Author + information
- Received June 27, 2019
- Revision received August 7, 2019
- Accepted August 31, 2019
- Published online October 21, 2019.
- Alberto Aimo, MDa,
- James L. Januzzi Jr., MDb,
- Antoni Bayes-Genis, MD, PhDc,
- Giuseppe Vergaro, MD, PhDa,d,
- Paolo Sciarrone, MDd,
- Claudio Passino, MDa,d and
- Michele Emdin, MD, PhDa,d,∗ ( )(, )@MicheleEmdin@JJheart_doc
- aInstitute of Life Sciences, Scuola Superiore Sant’Anna, Pisa, Italy
- bMassachusetts General Hospital and Baim Institute for Clinical Research, Boston, Massachusetts
- cHospital Universitari Germans Trias i Pujol, Badalona (Barcelona), CIBERCV, Barcelona, Spain
- dCardiology Department, Fondazione Toscana Gabriele Monasterio, Pisa, Italy
- ↵∗Address for correspondence:
Dr. Michele Emdin, Scuola Superiore Sant’Anna and Fondazione Toscana Gabriele Monasterio, Via G. Moruzzi 1—56124 Pisa, Italy.
• sST2 is released in response to vascular congestion, inflammatory, and pro-fibrotic stimuli.
• sST2 is a strong predictor of outcome in HF.
• The prognostic value of sST2 in HF is additive to natriuretic peptides.
Soluble suppression of tumorigenesis-2 (sST2) is released in response to vascular congestion and inflammatory and pro-fibrotic stimuli, and is a strong, independent predictor of mortality and heart failure (HF) hospitalization in patients with acute or chronic HF. sST2 meets 2 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. In particular, the prognostic value of sST2 is additive to natriuretic peptides and (in the case of chronic HF) to high-sensitivity troponin T. Nevertheless, 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. Four years after a consensus document on sST2, and following major advances in the comprehension of the clinical value of this biomarker, the authors felt it worthwhile to reappraise current knowledge on sST2 in HF.
Dr. Januzzi is supported in part by the Hutter Family Professorship; is a Trustee of the American College of Cardiology; has received grant support from Novartis Pharmaceuticals, Roche Diagnostics, Abbott, Singulex, and Prevencio; has received consulting income from Abbott, Janssen, Novartis, Pfizer, Merck, Roche Diagnostics, and Critical Diagnostics; and participates in Clinical Endpoint Committees/Data Safety Monitoring Boards for Abbott, AbbVie, Amgen, Boehringer Ingelheim, Janssen, and Takeda. Dr. Bayes-Genis has received grant support from Roche Diagnosis; has received lecture honoraria from Roche Diagnostics and Critical Diagnostics; and has received consulting income from Roche Diagnostics, Critical Diagnostics, and Novartis. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. David A. Morrow, MD, served as Guest Associate Editor for this paper.
- Received June 27, 2019.
- Revision received August 7, 2019.
- Accepted August 31, 2019.
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