Key result
Statin therapy mitigates the ~2.3-fold higher mortality linked to elevated PIV in acute HFpEF.
Why the study?
Although inflammation plays a role in the pathophysiology of HFpEF, this knowledge is not yet utilized in clinical practice, motivating an evaluation of the association between statin therapy, immune-inflammatory biomarkers, and 5-year mortality.
Does statin therapy at discharge modify the association between immune-inflammatory biomarkers and 5-year all-cause mortality in patients hospitalized for acute heart failure with preserved ejection fraction?
Cohort (n=311)
Does statin therapy at discharge modify the association between immune-inflammatory biomarkers and 5-year all-cause mortality in patients hospitalized for acute heart failure with preserved ejection fraction?
Immune-inflammatory biomarkers, particularly derived neutrophil-to-lymphocyte ratio and pan-immune-inflammation value, strongly predict 5-year mortality in statin-naïve patients with acute HFpEF, whereas statin therapy attenuates this prognostic risk.
Suggests potential statin benefit amid inflammatory risk in acute HFpEF; leaves open confirmation in randomized trials.
Background Heart failure with preserved ejection fraction (HFpEF) is characterized by diastolic dysfunction of left ventricle. There is evidence on the role of inflammation in the pathophysiology of HFpEF, however this knowledge is yet to be utilized in clinical practice. Purpose We conducted a study to evaluate the association between statin therapy, levels of immune–inflammatory biomarkers (IIBs), and 5-year mortality among patients with HFpEF in a Polish population. Methods We analyzed 311 HFpEF patients hospitalized for acute heart failure between 2009 and 2019 included in the Lesser Poland Cracovian Heart Failure Registry. Baseline clinical, echocardiographic, and laboratory data, including IIBs, were collected. Patients were stratified according to statin therapy at discharge, and all-cause mortality was assessed. Results Elevated systemic immune-inflammation index (SII) without statins was associated with the lowest survival, whereas high lymphocyte-to-monocyte ratio (LMR) and low pan-immune-inflammation value (PIV) among statin users conferred the best outcomes. LMR was associated with reduced mortality in HFpEF patients not receiving statins (OR 0.46, 95% CI 0.26–0.82). NLR (neutrophil to lymphocyte ratio) (OR 1.51, 95% CI 1.03–2.22, P=0.034), dNLR (derived NLR) (OR 1.92, 95% CI 1.07–3.45, P=0.029), SII (OR 2.09, 95% CI 1.19–3.67, P=0.010) and PIV (OR 2.32, 95% CI 1.13–4.78, P=0.023) independently predicted mortality in the non-statin group, with statins attenuating the prognostic value of dNLR (P for interaction = 0.042) and PIV (P for interaction = 0.036). Conclusions The IIBs, particularly dNLR and PIV, were strong predictors of mortality in statin-naïve HFpEF patients, whereas statin therapy attenuated their prognostic value.
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Stepien et al. (2026) conducted a cohort in Heart failure with preserved ejection fraction (HFpEF) hospitalized for acute heart failure (n=311). Statin therapy at discharge and immune-inflammatory biomarkers vs. No statin therapy at discharge was evaluated on 5-year all-cause mortality (OR 2.32, 95% CI 1.13-4.78, p=0.023). Statin therapy attenuated the mortality risk of elevated PIV (OR 2.32, 95% CI 1.13-4.78 in non-statin users; Pinteraction=0.036) and dNLR (Pinteraction=0.042) in acute HFpEF.
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