Role of Vitamin D Supplementation in Heart Failure Patients With Vitamin D Deficiency and Its Effects on Clinical Outcomes: A Literature Review

Abstract

Vitamin D deficiency has become a global pandemic affecting approximately one billion people worldwide. Much attention has been paid to the association of low serum 25-hydroxyvitamin D (25(OH)D) levels and various chronic diseases, especially heart failure (HF). A clear role of vitamin D deficiency has been established, with increased mortality and morbidity in heart failures. However, previous randomized control trials have failed to show improvement in clinical outcomes with calciferol supplementation in these patients. Therefore, it is still unclear whether calciferol therapy can be added to the standard care in congestive heart failure (CHF) patients with deficiency. Hence, to evaluate the role of vitamin D supplementation in CHF patients with low serum 25(OH)D, we conducted an extensive search in the PubMed and Google Scholar databases using various combinations of keywords. All potentially eligible studies that evaluated the effects of vitamin D supplementation on clinical outcomes in HF patients were retrieved and extensively studied. We also checked the references of all eligible studies to identify additional relevant publications. In this study, we reviewed various mechanisms of vitamin D affecting the cardiovascular system and examined the impact of deficiency on heart failures in terms of mortality and hospitalizations. In conclusion, vitamin D supplementation has failed to improve the clinical outcomes in HF patients. The possible long-term benefits of supplementation cannot be excluded. Therefore, for future clinical trials, we recommend considering large sample sizes, longer follow-up durations, along with optimal dosage and appropriate dosing frequency.

Is vitamin D deficiency a risk factor for all-cause mortality and rehospitalization in heart failure patients?: A systematic review and meta-analysis

“…[22] Finally, low vitamin D level leads to increase parathyroid hormone level, subsequently causing left ventricular hypertrophy and affecting systolic function. [23] The current meta-analysis suggested that HF patients with low serum 25-hydroxyvitamin D level should be received closely monitored and intensive treatment. HF patients with low 25-hydroxyvitamin D level may be potentially benefited by vitamin D supplementation.…”

Preoperative Evaluation of Refugee Children With Heart Disease

“…2 Vitamin D plays a role in regulation of the renin-angiotensin-aldosterone system; a deficiency can result in uninhibited renin-angiotensin-aldosterone system activation, causing worsening heart failure. 3 Selenium deficiency is uncommon in Canadian children. Low soil micronutrients in parts of the world can result in selenium deficiency.…”

“…4 Micronutrient replacement within a time-sensitive period has been shown to prevent myocyte death and restore overall heart function. 3 Refugee children present with failure to thrive and micronutrient deficiencies due to poor nutrition. 6 Infants with heart failure have an increased metabolic demand and have significantly higher caloric intake requirements.…”

Vitamin D supplementation and postoperative atrial fibrillation

“…2 In a study, it was revealed that the risk of hospitalization and mortality increased due to vitamin D deficiency in patients with heart failure. 3 The effects of vitamin D deficiency on atrial fibrillation (AF) are explained by direct effects on atrial tissue and indirect effects on cardiovascular risk factors. 4 Postoperative atrial fibrillation (PoAF) is an important problem that increases mortality and morbidity rates after cardiac surgery operations.…”

“…Apart from all these, its effects on atherosclerotic cardiovascular diseases, stroke, and cardiac remodeling have also been shown 2 . In a study, it was revealed that the risk of hospitalization and mortality increased due to vitamin D deficiency in patients with heart failure 3 . The effects of vitamin D deficiency on atrial fibrillation (AF) are explained by direct effects on atrial tissue and indirect effects on cardiovascular risk factors 4 …”