Matches in SemOpenAlex for { <https://semopenalex.org/work/W2034654450> ?p ?o ?g. }
Showing items 1 to 69 of
69
with 100 items per page.
- W2034654450 endingPage "1086" @default.
- W2034654450 startingPage "1085" @default.
- W2034654450 abstract "This editorial refers to ‘Relationship of serum sodium concentration to mortality in a wide spectrum of heart failure patients with preserved and with reduced ejection fraction: an individual patient data meta-analysis’, by D. Rusinaru et al., published in this issue on pages 1139–1146 and ‘Dysnatraemia in heart failure’, by N. Deubner et al., published in this issue on pages 1147–1154. A problem well stated is a problem half-solved Charles Kettering Hyponatraemia is the most common electrolyte abnormality in hospitalized patients and has been associated with cognitive impairment, risk of fall, longer hospital stay, and higher mortality. In patients hospitalized with decompensated heart failure (HF), it has additionally been associated with haemodynamic deterioration, and higher risk of rehospitalization.1 The first study that associated hyponatraemia with higher mortality in HF used a cut-off of 137 mEq/L to define hyponatraemia.2 Traditionally, however, hyponatraemia is defined as serum sodium ≤135 mEq/L.3 Little attention has been paid to scrutinizing the cut-off for serum sodium that defines hyponatraemia. In various survival models, levels as low as 130 mEq/L4 and as high as <140 mEq/L5 have been used to define hyponatraemia. The Seattle Heart Failure6 and the MUerte Subita en Insuficiencia Cardiaca (MUSIC)7 survival models used a cut-off of <138 mEq/L,6 whereas the United Kingdom Heart Failure Evaluation and Assessment Risk Trial (UK-HEART)5 used a cut-off of ≤140 mEq/L.5 Recently, there has been accumulating evidence to support reconsideration of the appropriate level that defines hyponatraemia. In a population-based study involving 671 participants with no history of cardiovascular disease, hyponatraemia defined as serum sodium <138 mEq/L was an independent predictor of death or myocardial infarction.8 Similarly, in a study that included all adult hospitalizations over a 7-year period (n = 53 236), hyponatraemia defined as serum sodium <138 mEq/L was independently associated with increased in-hospital mortality, discharge to a care facility, and hospital length of stay.9 An analysis from the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE) registry on 47 647 hospitalized patients with decompensated HF that was published 5 years ago reported that a serum sodium level <138 mEq/L was an independent predictor of in-hospital and 60-day mortality.10 Based on these data, an accompanying editorial called for a redefinition of hyponatraemia in patients with HF.11 Two separate studies have now reported on the association of hyponatraemia with outcomes in patients with HF with impaired as well as preserved left ventricular ejection fraction (LVEF) and with relatively long-term follow-up.11 Deubner et al.12 analysed data from the Interdisciplinary Network for Heart Failure (INH) Registry that included 1000 consecutively hospitalized patients with decompensated HF, 48% of whom had LVEF >40%. After 5 years of follow-up, 56% had died. Patients with either hyponatraemia (defined as sodium levels <135 mmol/L) or hypernatraemia (sodium >145 mmol/L) had a significantly higher mortality signalling a U-shaped relationship to mortality, thus providing support for earlier observations that hypernatraemia may very well be linked to worse outcomes.9,10,13 Perhaps more importantly, the study also demonstrated that patients with sodium levels <140 mmol/L exhibited higher mortality and this relationship was not influenced by LVEF. Rusinaru et al.14 analysed the data collected in the Meta-analysis Global Group in Chronic Heart failure (MAGGIC), a large individual patient data meta-analysis (n = 14 766), to assess the risk of death associated with hyponatraemia. The authors found that hyponatraemic (defined as sodium <135 mmol/L) patients with HF and either impaired or preserved LVEF had a substantially higher mortality. Importantly, a linear increase in the risk of 3-year mortality was identified at levels <140 mmol/L. These two studies provide a substantial contribution to our understanding of the crucial issue of defining hyponatraemia particularly in HF. Both studies confirm previous findings that hyponatraemia should be defined as sodium levels <140 mmol/L (Table 1). They also confirm that this definition applies equally to patients with HF and either impaired or preserved LVEF. The large number of patients enrolled in both studies coupled with a long-term follow-up provide convincing supportive evidence. One may question the practical value of redefining hyponatraemia. An argument could be made that the available data from the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan (EVEREST) suggesting that when hyponatraemia is defined as sodium levels <135 mmol/L treatment with the arginin vasopressin antagonist tolvaptan may improve outcomes imply that in order to improve outcomes, treatment of hyponatraemia should be confined to lower levels and redefining hyponatraemia at a higher level would not be expected to contribute to better outcomes. This view, however, may be short sighted. First, there are no firm data that indicate that treating hyponatraemia improves outcomes, let alone deciding the appropriate cut-off at which to do so. Whether hyponatraemia is a marker or a mediator is an unsettled issue.15 Secondly, defining hyponatraemia should not depend on whether raising sodium above certain levels by a certain drug improves outcomes or not because any therapeutic intervention may trigger undesirable effects that undermine its benefits. Thirdly, the larger issue is to advance and further our understanding of hyponatraemia, and a proper definition would widen our ability to obtain this knowledge. Further efforts addressing the issue of hyponatraemia must take into consideration the proper definition of hyponatraemia. Conflict of interest: none declared." @default.
