Summary: In a prespecified participant-level pooled analysis of three randomised trials (14,581 patients across the cardio-kidney-metabolic spectrum, free of arrhythmia at baseline), the nonsteroidal mineralocorticoid receptor antagonist finerenone modestly lowered the rate of new-onset atrial fibrillation or flutter compared with placebo (3.9% vs 4.7%; HR 0.83, 95% CI 0.71 to 0.97; P=0.019). The absolute risk reduction was roughly 0.8 percentage points over a median 2.9 years.
PICO Summary
| Element | Detail |
|---|---|
| Population | 14,581 participants free of atrial fibrillation/flutter at enrolment, pooled across the cardio-kidney-metabolic spectrum (FIDELIO-DKD and FIGARO-DKD in chronic kidney disease with type 2 diabetes, and FINEARTS-HF in heart failure with mildly reduced or preserved ejection fraction); multinational. |
| Intervention | Finerenone, a nonsteroidal mineralocorticoid receptor antagonist, at trial-specified doses (n=7,283 randomised to finerenone across the pooled cohort). |
| Comparison | Placebo on a background of standard care (n=7,298), randomised 1:1. |
| Outcome | New-onset atrial fibrillation/flutter (blinded adjudication): 286/finerenone (3.9%) vs 345/placebo (4.7%). HR 0.83 (95% CI 0.71 to 0.97; P=0.019). Absolute risk reduction approximately 0.8 percentage points; NNT approximately 125 over a median 2.9 years. Effect consistent by number of cardio-kidney-metabolic conditions (P interaction 0.87) and by trial (P 0.57). No safety or hyperkalaemia data were reported for this analysis. |
Finerenone and new-onset atrial fibrillation
FINE-HEART pooled analysis · 3 RCTs · median 2.9 y
Finerenone cut new-onset atrial fibrillation/flutter by 17% across the cardio-kidney-metabolic spectrum, but the small absolute benefit makes it a bonus rather than a standalone indication.
Expert Commentary
This pooled analysis is best read as hypothesis-strengthening rather than practice-defining. New-onset atrial fibrillation or flutter was a prespecified but non-primary endpoint, and the three constituent trials were powered for cardiorenal and heart-failure outcomes, not arrhythmia. Within those limits the signal is coherent: a relative risk reduction of 17% (HR 0.83), with confidence intervals that exclude no effect, and a result that was consistent across the cardio-kidney-metabolic spectrum and by trial. The mechanistic rationale, namely attenuation of fibrosis and inflammation through mineralocorticoid receptor blockade, is biologically plausible. The most important caveat is magnitude. The absolute risk reduction was only about 0.8 percentage points over nearly three years, implying a number-needed-to-treat near 125 for this single outcome, so atrial fibrillation prevention alone would not justify therapy. It should be weighed alongside the established renal and heart-failure benefits that already drive finerenone use. The trials were placebo-controlled and blindly adjudicated, which is reassuring, but the manufacturer (Bayer) sponsored them and several authors are employees, so independent confirmation is welcome. Can I use this with my patients? Yes, but as a secondary consideration: in a patient with chronic kidney disease and type 2 diabetes or with heart failure with preserved ejection fraction who already meets criteria for finerenone, a lower arrhythmia risk is a welcome bonus rather than a standalone indication. I would like to see a prospectively powered trial confirm the effect.
References
Pabon MA, Filippatos G, Claggett BL, et al. Finerenone reduces new-onset atrial fibrillation across the spectrum of cardio-kidney-metabolic syndrome: the FINE-HEART pooled analysis. J Am Coll Cardiol. 2025;85(17):1649-1660. doi:10.1016/j.jacc.2025.03.429