Author + information
- Salvatore Patanè, MD∗ ()
- ↵∗Cardiologia Ospedale San Vincenzo–Taormina (Me) Azienda Sanitaria Provinciale di Messina, Italy, Contrada Sirina, 98039 Taormina (Messina), Italy
I read the paper by van Vark et al. (1) with great interest and congratulate the authors on their excellent work. As the authors correctly state, soluble ST2, which is the form measured by current assays, acts as a decoy receptor for interleukin (IL)-33 and prevents the IL-33/ST2L interaction and subsequent cardioprotective cascade of events (1). The authors also correctly state that repeated ST2 measurements appear to be strong predictors of outcome in patients with acute heart failure, independent of repeatedly measured N-terminal pro–B-type natriuretic peptide. However, I would like to call attention to several points that need further clarification. Research has reported that micro–ribonucleic acid-487b promotes the protective response of IL-33 in the heart, binding to the IL-33 3′-untranslated region to activate IL-33 transcripts (2). Research has also reported that missense variants of IL1RL1 (the gene encoding ST2) map to the intracellular domain of ST2 (which is absent in sST2), resulting in increased levels of sST2 and altering immune and inflammatory signaling through the ST2/IL-33 pathway; this research suggests that much of the variation in sST2 production is driven by genetic factors (3,4). The findings of van Vark et al. (1) add significant information to previously published data, but evaluating the real effect of these aspects would also be useful for a better understanding of the value of serial ST2 measurements in patients with acute heart failure.
Please note: Dr. Patanè has reported that he has no relationships relevant to the contents of this paper to disclose.
- 2018 American College of Cardiology Foundation
- van Vark L.C.,
- Lesman-Leegte I.,
- Baart S.J.,
- et al.,
- for the TRIUMPH Investigators
- Wang E.W.,
- Jia X.S.,
- Ruan C.W.,
- Ge Z.R.