Background: Vitamin D deficiency is associated with heart failure (HF) events, and in animal models vitamin D down-regulates renin-angiotensin-aldosterone system hormones.
Methods: Patients with New York Heart Association (NYHA) functional class II-IV HF and a 25OH-D level ≤37.5 ng/mL received 50,000 IU vitamin D3 weekly (n = 31) or placebo (n = 33) for 6 months. Serum aldosterone, renin, echocardiography, and health status were determined at baseline and 6 months.
Results: Mean age of participants was 65.9 ± 10.4 years, 48% were women, 64% were African American, mean ejection fraction was 37.6 ± 13.9%, 36% were in NYHA functional class III, and 64% were in class II. The vitamin D group increased serum 25OH-D (19.1 ± 9.3 to 61.7 ± 20.3 ng/mL) and the placebo group did not (17.8 ± 9.0 to 17.4 ± 9.8 ng/mL). Aldosterone decreased in the vitamin D group (10.0 ± 11.9 to 6.2 ± 11.6 ng/dL) and not in the placebo group (8.9 ± 8.6 to 9.0 ± 12.4 ng/dL; P = .02). There was no difference between groups in renin, echocardiographic measures, or health status from baseline to 6 months. Modeling indicated that variables which predicted change in aldosterone included receiving vitamin D, increasing age, African American race, and lower glomerular filtration rate.
Conclusions: Vitamin D3 repletion decreases aldosterone in patients with HF and low serum vitamin D. Vitamin D may be an important adjunct to standard HF therapy. Further study will assess if vitamin D provides long-term benefit for patients with HF.
Keywords: Hormones; aldosterone; health status; heart failure; vitamin D.
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