American heart journal plus : cardiology research and practice · 2026
Dynamic change in soluble suppressor of tumorigenicity 2 (sST2) during acute decompensated heart failure with a reduced ejection fraction, and its mortality implications.
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Li Brian, Dowley Michaela, Langley Samantha, Cliffe Paraic, Whiting Stephen, Ganapathy Archana, Dimarco Anthony D, Barbagallo Rossella, Dungu Jason N, Savage Henry Oluwasefunmi
Аннотация
AIMS: To evaluate the association of soluble suppression of tumorigenicity 2 (sST2) concentrations measured at clinician-determined decompensation and recompensation, and their change between these states, with one-year mortality in acute decompensated heart failure (ADHF).
METHODS: Paired sST2 samples were obtained at decompensation and recompensation from 168 patients hospitalized with ADHF and a left ventricular ejection fraction of <50%. Associations with one-year all-cause mortality were assessed using Cox regression and Kaplan-Meier analysis. Discrimination was evaluated using receiver operating characteristic curves, with exploratory cut-offs derived using Youden's index.
RESULTS: The median age was 71.5 years (IQR 62-80.8), 39 (23.2%) were women, median LVEF was 26% (IQR 17.5-32.5), and 158 (94.1%) had NYHA class III or IV symptoms. During one-year follow-up, 34 patients (20.2%) died. Each doubling of decompensation sST2 was associated with higher mortality after adjustment for creatinine (HR 1.67, 95% CI 1.23-2.25). Recompensation sST2 remained associated with mortality after adjustment for creatinine and NT-proBNP (HR per doubling 1.71, 95% CI 1.18-2.48). The respective areas under the curve were 0.686 and 0.688, with exploratory cut-offs of 66.5 and 57 ng/mL. Unchanged or increased sST2 was associated with higher mortality than decreased sST2 in unadjusted analysis (HR 2.76, 95% CI 1.37-5.59, p = 0.003).
CONCLUSION: Elevated sST2 at decompensation and unchanged or increased concentrations during recompensation were associated with one-year mortality in patients with ADHF. These findings support further evaluation of sST2 as an adjunctive prognostic biomarker in this setting; the cohort-derived cut-offs require validation.
METHODS: Paired sST2 samples were obtained at decompensation and recompensation from 168 patients hospitalized with ADHF and a left ventricular ejection fraction of <50%. Associations with one-year all-cause mortality were assessed using Cox regression and Kaplan-Meier analysis. Discrimination was evaluated using receiver operating characteristic curves, with exploratory cut-offs derived using Youden's index.
RESULTS: The median age was 71.5 years (IQR 62-80.8), 39 (23.2%) were women, median LVEF was 26% (IQR 17.5-32.5), and 158 (94.1%) had NYHA class III or IV symptoms. During one-year follow-up, 34 patients (20.2%) died. Each doubling of decompensation sST2 was associated with higher mortality after adjustment for creatinine (HR 1.67, 95% CI 1.23-2.25). Recompensation sST2 remained associated with mortality after adjustment for creatinine and NT-proBNP (HR per doubling 1.71, 95% CI 1.18-2.48). The respective areas under the curve were 0.686 and 0.688, with exploratory cut-offs of 66.5 and 57 ng/mL. Unchanged or increased sST2 was associated with higher mortality than decreased sST2 in unadjusted analysis (HR 2.76, 95% CI 1.37-5.59, p = 0.003).
CONCLUSION: Elevated sST2 at decompensation and unchanged or increased concentrations during recompensation were associated with one-year mortality in patients with ADHF. These findings support further evaluation of sST2 as an adjunctive prognostic biomarker in this setting; the cohort-derived cut-offs require validation.