Vitamin D Deficiency Predicts Poor Clinical Outcomes in Heart Failure Patients Undergoing Cardiac Resynchronization Therapy.


Journal

Disease markers
ISSN: 1875-8630
Titre abrégé: Dis Markers
Pays: United States
ID NLM: 8604127

Informations de publication

Date de publication:
2019
Historique:
received: 01 02 2019
accepted: 06 05 2019
entrez: 19 11 2019
pubmed: 19 11 2019
medline: 28 4 2020
Statut: epublish

Résumé

Resynchronization therapy (CRT) improves mortality and induces reverse remodeling in heart failure (HF) patients with reduced ejection fraction and wide QRS. Nonetheless, some patients do not improve despite the optimal medical therapy and right indications for device implantation. Therefore, finding biomarkers suitable for identification of those patients is crucial. Vitamin D plays a classic hormonal role in the regulation of bone metabolism and also has physiological functions in wide range of nonskeletal tissues. Based on recent studies, low levels of vitamin D seem to directly contribute to pathogenesis and worsening of HF. We planned to assess the role of vitamin D levels on clinical outcomes of HF patients undergoing CRT. We enrolled 136 HF patients undergoing CRT. Total plasma vitamin D levels were measured at baseline and 6 months later. Primary endpoint was 5-year all-cause mortality; secondary endpoint was lack of good clinical response, defined as less than 15% increase of left ventricular ejection fraction after six months. During follow-up, 58 patients reached the primary, and 45 patients reached the secondary endpoint. Vitamin D levels less than 24.13 ng/mL predicted 5-year mortality ( Our study showed that vitamin D deficiency has a significant impact in heart failure patients; it is an independent predictor of lack of midterm clinical response and long-term mortality in patients undergoing CRT. Therefore, monitoring vitamin D status of heart failure patients could be of clinical significance.

Sections du résumé

BACKGROUND AND AIMS OBJECTIVE
Resynchronization therapy (CRT) improves mortality and induces reverse remodeling in heart failure (HF) patients with reduced ejection fraction and wide QRS. Nonetheless, some patients do not improve despite the optimal medical therapy and right indications for device implantation. Therefore, finding biomarkers suitable for identification of those patients is crucial. Vitamin D plays a classic hormonal role in the regulation of bone metabolism and also has physiological functions in wide range of nonskeletal tissues. Based on recent studies, low levels of vitamin D seem to directly contribute to pathogenesis and worsening of HF. We planned to assess the role of vitamin D levels on clinical outcomes of HF patients undergoing CRT.
METHODS AND RESULTS RESULTS
We enrolled 136 HF patients undergoing CRT. Total plasma vitamin D levels were measured at baseline and 6 months later. Primary endpoint was 5-year all-cause mortality; secondary endpoint was lack of good clinical response, defined as less than 15% increase of left ventricular ejection fraction after six months. During follow-up, 58 patients reached the primary, and 45 patients reached the secondary endpoint. Vitamin D levels less than 24.13 ng/mL predicted 5-year mortality (
CONCLUSION CONCLUSIONS
Our study showed that vitamin D deficiency has a significant impact in heart failure patients; it is an independent predictor of lack of midterm clinical response and long-term mortality in patients undergoing CRT. Therefore, monitoring vitamin D status of heart failure patients could be of clinical significance.

Identifiants

pubmed: 31737126
doi: 10.1155/2019/4145821
pmc: PMC6815629
doi:

Substances chimiques

Biomarkers 0
Peptide Fragments 0
pro-brain natriuretic peptide (1-76) 0
Natriuretic Peptide, Brain 114471-18-0
Vitamin D 1406-16-2

Types de publication

Journal Article Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

4145821

Informations de copyright

Copyright © 2019 P. Perge et al.

Déclaration de conflit d'intérêts

The authors declare that there is no conflict of interest regarding the publication of this article.

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Auteurs

P Perge (P)

Heart and Vascular Center, Semmelweis University, Városmajor utca 68, Budapest 1122, Hungary.

A M Boros (AM)

Heart and Vascular Center, Semmelweis University, Városmajor utca 68, Budapest 1122, Hungary.

L Gellér (L)

Heart and Vascular Center, Semmelweis University, Városmajor utca 68, Budapest 1122, Hungary.

I Osztheimer (I)

Heart and Vascular Center, Semmelweis University, Városmajor utca 68, Budapest 1122, Hungary.

Sz Szilágyi (S)

Heart and Vascular Center, Semmelweis University, Városmajor utca 68, Budapest 1122, Hungary.

T Tahin (T)

Heart and Vascular Center, Semmelweis University, Városmajor utca 68, Budapest 1122, Hungary.

A Apor (A)

Heart and Vascular Center, Semmelweis University, Városmajor utca 68, Budapest 1122, Hungary.

K V Nagy (KV)

Heart and Vascular Center, Semmelweis University, Városmajor utca 68, Budapest 1122, Hungary.

E Zima (E)

Heart and Vascular Center, Semmelweis University, Városmajor utca 68, Budapest 1122, Hungary.

L Molnár (L)

Heart and Vascular Center, Semmelweis University, Városmajor utca 68, Budapest 1122, Hungary.

B Merkely (B)

Heart and Vascular Center, Semmelweis University, Városmajor utca 68, Budapest 1122, Hungary.

G Széplaki (G)

Heart and Vascular Center, Semmelweis University, Városmajor utca 68, Budapest 1122, Hungary.

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