title: ST2 pathogenetic profile in ambulatory heart failure patients.
abstract: BACKGROUND
  Soluble ST2 is involved in multiple pathogenic pathways, including cardiac strain, inflammation, and myocardial necrosis with remodeling. The relative weight of ST2 and the point at which its prognostic value in heart failure (HF) is affected by different degrees of myocardial strain, inflammation, necrosis, and remodeling is unknown.
  
  
  RESULTS
  We examined whether soluble ST2 levels improves HF risk stratification relative to other biomarkers representative of multiple pathogenic pathways-N-terminal pro-B-type natriuretic peptide (NT-proBNP; strain), high-sensitivity C-reactive protein (hsCRP; inflammation), and galectin-3 and high-sensitivity troponin T (hsTnT; necrosis and remodeling)-in 1,015 patients with mean left ventricular ejection fraction (LVEF) 33.5%. Mean follow-up was 4.2 ± 2.1 years. The correlation with soluble ST2 was highest with NT-proBNP (r = 0.32; P < .001) and lowest with galectin-3 (r = 0.15; P < .001). ST2 levels increased with increasing concentrations of the other biomarkers (P < .001 in all cases). During follow-up, 467 patients died. Soluble ST2 remained an independent prognosticator of risk at every tertile of each biomarker. This was observed even after adjusting for clinical parameters.
  
  
  CONCLUSIONS
  Soluble ST2 may be regarded as a 3-in-1 prognosis biomarker in HF. ST2 provides valuable long-term risk stratification information in HF beyond that reported by other biomarkers of stretch, inflammation, necrosis, and remodeling.
authors.affiliation: Heart Failure Unit, Cardiology Department, Hospital Universitari Germans Trias i Pujol, Badalona, Spain; Department of Medicine, Autonomous University of Barcelona, Barcelona, Spain. Electronic address: abayesgenis@gmail.com.
authors.forename: Antoni
authors.initials: A
authors.lastname: Bayes-Genis
authors.affiliation: Cardiology Division, Medicine Department, Massachusetts General Hospital, Boston, Massachusetts, USA.
authors.forename: James L
authors.initials: JL
authors.lastname: Januzzi
authors.affiliation: Cardiology Division, Medicine Department, Massachusetts General Hospital, Boston, Massachusetts, USA.
authors.forename: Hanna K
authors.initials: HK
authors.lastname: Gaggin
authors.affiliation: Heart Failure Unit, Cardiology Department, Hospital Universitari Germans Trias i Pujol, Badalona, Spain; Department of Medicine, Autonomous University of Barcelona, Barcelona, Spain.
authors.forename: Marta
authors.initials: M
authors.lastname: de Antonio
authors.affiliation: Cardiology Division, Medicine Department, Massachusetts General Hospital, Boston, Massachusetts, USA.
authors.forename: Shweta R
authors.initials: SR
authors.lastname: Motiwala
authors.affiliation: Heart Failure Unit, Cardiology Department, Hospital Universitari Germans Trias i Pujol, Badalona, