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The effect of vitamin d on aldosterone and health status in patients with heart failure.

ABSTRACT: Vitamin D deficiency is associated with heart failure (HF) events, and in animal models vitamin D down-regulates renin-angiotensin-aldosterone system hormones.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.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.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.

SUBMITTER: Boxer RS

PROVIDER: S-EPMC4117205 | biostudies-literature | 2014 May

REPOSITORIES: biostudies-literature

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The effect of vitamin d on aldosterone and health status in patients with heart failure.

Boxer Rebecca S RS Hoit Brian D BD Schmotzer Brian J BJ Stefano Gregory T GT Gomes Amanda A Negrea Lavinia L

Journal of cardiac failure 20140204 5

<h4>Background</h4>Vitamin D deficiency is associated with heart failure (HF) events, and in animal models vitamin D down-regulates renin-angiotensin-aldosterone system hormones.<h4>Methods</h4>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.<h4>Results</h4>Me ...[more]

PMID: 24508026

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Project description:Objective1,25-Dihydroxyvitamin D (1,25([OH]2D) is considered to be a negative endogenous regulator of the renin-angiotensin-aldosterone system (RAAS), but the effect of vitamin D supplementation on the RAAS is inconclusive.DesignIn this prespecified secondary analysis of a randomized controlled trial, we assessed in 165 patients with heart failure (vitamin D group: n = 83; placebo group: n = 82) the effect of three years of vitamin D supplementation with 4000 IU daily on parameters of the RAAS (renin and aldosterone) and on circulating 1,25(OH)2D, plasma phosphate, and fibroblast growth factor (FGF)-23. We assessed age- and baseline-adjusted between-group differences at study termination.ResultsAlmost all patients were under treatment with beta-blockers, inhibitors of the RAAS, and diuretics. Initially, the frequency of concentrations above the laboratory-specific reference range (renin: >23.9 mIU/L; aldosterone: >232 ng/L) in the vitamin D and placebo group was 87.7% and 92.7%, respectively (renin), and 24.1% and 32.5%, respectively (aldosterone). Vitamin D increased adjusted 1,25(OH)2D concentrations significantly (mean treatment effect and 95% CI: 18.3 pmol/L,7.3 to 29.3 pmol/L; P < 0.001) but had no significant effects on phosphate (0.18 mmol/L, -0.00 to 0.35 mmol/L; P = 0.051), FGF-23 (685 RU/mL, -213 to 1585 RU/mL; P = 0.134), renin (312 mIU/L, -279 to 902 ng/L; P = 0.298), or aldosterone (-0.19 ng/L, -5.09 to 4.70 ng/L; P = 0.938). Vitamin D supplementation was, however, associated with an increase in renin concentrations in the subgroup with baseline 25-hydroxyvitamin D below 30 nmol/L (n = 67; 1365 mIU/, 343 to 2386 mIU/L; P = 0.010).ConclusionsIn patients with advanced heart failure treated according to evidence-based guidelines, vitamin D supplementation did not significantly influence parameters of the RAAS in the entire study cohort but was associated with an increase in plasma renin concentrations in the subgroup with low baseline 25-hydroxyvitamin D concentrations.

Project description:AimsThis study aims to assess long-term changes in left ventricular ejection fraction (LVEF) together with echocardiographic markers of cardiac remodelling and their association with prognosis and patient-reported quality of life (QoL).Methods and resultsWe conducted a retrospective analysis of serial echocardiograms performed between January 2009 and December 2019 in 1089 patients (median age 63 years, 71.0% men) enrolled in the Mazankowski Heart Function Clinic Registry who had at least two echocardiograms separated by ≥12 months. We classified the patients into four subgroups by their baseline and LVEF trajectories: persistent heart failure with reduced ejection fraction (persistent HFrEF, n = 364), recovered ejection fraction (HFrecEF, n = 325), transient recovery in ejection fraction (HFtrecEF, n = 117), and preserved ejection fraction (HFpEF, n = 283); 4490 echocardiograms were included in the present analysis, with 4.1 ± 1.8 echocardiograms available per patient during follow-up. Reductions in echocardiographic markers of cardiac remodelling, including LVIDd [adjusted odds ratio (aOR): 2.22, 95% confidence interval (CI) 1.75-2.86], LVIDs (aOR: 2.44, 95% CI 2.00-2.94), left ventricular mass index (aOR: 1.15, 95% CI 1.09-1.22), E/e' ratio (aOR: 1.15, 95% CI 1.02-1.30), left atrial volume index (aOR: 1.10, 95% CI 1.03-1.16), along with an increase in the maximum recommended daily dose of renin-angiotensin system inhibitors (aOR: 1.04, 95% CI 1.01-1.07) and mineralocorticoid-receptor antagonists (aOR: 1.06, 95% CI 1.01-1.11) at 2 years, strongly predicted the HFrecEF classification, which was further sustained at 5 years of follow-up. However, changes in these parameters were mostly absent in patients experiencing only a transient recovery in LVEF (HFtrecEF), closely resembling patients with persistent HFrEF. In the multivariable analysis, HFrecEF patients had lower risk of all-cause mortality alone [adjusted hazard ratio (aHR): 0.46, 95% CI 0.23-0.93], and composite all-cause (aHR: 0.59, 95% CI 0.49-0.73), cardiovascular (aHR: 0.47, 95% CI 0.36-0.61), and heart failure (aHR: 0.50, 95% CI 0.35-0.70) related hospitalizations with mortality than patients with persistent HFrEF. QoL assessed through the shortened Kansas City Cardiomyopathy Questionnaire-12 at the end of follow-up was greater in patients with HFrecEF by 5.2, 12.4, and 9.4 points than persistent HFrEF, HFtrecEF, and HFpEF, respectively.ConclusionsPatients with HFrecEF experienced progressive normalization in echocardiographic markers of cardiac remodelling characterized by reductions in left ventricular dimensions and mass in tandem with reductions in left atrial volume and E/e' ratio, which is associated with better prognosis and QoL.

