Finerenone and serum sodium in patients with heart failure and mildly reduced or preserved ejection fraction: an analysis of FINEARTS-HF
R Ono, K Docherty, A Henderson, B Claggett, A Desai, C Lam, B Pitt, M Senni, A Voors, F Zannad, M Vaduganathan, P Jhund, S Solomon, J McMurrayAbstract
Background
Older observational studies in cirrhosis and heart failure (HF) suggest that treatment with spironolactone is frequently associated with hyponatraemia, which is mechanistically plausible given the known actions of aldosterone. However, the effect of the nonsteroidal mineralocorticoid receptor antagonist (nsMRA) finerenone on serum sodium concentration (and according to sodium concentration) is unknown.
Purpose
To evaluate the effect of the nsMRA finerenone, compared with placebo, on serum sodium concentration in patients with HF and mildly reduced or preserved ejection fraction (HFmrEF/HFpEF) enrolled in FINEARTS-HF (Finerenone Trial to Investigate Efficacy and Safety Superior to Placebo in Patients with Heart Failure).
Methods
The primary outcome of FINEARTS-HF was a composite of total (first and recurrent) HF events and cardiovascular death. Serum sodium changes were assessed by treatment group, and the effects of finerenone compared with placebo were evaluated according to baseline sodium concentration.
Results
Among 5,855 patients (98%) with available baseline sodium levels, 2,632 (45.0%) were in tertile 1 (T1: sodium concentration 117-140 mmol/L), 1,773 (30.3%) in tertile 2 (T2: 141-142 mmo/L), and 1,450 (24.8%) in tertile 3 (T3: 143-154 mmol/L). Patients with lower sodium levels were more frequently male and more likely to have a history of diabetes and HF hospitalization. They had lower systolic blood pressure, eGFR, and NT-proBNP levels and were less likely to have atrial fibrillation. Serum sodium concentration was slightly but significantly reduced by finerenone compared with placebo at 1 month (mean difference [95% CI], −0.94 [−1.07 to −0.81] mmol/L) and at 3 months (−1.07 [−1.21 to −0.94] mmol/L) after randomization, with the small difference persisting throughout follow-up (Figure 1). Finerenone, compared with placebo, reduced the risk of the primary endpoint across tertiles of baseline sodium concentration: T1, relative risk (RR) for finerenone versus placebo = 0.82 (95% CI: 0.68–0.98); T2, RR 0.85 (95% CI: 0.66–1.09); and T3, RR 0.91 (95% CI: 0.68–1.21) (Pinteraction=0.87). Figure 2 shows the incidence rate of the primary endpoint (and its components) across the range of baseline sodium concentration analysed as a continuous variable, according to treatment assignment.
Conclusions
As used in FINEARTS-HF, finerenone led to only a small (approximately 1 mmol/L) reduction in serum sodium concentration during follow-up. The benefit of finerenone was consistent across baseline tertiles of sodium concentration.Figure 1Figure 2