Author + information
- Received October 11, 2018
- Revision received November 27, 2018
- Accepted November 27, 2018
- Published online March 4, 2019.
- Domingo A. Pascual-Figal, MD, PhDa,b,c,∗ (, )
- Antoni Bayes-Genis, MD, PhDc,d,
- Maria C. Asensio-Lopez, MSca,
- Alvaro Hernández-Vicente, BSca,
- Iris Garrido-Bravo, MD, PhDa,
- Francisco Pastor-Perez, MD, PhDa,
- Javier Díez, MD, PhDc,e,f,g,
- Borja Ibáñez, MD, PhDb,c,h and
- Antonio Lax, PhDa
- aCardiology Department, Hospital Virgen de la Arrixaca, IMIB-Arrixaca, University of Murcia, Murcia, Spain
- bCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, España
- cCIBERCV, Madrid, Spain
- dHeart Institute, Hospital Universitari Germans Trias i Pujol, Badalona, Spain
- eDepartments of Nephrology, and Cardiology and Cardiac Surgery, University of Navarra Clinic, Pamplona, Spain
- fProgram of Cardiovascular Diseases, Centre for Applied Medical Research, University of Navarra, Pamplona, Spain
- gInstituto de Investigación Sanitaria de Navarra, IDISNA, Pamplona, Spain
- hIIS-Fundación Jiménez Díaz University Hospital, Madrid, Spain
- ↵∗Address for correspondence:
Dr. Domingo A. Pascual-Figal, Cardiology Department, University of Murcia, LAIB, Room 2.52, Avenue Buenavista s/n, 30120 Murcia, Spain.
Background Soluble ST2 (sST2), which is the soluble form of interleukin (IL)-1 receptor-like 1, identifies risk in acutely decompensated heart failure (ADHF). IL-1β is an inflammatory cytokine that has deleterious effects in myocardial remodeling and function. IL-1β inhibition has beneficial effects after acute myocardial infarction. However, the role of IL-1β in ADHF and its relationship to ST2 remain unclear.
Objectives This study sought to investigate the relationship between IL-1β and sST2, and the prognostic impact of such a relationship in patients with ADHF.
Methods This study examined 316 consecutive patients who were hospitalized with ADHF (72 ± 12 years of age, 57% male, and left ventricular ejection fraction 45 ± 17%). Blood samples were collected at presentation, and IL-1β and sST2 levels were measured. All-cause mortality was obtained for all patients at 1 year.
Results The IL-1β concentration at presentation was associated with prior HF hospitalizations, functional impairment, and higher N-terminal pro–B-type natriuretic peptide and high-sensitivity troponin T concentrations. IL-1β was higher in patients who died during the year after hospitalization (n = 52, 16.5%) (p = 0.005), and the optimal threshold was identified with levels over 49.1 pg/ml (hazard ratio: 2.5; 95% confidence interval: 1.43 to 4.49; p = 0.0014). Circulating IL-1β positively correlated with sST2 (ρ = 0.65; p < 0.001). Considering the prognostic thresholds of IL-1β (≥49.1 pg/ml) and sST2 (≥35.0 ng/ml) concentrations: all patients with low sST2 also presented with low IL-1β; among patients with high sST2, only those with also high IL-1β had a significantly higher risk of death (30% vs. 14%; hazard ratio: 2.52; 95% confidence interval: 1.40 to 4.56; p = 0.002).
Conclusions Circulating IL-1β concentrations are clinically meaningful in ADHF patients and interplay with the predictive ability of sST2. IL-1 axis-related inflammation signaling may represent a therapeutic target in ADHF.
This work has been supported by grants PI14/01637 and PI17/01742 from “Instituto de Salud Carlos III,” Madrid, Spain, and grant PI14/19334 from “Fundación Séneca de Ciencia y Tecnología de la Región de Murcia,” Murcia, Spain. Dr. Pascual-Figal has received grant support from Roche Diagnostics; and has received educational fees from Novartis. Dr. Bayes-Genis has received speaker fees from Novartis, Roche, and Critical Diagnostics. Dr. Díez has received educational fees from Novartis. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Listen to this manuscript's audio summary by Editor-in-Chief Dr. Valentin Fuster on JACC.org.
- Received October 11, 2018.
- Revision received November 27, 2018.
- Accepted November 27, 2018.
- 2019 American College of Cardiology Foundation
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