Finerenone after FINEARTS-HF: evidence boundaries and implementation in heart failure with LVEF ≥40%

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  Figure 1. CKM burden, MR overactivation, and finerenone action in heart failure with LVEF ≥40%. CKM features such as CKD, albuminuria, T2D, obesity or visceral adiposity, hypertension, AF, inflammation, and recurrent congestion may promote MR overactivation in HF with LVEF ≥40%. MR overactivation links CKM stress to kidney–vascular effects, endothelial and microvascular dysfunction, and remodeling or fibrosis, contributing to sodium retention, congestion, potassium vulnerability, inflammation, impaired relaxation, extracellular-matrix turnover, fibrosis, stiffness, worsening HF events, and persistent symptoms. Finerenone antagonizes MR signaling and, in FINEARTS-HF, reduced the prespecified composite of cardiovascular death and total worsening HF events, mainly by reducing worsening HF events; cardiovascular death alone was not significantly reduced. Safe implementation requires confirmation of HF, exclusion of mimickers, baseline potassium and eGFR assessment, interaction review, laboratory reassessment around 4 weeks, and integration with SGLT2 inhibitors, decongestion, and comprehensive HF care. CKM features organize risk and monitoring intensity but should not be treated as diagnostic…

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  Figure 2. Practical implementation of finerenone in heart failure with LVEF ≥40%. Finerenone implementation in HF with LVEF ≥40% should follow a safeguard-based sequence: confirm symptomatic HF with objective evidence and LVEF ≥40%, exclude mimickers or dominant alternative causes of symptoms, verify local label eligibility and follow-up feasibility, and assess baseline serum potassium, eGFR, and renal stability. Finerenone should be used for chronic risk reduction, not rescue decongestion or replacement of loop diuretics. Initiation should be delayed or reassessed in patients with high potassium, low or unstable eGFR, acute illness or acute kidney injury, or no feasible laboratory follow-up. Before treatment, clinicians should review CYP3A4 inhibitors, potassium supplements, NSAIDs, RAAS inhibitors, diuretic changes, and dehydration risk. HF-specific dosing should be based on eGFR and adjusted according to potassium and eGFR. Laboratory testing should be repeated around 4 weeks after initiation or dose change, with continuation, dose adjustment, or temporary interruption guided by potassium, renal function, acute illness, intake, and hydration status. Higher monitoring intensity is…