skip to main content

Transient Hyponatremia During Hospitalization for Acute Heart Failure.(Report)

Verbrugge, Frederik H. ; Grodin, Justin L. ; Mullens, Wilfried ; Taylor, David O. ; Starling, Randall C. ; Tang, W.H. Wilson

American Journal of Medicine, 2016, Vol.129(6), p.620 [Periódico revisado por pares]

Texto completo disponível

Citações Citado por
  • Título:
    Transient Hyponatremia During Hospitalization for Acute Heart Failure.(Report)
  • Autor: Verbrugge, Frederik H. ; Grodin, Justin L. ; Mullens, Wilfried ; Taylor, David O. ; Starling, Randall C. ; Tang, W.H. Wilson
  • Assuntos: Heart Failure – Analysis ; Natriuretic Peptides – Analysis ; Medical Research – Analysis ; Heart – Analysis ; Urea – Analysis ; Furosemide – Analysis ; Hyponatremia – Analysis
  • É parte de: American Journal of Medicine, 2016, Vol.129(6), p.620
  • Descrição: To access, purchase, authenticate, or subscribe to the full-text of this article, please visit this link: http://dx.doi.org/10.1016/j.amjmed.2016.01.016 Byline: Frederik H. Verbrugge, MD, PhD (a,b,c), Justin L. Grodin, MD, MPH (a), Wilfried Mullens, MD, PhD (b,d), David O. Taylor, MD (a), Randall C. Starling, MD, MPH (a), W.H. Wilson Tang, MD [tangw@ccf.org] (a,*) Keywords Diuretics; Heart failure; Prognosis; Sodium Abstract Objective The objective was to study whether the temporal pattern of transient hyponatremia development in acute heart failure might provide insight into its pathophysiology and prognostic relevance. Methods A post hoc analysis of the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) and Diuretic Optimization Strategies Evaluation in Acute Heart Failure (DOSE AHF) studies was performed (n = 716). Patients were stratified according to the temporal pattern of hyponatremia development: (1) no hyponatremia, (2) persistent hyponatremia, (3) decompensation hyponatremia disappearing with decongestive treatment, and (4) treatment-induced hyponatremia. Results Transient decompensation versus no hyponatremia was associated with significantly elevated blood urea nitrogen/creatinine ratio (P < .001), plasma renin activity (P < .001), and plasma aldosterone levels (P < .001) at baseline. Disease severity characteristics of such patients were intermediate between no and persistent hyponatremia. In contrast, patients with treatment-induced versus no hyponatremia had similar baseline characteristics and comparable natriuretic peptide levels, and both groups had little neurohumoral activation at baseline. Diuretic efficacy, defined as net fluid balance (milliliters) per 40 mg furosemide-equivalent dose administered, was lower in patients with persistent or treatment-induced hyponatremia versus decompensation hyponatremia or no hyponatremia, respectively. The former versus latter groups also had more pronounced neurohumoral activation with decongestive treatment. The risk for all-cause mortality (hazard ratio, 2.50; 95% confidence interval, 1.50-4.19; P < .001) and death or heart failure readmission (hazard ratio, 2.18; 95% confidence interval, 1.60-2.97; P < .001) was significantly elevated in patients with persistent versus no hyponatremia, with the risk of decompensation and treatment hyponatremia situated in between. Conclusions Transient hyponatremia is prognostically relevant, but it has a heterogeneous cause according to its temporal pattern of development. Author Affiliation: (a) Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Ohio (b) Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium (c) Doctoral School for Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium (d) Biomedical Research Institute, Department of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium * Requests for reprints should be addressed to W. H. Wilson Tang, MD, Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, 9500 Euclid Ave, Desk J3-4, Cleveland, OH 44195. (footnote) Funding: FHV is supported by a PhD fellowship of the Research Foundation--Flanders (FWO, 11L8214N). FHV and WM are researchers for the Limburg Clinical Research Program UHasselt-ZOL-Jessa, supported by the foundation Limburg Sterk Merk, Hasselt University, Ziekenhuis Oost-Limburg, and Jessa Hospital. WHWT is supported by the National Institutes of Health grant R01HL103931. (footnote) Conflict of Interest: None. (footnote) Authorship: All authors had access to the data and played a role in writing this manuscript.
  • Idioma: Inglês

Buscando em bases de dados remotas. Favor aguardar.