Finerenone across the HFpEF and HFmrEF spectrum: a step towards multi-pillar care?

Heart failure (HF) remains one of the leading causes of morbidity and mortality worldwide, with an increasingly significant health and socioeconomic burden. In recent years, the understanding of this syndrome has progressively evolved beyond the traditional classification based on left ventricular ejection fraction (LVEF). It is now widely recognized that the clinical severity of HF spans the entire LVEF spectrum, including both preserved (HFpEF) and mildly reduced ejection fraction (HFmrEF) phenotypes. Although HFpEF and HFmrEF collectively account for approximately half of all HF cases, effective therapeutic options remain limited. The most recent European Society of Cardiology (ESC) guidelines1 recommend the use of sodium–glucose co-transporter-2 inhibitors (SGLT2i) based on the favourable outcomes of the DELIVER and EMPEROR-Preserved trials.2,3 Despite these advances, there is an important unmet clinical need for complementary therapies capable of modulating the underlying pathophysiological mechanisms of HF, including myocardial inflammation and fibrosis. Within this context, the FINEARTS-HF trial investigated the efficacy and tolerability of finerenone in patients with HF and LVEF >40%. Finerenone is a non-steroidal mineralocorticoid receptor antagonist (MRA) characterized by higher receptor selectivity and more favourable hormonal safety profile compared with traditional steroidal MRAs. Furthermore, finerenone demonstrated anti-fibrotic effects in pre-clinical models.4 The FINEARTS-HF trial showed that finerenone treatment reduced the composite endpoint of cardiovascular death and HF hospitalization by 16%, while maintaining a favourable safety profile, in patients with HFmrEF and HFpEF.5