Dynamic change in soluble suppressor of tumorigenicity 2 (sST2) during acute decompensated heart failure with a reduced ejection fraction, and its mortality implications

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 sST 2 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.