Prognostic Value of Serial Measurements of Soluble Suppression of Tumorigenicity 2 and Galectin-3 in Ambulatory Patients With Chronic Heart Failure

• sST2 and galectin-3 target pathways leading to myocardial fibrosis.
• In time-dependent multivariate analysis, sST2 is an independent predictor.
• sST2 demonstrated incremental value in reclassifying patients to higher risk.
• Serial monitoring of sST2 but not galectin-3 identifies highest-risk HF outpatients.

BackgroundB-Type natriuretic peptides (BNP) and cardiac troponin T (cTnT) predict cardiovascular events in heart failure (HF) patients, but additional refinement in risk stratification may be possible by targeting pathways leading to fibrosis. We aimed to assess the value of serial measurements of soluble suppression of tumorigenicity 2 (sST2) and galectin-3 to identify risk for adverse pathophysiologic processes.MethodsNew York Heart Association (NYHA) functional class III–IV HF patients (n = 180; LVEF ≤40%) were prospectively evaluated with biomarkers collected every 3 months over 2 years and analyzed regarding a primary end point of death/cardiac transplantation and a secondary end point of HF-related hospitalization or death/transplantation.ResultsTime-dependent univariate analyses demonstrated that elevations of sST2 (≥49.3 ng/mL male, ≥33.5 ng/mL female) and galectin-3 (≥22.1 ng/mL) were predictive of the primary and secondary end points. In multivariate models adjusted for BNP, cTnT, and clinical variables, sST2 but not galectin-3 remained an independent predictor (hazard ratio 3.22, 95% confidence interval 1.76–5.89; P < .001). With serial measurements, only sST2 demonstrated incremental value in reclassifying patients to higher risk.ConclusionsSerial monitoring of sST2 (indicating myocardial fibrosis and remodeling) and cTnT (reflecting myocardial injury) identifies highest-risk HF outpatients and may be valuable to guide patient tailored therapy during follow-up evaluations. Serial galectin-3 monitoring in ambulatory HF patients may not be of benefit.