- W2034654450 created "2016-06-24" @default.
- W2034654450 creator A5017806292 @default.
- W2034654450 creator A5059591399 @default.
- W2034654450 date "2012-10-01" @default.
- W2034654450 modified "2023-10-12" @default.
- W2034654450 title "Defining hyponatraemia: a call for action" @default.
- W2034654450 cites W1501096814 @default.
- W2034654450 cites W1521342393 @default.
- W2034654450 cites W2028044474 @default.
- W2034654450 cites W2034129937 @default.
- W2034654450 cites W2037211180 @default.
- W2034654450 cites W2057462924 @default.
- W2034654450 cites W2063369692 @default.
- W2034654450 cites W2074330505 @default.
- W2034654450 cites W2074852127 @default.
- W2034654450 cites W2077277741 @default.
- W2034654450 cites W2096108188 @default.
- W2034654450 cites W2103679597 @default.
- W2034654450 cites W2108600107 @default.
- W2034654450 cites W2116296294 @default.
- W2034654450 cites W4254729059 @default.
- W2034654450 doi "https://doi.org/10.1093/eurjhf/hfs140" @default.
- W2034654450 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22941948" @default.
- W2034654450 hasPublicationYear "2012" @default.
- W2034654450 type Work @default.
- W2034654450 sameAs 2034654450 @default.
- W2034654450 citedByCount "1" @default.
- W2034654450 countsByYear W20346544502018 @default.
- W2034654450 crossrefType "journal-article" @default.
- W2034654450 hasAuthorship W2034654450A5017806292 @default.
- W2034654450 hasAuthorship W2034654450A5059591399 @default.
- W2034654450 hasBestOaLocation W20346544501 @default.
- W2034654450 hasConcept C126322002 @default.
- W2034654450 hasConcept C164705383 @default.
- W2034654450 hasConcept C177713679 @default.
- W2034654450 hasConcept C2776703092 @default.
- W2034654450 hasConcept C2778198053 @default.
- W2034654450 hasConcept C71924100 @default.
- W2034654450 hasConcept C78085059 @default.
- W2034654450 hasConceptScore W2034654450C126322002 @default.
- W2034654450 hasConceptScore W2034654450C164705383 @default.
- W2034654450 hasConceptScore W2034654450C177713679 @default.
- W2034654450 hasConceptScore W2034654450C2776703092 @default.
- W2034654450 hasConceptScore W2034654450C2778198053 @default.
- W2034654450 hasConceptScore W2034654450C71924100 @default.
- W2034654450 hasConceptScore W2034654450C78085059 @default.
- W2034654450 hasIssue "10" @default.
- W2034654450 hasLocation W20346544501 @default.
- W2034654450 hasLocation W20346544502 @default.
- W2034654450 hasOpenAccess W2034654450 @default.
- W2034654450 hasPrimaryLocation W20346544501 @default.
- W2034654450 hasRelatedWork W2051712573 @default.
- W2034654450 hasRelatedWork W2077083067 @default.
- W2034654450 hasRelatedWork W2091139515 @default.
- W2034654450 hasRelatedWork W2319805938 @default.
- W2034654450 hasRelatedWork W2355594703 @default.
- W2034654450 hasRelatedWork W2367757763 @default.
- W2034654450 hasRelatedWork W2745017169 @default.
- W2034654450 hasRelatedWork W3033076790 @default.
- W2034654450 hasRelatedWork W3155674270 @default.
- W2034654450 hasRelatedWork W3187572025 @default.
- W2034654450 hasVolume "14" @default.
- W2034654450 isParatext "false" @default.
- W2034654450 isRetracted "false" @default.
- W2034654450 magId "2034654450" @default.
- W2034654450 workType "article" @default.