The following are key points to remember from this state-of-the-art review on the clinical and prognostic significance of soluble suppression of tumorigenesis-2 (sST2) in heart failure (HF):

1. sST2 is released in response to vascular congestion and inflammatory and profibrotic stimuli, and is a strong, independent predictor of mortality and HF hospitalization in patients with acute or chronic HF.
2. sST2 meets two fundamental criteria for clinically useful biomarkers: accurate, repeated measurements are available at a reasonable cost, and the biomarker provides information not already available from a careful clinical assessment.
3. Furthermore, the prognostic value of sST2 is additive to natriuretic peptides and (in the case of chronic HF) to high-sensitivity troponin T.
4. The 2013 American College of Cardiology Foundation/American Heart Association HF guidelines recommended to assess biomarkers of inflammation and fibrosis to refine prognostic stratification, with a low class of recommendation (Class IIb; Level of Evidence B for chronic HF, Level of Evidence A for acute HF) and do not cite or recommend any specific biomarker.
5. The 2017 update of these guidelines includes a similar recommendation for chronic HF, whereas acute HF is not mentioned.
6. The 2016 European Society of Cardiology HF guidelines state that the evidence of sST2 and other emerging biomarkers is still not so compelling to recommend their use in clinical practice.
7. Based on available data, it seems reasonable to suggest that sST2 be measured at least on admission for acute HF, and at the planned discharge. Patients whose sST2 levels do not decrease might be considered to be at higher risk, which may suggest a prolongation of the hospital stay, a more rapid up-titration of HF drugs (after hemodynamic stabilization), as well as more frequent visits after discharge or the use of monitoring systems to detect pulmonary congestion.
8. In chronic HF, sST2 measurement may possibly be a valuable tool for risk stratification, either alone or together with natriuretic peptides and troponins, but the possibility to guide HF treatment on this basis (e.g., up-titrating or switching drugs, or deciding whether to refer a patient with nonischemic dilated cardiomyopathy and mild systolic dysfunction for defibrillator implantation) remains to be investigated.
9. It should be noted that the need for a multibiomarker approach to risk stratification and the role of sST2 as a guide to therapy decision making remain to be established.
10. Future studies need to establish if a sST2-guided management of acute or chronic HF patients could have a positive effect on patient symptoms and disease evolution and on hard clinical outcomes.

Keywords: Biomarkers, Carcinogenesis, Cardiomyopathy, Dilated, Defibrillators, Heart Failure, Hemodynamics, Inflammation, Length of Stay, Natriuretic Peptides, Secondary Prevention, Troponin, Troponin T

< Back to Listings