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This editorial refers to ‘Effects of serelaxin in subgroups of patients with acute heart failure: results from RELAX-AHF’[†][1], by M. Metra et al. , on page 3128 The lifetime likelihood of developing heart failure (HF) is ∼20% over 40 years of age, and acute heart failure (AHF) remains the most common cause of hospitalization in people older than 65 years, with increasing incidence, and substantial morbidity and mortality.1 Whereas success in treating chronic HF has been achieved throughout the last decades, treatment options for AHF have failed to demonstrate any substantial clinical benefit in randomized prospective trials.1Serelaxin is a recombinant human relaxin-2 vasoactive peptide that causes systemic and renal vasodilation. The mechanism of action of serelaxin involves activation of the endothelin type B receptor (ETB-receptor) and stimulation of nitric oxide production, that mediate systemic and renal vasodilation and natriuresis.2 In a dose-finding study (Pre-RELAX-AHF), i.v. infusion of serelaxin over 24 h was associated with significant relief of dyspnoea and a reduction of cardiovascular death or readmission due to heart or renal failure at day 60.3 In the RELAX-AHF study enrolling 1161 patients admitted to hospital for AHF treatment, serelaxin was associated with dyspnoea relief, as evidenced by the visual analogue scale (VAS) area under the curve from baseline to day 5.4 For the two key secondary endpoints (cardiovascular death or readmission to hospital for HF or renal failure), no significant effect was found with serelaxin. However, in a longer follow-up, a significant reduction in cardiovascular deaths and all-cause deaths at 180 days was observed.4Two distinctive peculiarities characterize the … [1]: #fn-2

RELAX-AHF: consistency across subgroups and new hypotheses generated