Transient Hyponatremia During Hospitalization for Acute Heart Failure

Abstract

Objective 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 ESCAPE and 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-value<0.001), plasma renin activity (P-value<0.001), and plasma aldosterone levels (P-value<0.001) 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, comparable natriuretic peptide levels, and both groups had little neurohumoral activation at baseline. Diuretic efficacy, defined as net fluid balance [mL] 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 [HR (95%CI) = 2.50 (1.50-4.19); P-value<0.001] and death or heart failure readmission [HR (95%CI) = 2.18 (1.60-2.97); P-value<0.001] 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 has a heterogeneous etiology according to its temporal pattern of development.

Impact of Ultrafiltration on Serum Sodium Homeostasis and its Clinical Implication in Patients With Acute Heart Failure, Congestion, and Worsening Renal Function

“…The authors reported that TIH was observed in 14.3% of the patients in ADHF. 26 In the current study, TIH was observed in 24.5% of patients. Consistent with previous studies, patients with TIH had similar outcomes compared to those who did not experience any hyponatremia during the treatment.…”

“…Consistent with previous studies, patients with TIH had similar outcomes compared to those who did not experience any hyponatremia during the treatment. 26 More advanced chronic kidney disease patients may explain a higher prevalence of TIH in our study. Development of TIH is not necessarily a bad sign unless hyponatremia persists after decongestion therapy; however, care is needed for their potential risks to persistent hyponatremia because patients who developed TIH may have co-existing sodium depletion.…”

Predictors of Long-Term Mortality in Patients With Acute Heart Failure

“…[39][40][41] A report from the HARVEST registry also revealed that hyponatremia and worsening sodium levels were associated with mortality in patients hospitalized for AHF. 42) In our results, serum sodium is considered to be an independent mortality predictor which was in relation to a 12.0% increase in mortality risk for each 1U decrease (HR 0.880, 95%CI 0.822-0.943).…”

Hyponatremia in Acute Heart Failure in Relation to Hematocrit Levels: Clinical Relevance and Prognostic Implication

“…A recent subanalysis of the ESCAPE and DOSE trials showed that persistent hyponatremia had a significantly increased risk of death and rehospitalization when compared to patients without hyponatremia [6]. Similarly, Donzé et al [27] demonstrated that severe discharge persistent hyponatremia was related to death at 30 days or rehospitalization.…”

“…Hyponatremia, defined as serum sodium < 135 mEq/L, is a common electrolyte disturbance encountered in 15-25% of patients with AHF before and during decongestion and has been associated with impaired diuretic response and adverse events [4][5][6]. Hyponatremia may be the result of either effectively low sodium levels, mostly related to intensive use of diuretic therapy (i.e., depletion) or alternatively hemodilution, with the latter reflecting neurohormonal activation and plasma osmolality changes [7].…”