Prognostic Value of Soluble Suppression of Tumorigenicity-2 in Chronic Heart Failure: A Meta-Analysis.


Journal Article

OBJECTIVES: The purpose of this study was to perform the first meta-analysis of currently available data. BACKGROUND: Soluble suppression of tumorigenesis 2 (sST2) plasma concentration is elevated in chronic heart failure (CHF) and helps to predict prognosis in this setting, although the evidence is limited. METHODS: Three databases (Medline, Cochrane Library, and Scopus) were searched. Inclusion criteria were: follow-up studies; papers published in English; enrollment of CHF outpatients; available data on hazard ratio (HR) for the log2 ST2 (so that the reported HRs represent the risk per doubling of sST2) and 95% confidence interval (CI) for all-cause death, and possibly also for cardiovascular (CV) death; and use of standardized sST2 assay. Exclusion criteria were: sST2 considered only as an element of a prognostic score, and studies on patients with end-stage HF. RESULTS: Seven studies were finally included for all-cause death, with a global population of 6,372 patients; data on CV death were available for 5 studies, totaling 5,051 patients. The HR was 1.75 (95% CI: 1.37 to 2.22) for all-cause death and 1.79 (95% CI: 1.22 to 2.63) for CV death (both p < 0.001). Significant heterogeneity among studies was detected in the quantification of sST2 predictive value, attributable to marked differences in pharmacological treatment among trials. The predictive power of sST2 was greater when patients were managed according to present guideline-recommended medical treatment. CONCLUSIONS: sST2 is a predictor of both all-cause and CV death in CHF outpatients. The present meta-analysis supports the use of sST2 for risk stratification in patients with stable CHF.

Full Text

Duke Authors

Cited Authors

  • Aimo, A; Vergaro, G; Passino, C; Ripoli, A; Ky, B; Miller, WL; Bayes-Genis, A; Anand, I; Januzzi, JL; Emdin, M

Published Date

  • April 2017

Published In

Volume / Issue

  • 5 / 4

Start / End Page

  • 280 - 286

PubMed ID

  • 27816512

Pubmed Central ID

  • 27816512

Electronic International Standard Serial Number (EISSN)

  • 2213-1787

Digital Object Identifier (DOI)

  • 10.1016/j.jchf.2016.09.010


  • eng

Conference Location

  • United States