Why the study?
Does elevated serum uric acid increase recorded all-cause mortality in hospitalized patients with exacerbated/decompensated chronic heart failure?
Observational (n=553)
No
Does elevated serum uric acid increase recorded all-cause mortality in hospitalized patients with exacerbated/decompensated chronic heart failure?
Serum uric acid is a marker of disease severity in hospitalized heart failure patients, but it does not provide independent prognostic value for mortality when accounting for established biomarkers like NT-proBNP and LVEF.
Elevated UA was associated with higher mortality risk in hospitalized HF; leaves open incremental prognostic value beyond NT-proBNP and need for trials.
Serum uric acid (UA) is a routinely measured laboratory parameter, and elevated levels have been associated with adverse cardiovascular outcomes. However, its prognostic role in hospitalized patients with heart failure remains insufficiently clarified. The aim of this study was to evaluate the association between serum UA levels and recorded all-cause mortality in hospitalized patients with heart failure and to assess whether UA provides additional prognostic information beyond N-terminal pro-B-type natriuretic peptide (NT-proBNP), C-reactive protein (CRP), creatinine, and left ventricular ejection fraction (LVEF). This retrospective observational study included patients hospitalized with exacerbated/decompensated chronic heart failure at University Hospital “Tsaritsa Yoanna – ISUL” between September 2023 and October 2025. Patients meeting the predefined study criteria and with available serum UA measurements were included. Demographic characteristics, cardiovascular comorbidities, LVEF, NT-proBNP, CRP, and creatinine were analyzed. Patients were stratified into quintiles according to serum UA levels. The primary outcome was recorded all-cause mortality at the time of data extraction. Correlation analyses and univariable and multivariable logistic regression analyses were performed. A total of 553 patients were included; mean age was 72.4 ± 11.6 years. Mortality status was available for 552 patients, and recorded all-cause mortality was observed in 138 patients (25.0%). Higher UA quintiles were associated with higher NT-proBNP, CRP, and creatinine levels, and with lower LVEF. Recorded all-cause mortality differed significantly across UA quintiles, with the highest proportion in the highest quintile (36.7%; p = 0.019). In the clinically adjusted model including uric acid-lowering therapy, the highest UA quintile (>562 μmol/L) was associated with recorded all-cause mortality (OR 2.14; 95% CI 1.15–4.01; p = 0.017). After further adjustment for NT-proBNP, CRP, creatinine, and LVEF, this association was attenuated and was no longer statistically significant. In hospitalized patients with heart failure and available serum UA measurements, higher serum UA levels were associated with adverse cardiorenal-inflammatory profiles and recorded all-cause mortality. However, this association was attenuated after adjustment for established biomarkers and LVEF. These findings support serum UA as an integrative marker of disease severity, with limited incremental prognostic information beyond established biomarkers in the present cohort.
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Krastev et al. (2026) conducted an observational in exacerbated/decompensated chronic heart failure (n=553). Elevated serum uric acid (highest quintile >562 μmol/L) vs. Lower serum uric acid quintiles was evaluated on recorded all-cause mortality at the time of data extraction (OR 2.14, 95% CI 1.15-4.01, p=0.017).
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