whether VDD belongs to prognostic markers of worse outcomes in HF or is instead their potential cause. Therefore, the clinical utility of VD in HF management remains underexplored. This review aims to assess the evidence regarding vitamin D status and its supplementation in the context of HF, with a focus on different HF phenotypes: reduced (HFrEF), mildly reduced (HFmrEF), and preserved ejection fraction (HFpEF). The aim is to synthesize findings from novel observational studies, randomized controlled trials, and meta-analyses that shed light onto this intricate relationship and may be valuable in everyday clinical practice.