Finerenone’s Efficacy in HF Unaffected by Concomitant CKM Components

Finerenone’s efficacy and safety in heart failure (HF) are not impacted by the presence of ≥1 cardio-kidney-metabolic (CKM) condition at baseline, according to a secondary analysis of FINEARTS-HF.1

These data were presented at the European Society of Cardiology (ESC) Congress 2026 in Munich, Germany, by John Ostrominski, MD, a fellow in cardiovascular medicine and an obesity medicine specialist at Brigham and Women’s Hospital.1

“This is really a snapshot view of those who were eligible for the trial at randomization, so we’re a bit limited in what we can say in terms of how often or how prominently these conditions were drivers of the condition,” Ostrominski told HCPLive in an exclusive interview. “But I do think it has implications for the causality of at least HFpEF and the breadth of the view that’s needed to really engage in comprehensive care in this population.”

FINEARTS-HF was a randomized, double-blind, international, multicenter, parallel-group, event-driven trial comparing finerenone to placebo in patients with HF with preserved ejection fraction (HFpEF). Eligible patients were required to be ≥40 years old with symptomatic HF, a left ventricular ejection fraction (LVEF) of ≥40%, evidence of structural heart disease, and elevated natriuretic peptide levels.2

Eligible patients were randomly assigned in a 1:1 ratio to either finerenone or matching placebo on top of standard therapy. Finerenone was administered at a maximum of 20 mg or 40 mg once daily, depending on baseline estimated glomerular filtration rate (eGFR). The study’s primary outcome was a composite of total worsening HF events and cardiovascular death. Secondary outcomes included total worsening HF events, change from baseline in the total symptom score from the Kansas City Cardiomyopathy Questionnaire (KCCQ), and improvement in New York Heart Association (NYHA) functional class by month 12.2

A total of 6016 patients were enrolled in the trial. Mean (+/- standard deviation [SD]) LVEF was 53 +/- 8%, and 69.1% of patients were in NYHA functional class II. 1219 patients were enrolled during or ≤7 days after an HF event. At baseline, 84.9% of patients were receiving beta-blockers, 35.9% were receiving angiotensin-converting enzyme inhibitors, 35% were receiving angiotensin-receptor blockers, 8.5% were receiving angiotensin receptor-neprilysin inhibitors, and 13.6% were receiving SGLT2 inhibitors.2

Over a median follow-up of 32 months, investigators recorded 1083 primary-outcome events among 624 of 3003 patients in the finerenone arm. Another 1283 primary-outcome events occurred in 719 of the 2998 patients assigned to receive placebo (rate ratio [RR], 0.84; 95% CI, 0.74 to 0.95; P = .007). The total number of worsening HF events was 842 in the finerenone arm versus 1024 in the placebo arm (RR, 0.82; 95% CI, 0.71 to 0.94; P = .006).2

In the present analysis, Ostrominski and colleagues examined the same patient population for the presence of ≥1 aspect of CKM syndrome. These included cardiovascular disease, defined as a history of atherosclerotic cardiovascular disease (ASCVD) or atrial fibrillation/flutter, chronic kidney disease (CKD), or metabolic disease, defined as either obesity, type 2 diabetes, or history of metabolic dysfunction-associated steatotic liver disease.1

Of the 6001 patients who ultimately completed FINEARTS-HF, 5977 had ≥1 concomitant CKM component. Of these, 619 had 0-1 overlapping components, 2170 had 2 overlapping components, and 3212 had 3 overlapping components. Those with 2 (adjusted RR, 1.32; 95% CI, 1.02-1.72) and 3 (adjusted RR, 2.58; 95% CI, 2.01-3.32) components saw incrementally higher rates of the primary composite outcome of cardiovascular death and total HF events after a median follow-up of 2.7 years. However, the benefits of finerenone on cardiovascular death and HF events appeared consistent irrespective of the number of CKM components.1

“I suspect that the broad message here is that this profile, these intersectional diseases, is very much consistent with how we’re increasingly viewing HFpEF and HFrEF as a disease that is really mediated, but also sort of feeding back into these general profiles and pathways of multiple long-term conditions,” Ostrominski said. “This message has important implications for how we think about the disease, but there are certain things that we just didn’t quite have access to in the trial, and so it’s important to acknowledge these limitations.”

Editors’ Note: Ostrominski reports receiving grant support from the National Institutes of Health.

References

1. Ostrominski J. Cardiovascular-kidney-metabolic overlap and finerenone in heart failure: insights from the FINEARTS-HF Trial. Presented at the European Society of Cardiology (ESC) Congress 2026, Munich, Germany. August 28-31, 2026.

2. Pabon MA, Vardeny O, Vaduganathan M, et al. Finerenone in heart failure with improved ejection fraction. JAMA Cardiology. 2025;10(7):740. doi:10.1001/jamacardio.2025.1101