Key result
Higher CONUT score linked to ~13% higher composite outcome risk per point in HFpEF.
Why the study?
The incremental prognostic value of a simple nutritional score beyond NT-proBNP in HFpEF, as well as the clinical relevance of effect modification by systemic inflammation, had not been established.
Does the Controlling Nutritional Status (CONUT) score improve prognostic prediction of composite clinical events (all-cause mortality, cardiovascular death, HF hospitalisation, or sudden cardiac death) beyond NT-proBNP in patients with HFpEF?
Cohort (n=1,061)
No
Does the Controlling Nutritional Status (CONUT) score improve prognostic prediction of composite clinical events (all-cause mortality, cardiovascular death, HF hospitalisation, or sudden cardiac death) beyond NT-proBNP in patients with HFpEF?
The CONUT nutritional score provides incremental prognostic value beyond NT-proBNP for predicting adverse clinical outcomes in HFpEF, particularly among patients with elevated systemic inflammation (hsCRP ≥3 mg/L).
CONUT may refine HFpEF risk stratification amid inflammation; hypothesis-generating and requires prospective validation before practice change.
Background Despite the recognised co-occurrence of malnutrition and systemic inflammation in heart failure with preserved ejection fraction (HFpEF), the incremental prognostic value of a simple nutritional score beyond NT-proBNP—and the clinical relevance of inflammation-driven effect modification—has not been established. Aims We evaluated the prognostic utility of the Controlling Nutritional Status (CONUT) score in HFpEF, tested effect modification by inflammation (hsCRP), compared CONUT with PNI and GNRI, and quantified incremental utility using NRI and decision-curve analysis (DCA). Methods From a retrospective single-centre HFpEF registry (n=2,190), 1,061 patients with complete NT-proBNP and hsCRP were analysed. CONUT (albumin, cholesterol, lymphocyte count) was evaluated alongside PNI and GNRI. The primary composite comprised all-cause mortality, cardiovascular death, HF hospitalisation, or sudden cardiac death. Cox models adjusted for age, sex, BMI, eGFR, LVEF, log(NT-proBNP), comorbidities and therapy, including a pre-specified CONUT×hsCRP interaction (≥3 vs <3 mg/L). Incremental utility was assessed by ΔC-index, category-free NRI, and 1-year DCA. Results Over a median follow-up of 2.8 years, 400 composite events and 284 all-cause deaths occurred. CONUT was independently associated with the composite outcome (adjusted HR 1.129 per point; 95% CI 1.084–1.175; P<0.001). Discrimination gains were modest (ΔC-index 0.0080), but reclassification improved (category-free NRI 2.3%, bootstrap 95% CI 0.9–4.0%; P=0.002), outperforming PNI and GNRI. Clinical+CONUT increased net benefit on 1-year DCA across 10–30% thresholds (30%: 0.85 fewer missed events/100). Interaction was significant (P=0.014): HR per point 1.153 with hsCRP ≥3 mg/L vs 1.082 with hsCRP <3 mg/L. Conclusions CONUT provides incremental prognostic and clinical utility beyond NT-proBNP, particularly with elevated hsCRP, defining a malnutrition–inflammation phenotype that may inform triage and nutritional evaluation. As a retrospective single-centre study without external validation, prospective confirmation is required.
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Yang et al. (2026) conducted a cohort in Heart failure with preserved ejection fraction (HFpEF) (n=1,061). Controlling Nutritional Status (CONUT) score vs. Prognostic Nutritional Index (PNI) and Geriatric Nutritional Risk Index (GNRI) was evaluated on Composite of all-cause mortality, cardiovascular death, HF hospitalisation, or sudden cardiac death (HR 1.129 per point, 95% CI 1.084-1.175, p=<0.001). The CONUT score was independently associated with the primary composite outcome in HFpEF (adjusted HR 1.129 per point; 95% CI 1.084–1.175; P<0.001), particularly with elevated hsCRP.
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