No abstract

BackgroundVitamin D status may influence heart failure (HF) patient outcomes by affecting b-type natriuretic peptide (BNP), parathyroid hormone (PTH), and enhancing cardiac contractility. Vitamin D deficiency is associated with morbidity and mortality in HF patients. The objective of this study was to determine if vitamin D3 at a comparatively high dose would replete 25-hydroxyvitamin D (25(OH)D) stores, improve BNP, PTH, cardiopulmonary function, reduce inflammatory markers, and improve quality of life (QOL) in HF patients.MethodsThis was a 6 month, parallel group, double-blind, placebo-controlled, single clinic center, randomized trial of supplemental vitamin D3 using a dose of 10,000 IU daily or placebo in 40 vitamin D deficient or insufficient (25(OH)D level ≤ 32 ng/ml) patients with stable New York Heart Association Class II-III HF in a specialty cardiology clinic. All variables were measured at baseline and 6 months. Values between the two treatment groups were assessed using Student’s t-test or Mann-Whitney Test. Univariate analysis of covariance was conducted to adjust for variance in baseline 25(OH)D.ResultsAll results were adjusted for baseline 25(OH)D. The change in BNP from baseline was ∆ +30 ± 950 pg/ml for treatment vs. placebo ∆ +400 ± 1900 pg/ml, p = 0.003. 25(OH)D serum levels rose by 49 ± 32 ng/ml in the treatment group vs 4 ± 10 ng/ml in the placebo group, p < 0.001. PTH and exercise chronotropic response index improved in the treatment group vs placebo group, respectively, but both were attenuated by adjustment ((∆-20 ± 20 pg/ml vs ∆ + 7 ± 53 pg/ml respectively (p = 0.01, adjusted p = 0.07)) and (∆ + 0.13 ± 0.26 vs. ∆-0.03 ± 02.9 respectively, p < 0.01, adjusted p = 0.17)). Other measured cardiopulmonary parameters remained unchanged. High sensitivity C-reactive protein (hsCRP) remained unchanged for women, but improved for men (∆-2 ± 4 treatment versus ∆2 ± 5 mg/L placebo, p = 0.05). QOL scores, including composite overall and clinical summary scores significantly improved in treatment compared to placebo (∆ + 10 ± 15 versus −6 ± 15, p < 0.01 and ∆ + 8 ± 14 versus −8 ± 18, p = 0.01, respectively).ConclusionsRepletion of 25(OH)D may improve QOL in HF patients and may help to normalize BNP, PTH, and hsCRP.Trial registrationClinicaltrials.gov, Trial Registration Number: NCT01636570, First registered 3 July 2012.Electronic supplementary materialThe online version of this article (10.1186/s12872-017-0707-y) contains supplementary material, which is available to authorized users.

No abstract

No abstract

No abstract

No abstract

Background: Vitamin D deficiency has been associated with cardiovascular mortality and sudden cardiac death in heart failure patients. Vitamin D may influence parathyroid hormone, the renin-angiotensin axis, natriuretic peptide gene expression, cardiac contractility, and cardiopulmonary function. Heart Failure (HF) studies using vitamin D to date have typically not used adequate repletion doses. Objectives: The primary objectives of this research were to determine if vitamin D repletion over a six month period in New York Heart Association (NYHA) Class II-III HF patients would result in a change in neurohormonal markers, cardiopulmonary exercise parameters, circulating 25- hydroxyvitamin D, and quality of life. Methods: A randomized, double-blinded, placebo-controlled trial assessing adjunctive Vitamin D3 supplementation in the treatment of NYHA Class II-III HF patients was conducted. Patients received 10,000 International Units (IU) per day of vitamin D3 or placebo for 6 months. Inclusion Criteria: 1) 25-hydroxyvitamin D level ≤32 ng/ml 2) stable medical regimen for 3 months. Exclusion Criteria: 1) any clinically unstable medical disorder 2) supplementation of vitamin D3 or D2 of greater than or equal to 2,000 IU/day. Study endpoints were: 1) B-type Natriuretic Peptide (BNP), 2) cardiopulmonary exercise parameters using Shape HF, 3) 25-hydroxyvitamin D, 4) intact parathyroid hormone (PTH), and 5) quality of life with the Kansas City Cardiomyopathy Questionnaire (KCCQ). Statistical analysis included independent samples t-test and multivariate regression. Results: A total of 34 patients completed the study. When adjusted for baseline 25-hydroxyvitamin D, the difference between groups for BNP was significant ([[Unable to Display Character: &#8710;]]540 ±1928 pg/ml placebo vs [[Unable to Display Character: &#8710;]] 35 pg/ml ±1054 pg/ml treatment p=0.009). 25-hydroxyvitamin D was [[Unable to Display Character: &#8710;]]48.9 ±32 ng/ml treatment vs [[Unable to Display Character: &#8710;]]3.6 ± 9.4 ng/ml placebo, p<0.001 (mean 68 ng/ml treatment vs 23 ng/ml placebo). No toxicity was observed with treatment. PTH and exercise chronotropic response index trended towards improvement in the treatment group vs placebo group, respectively (([[Unable to Display Character: &#8710;]]-20 ±20 pg/ml vs [[Unable to Display Character: &#8710;]]7 ±54pg/ml (p=0.06)) and ([[Unable to Display Character: &#8710;]]0.13±0.26 versus [[Unable to Display Character: &#8710;]]-0.03 ± 0.23, p=0.12)). KCCQ quality of life total symptom ([[Unable to Display Character: &#8710;]]16 ±16 treatment vs [[Unable to Display Character: &#8710;]]-12 ±15 placebo, p< 0.001) and individual scores significantly improved from baseline in the treatment group. Conclusions: Preliminary results show that vitamin D3 treatment of 10,000 IU/day in heart failure patients is safe, results in adequate circulating 25-hydroxyvitamin D levels, and achieves improvement in surrogate endpoint markers of HF outcomes.

No abstract