Project description:Rationale & objectiveHeart failure treatment relies on loop diuretics to induce natriuresis and decongestion, but the therapy is often limited by diuretic resistance. We explored the association of renin-angiotensin-aldosterone system (RAAS) activation with diuretic response.Study designObservational cohort.Setting & populationEuvolemic ambulatory adults with chronic heart failure were administered torsemide in a monitored environment.PredictorsPlasma total renin, active renin, angiotensinogen, and aldosterone levels. Urine total renin and angiotensinogen levels.OutcomesSodium output per doubling of diuretic dose and fractional excretion of sodium per doubling of diuretic dose.Analytical approachRobust linear regression models estimated the associations of each RAAS intermediate with outcomes.ResultsThe analysis included 56 participants, and the median age was 65 years; 50% were women, and 41% were Black. The median home diuretic dose was 80-mg furosemide equivalents. In unadjusted and multivariable-adjusted models, higher levels of RAAS measures were generally associated with lower diuretic efficiency. Higher plasma total renin remained significantly associated with lower sodium output per doubling of diuretic dose (β = -0.41 [-0.76, -0.059] per SD change) with adjustment; higher plasma total and active renin were significantly associated with lower fractional excretion of sodium per doubling of diuretic dose (β = -0.48 [-0.83, -0.14] and β = -0.51 [-0.95, -0.08], respectively) in adjusted models. Stratification by RAAS inhibitor use did not substantially alter these associations.LimitationsSmall sample size; highly selected participants; associations may not be causal.ConclusionsAmong multiple measures of RAAS activation, higher plasma total and active renin levels were consistently associated with lower diuretic response. These findings highlight the potential drivers of diuretic resistance and underscore the need for high-quality trials of decongestive therapy enhanced by RAAS blockade.

Project description:ImportanceMany patients with chronic heart failure experience reduced health status despite receiving conventional therapy.ObjectiveTo determine whether a symptom and psychosocial collaborative care intervention improves heart failure-specific health status, depression, and symptom burden in patients with heart failure.Design, setting, and participantsA single-blind, 2-arm, multisite randomized clinical trial was conducted at Veterans Affairs, academic, and safety-net health systems in Colorado among outpatients with symptomatic heart failure and reduced health status recruited between August 2012 and April 2015. Data from all participants were included regardless of level of participation, using an intent-to-treat approach.InterventionsPatients were randomized 1:1 to receive the Collaborative Care to Alleviate Symptoms and Adjust to Illness (CASA) intervention or usual care. The CASA intervention included collaborative symptom care provided by a nurse and psychosocial care provided by a social worker, both of whom worked with the patients' primary care clinicians and were supervised by a study primary care clinician, cardiologist, and palliative care physician.Main outcomes and measuresThe primary outcome was patient-reported heart failure-specific health status, measured by difference in change scores on the Kansas City Cardiomyopathy Questionnaire (range, 0-100) at 6 months. Secondary outcomes included depression (measured by the 9-item Patient Health Questionnaire), anxiety (measured by the 7-item Generalized Anxiety Disorder Questionnaire), overall symptom distress (measured by the General Symptom Distress Scale), specific symptoms (pain, fatigue, and shortness of breath), number of hospitalizations, and mortality.ResultsOf 314 patients randomized (157 to intervention arm and 157 to control arm), there were 67 women and 247 men, mean (SD) age was 65.5 (11.4) years, and 178 (56.7%) had reduced ejection fraction. At 6 months, the mean Kansas City Cardiomyopathy Questionnaire score improved 5.5 points in the intervention arm and 2.9 points in the control arm (difference, 2.6; 95% CI, -1.3 to 6.6; P = .19). Among secondary outcomes, depressive symptoms and fatigue improved at 6 months with CASA (effect size of -0.29 [95% CI, -0.53 to -0.04] for depressive symptoms and -0.30 [95% CI, -0.55 to -0.06] for fatigue; P = .02 for both). There were no significant changes in overall symptom distress, pain, shortness of breath, or number of hospitalizations. Mortality at 12 months was similar in both arms (10 patients died receiving CASA, and 13 patients died receiving usual care; P = .52).Conclusions and relevanceThis multisite randomized clinical trial of the CASA intervention did not demonstrate improved heart failure-specific health status. Secondary outcomes of depression and fatigue, both difficult symptoms to treat in heart failure, improved.Trial registrationclinicaltrials.gov Identifier: NCT01739686.

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The effect of vitamin d on aldosterone and health status in patients with heart failure.

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The effect of vitamin d on aldosterone and health status in patients with heart failure.

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