Association between serum sodium level trajectories and survival in patients with heart failure

Abstract

Aims The effect of changes in serum sodium levels on the survival of patients with heart failure (HF) is unclear. We aimed to analyse the impact of serum sodium level trajectories on survival in intensive care unit (ICU) patients with HF. Methods A total of 4760 patients diagnosed with HF between 2001 and 2012 from the Medical Information Mart for Intensive Care III (MIMIC‐III) database were extracted. Of these patients, 1132 patients who died within 48 h of ICU admission were excluded, and 3628 patients were included in this retrospective cohort study. Sodium levels were measured at baseline, 6, 12, 18, 24, 30, 36, 42, and 48 h. Patients were divided into hyponatremia, normal, and hypernatremia groups based on baseline sodium levels, and trajectory modelling was performed for each group separately. Group‐based trajectory model (GBTM) method was utilized to identify serum sodium levels trajectories. Results The number of patients with hyponatremia (<135 mmol/L), normal sodium levels (135–145 mmol/L), and hypernatremia (>145 mmol/L) at baseline were 594 (16.37%), 2,738 (75.47%), and 296 (8.16%), respectively. A total of seven trajectory groups were identified, including hyponatremia‐slow rise group [initial levels (IL), 128.48 ± 5.42 mmol/L; end levels (EL), 131.23 ± 3.83 mmol/L], hyponatremia‐rapid rise to normal group (IL, 132.13 ± 2.18 mmol/L; EL, 137.46 ± 3.68 mmol/L), normal‐slow decline group (IL, 137.65 ± 2.15 mmol/L; EL, 134.50 ± 2.54 mmol/L), normal‐steady‐state group (IL, 139.20 ± 2.26 mmol/L; EL, 139.04 ± 2.58 mmol/L), normal‐slow rise group (IL, 140.94 ± 2.37 mmol/L; EL, 143.43 ± 2.89 mmol/L), hypernatremia‐rapid decline to normal group (IL, 146.31 ± 1.98 mmol/L; EL, 140.71 ± 3.61 mmol/L), and hypernatremia‐slow decline group (IL, 148.89 ± 5.54 mmol/L; EL, 146.28 ± 3.90 mmol/L). The results showed that hyponatremia‐slow rise group [hazard ratio (HR) = 1.35; 95% confidence interval (CI), 1.01–1.80, P = 0.040], hyponatremia‐rapid rise to normal group (HR = 1.37; 95% CI, 1.11–1.71, P = 0.004), hypernatremia‐rapid decline to normal group (HR = 1.46; 95% CI, 1.08–1.97, P = 0.014), and hypernatremia‐slow decline group (HR = 1.49; 95% CI, 1.07–2.07, P = 0.018) trajectories were associated with an increased risk of 1‐year mortality in HF patients compared with normal‐steady‐state group. After adjustment for all confounders, hyponatremia‐rapid rise to normal group (HR = 1.26, 95% CI; 1.01–1.57, P = 0.038) and hypernatremia‐rapid decline to normal group (HR = 1.36; 95% CI, 1.01–1.84, P = 0.047) trajectories were still related to an increased risk of 1‐year mortality in patients with HF. Conclusions Serum sodium level trajectories were associated with mortality in patients with HF. Association between serum sodium level trajectorie...

Hyponatraemia and changes in natraemia during hospitalization for acute heart failure and associations with in‐hospital and long‐term outcomes – from the ESC‐HFA EORP Heart Failure Long‐Term Registry

“…The association between reversal of hyponatraemia and improved survival has been reported previously 3,10,25 . In a recent study of 3628 AHF patients, with serum sodium concentrations measured every 6 h since admission, rapid changes in serum sodium (both rapid decline from hypernatraemia, and in contrast to in our study, rapid increase from hyponatraemia) were related to increased 1‐year mortality but in this case conceivably, the rapidity of change may have been a marker of underlying severity of sodium derangements 26 …”

“…to in our study, rapid increase from hyponatraemia) were related to increased 1-year mortality but in this case conceivably, the rapidity of change may have been a marker of underlying severity of sodium derangements. 26 Notably, in our study, the association of hyponatraemia with long-term outcomes was observed only for mortality (all-cause, cardiovascular and HF), but not for first hospitalizations (all-cause, cardiovascular or HF). Lack of association between hyponatraemia and subsequent HF hospitalizations could be partially explained by more intensive diuretic treatment of hyponatraemic patients at hospital discharge compared to the reference group.…”

Loop diuretics in heart failure: The objective markers to guide the therapy are needed

“…First of all, due to their mode of action, diuretics remove water through sodium‐related mechanisms, which in the long run may lead to sodium depletion. Although it has never been demonstrated, at least part of the ominous signs of heart failure—hyponatremia and hypochloremia—may be related to chronic exposure to loop diuretics 2–4 . On the other hand, because sodium is needed for an adequate diuretic response (to loop diuretics), and at the same time, loop diuretics remove sodium from the body, a sort of vicious circle is created that hinders the diuretic response in the long run.…”

“…Although it has never been demonstrated, at least part of the ominous signs of heart failure—hyponatremia and hypochloremia—may be related to chronic exposure to loop diuretics. 2 , 3 , 4 On the other hand, because sodium is needed for an adequate diuretic response (to loop diuretics), and at the same time, loop diuretics remove sodium from the body, a sort of vicious circle is created that hinders the diuretic response in the long run. In this mechanism (sodium depletion), diuretics probably indirectly activate the renin‐angiotensin‐aldosterone (RAA) system, which is meant to keep sodium homeostasis in our body.…”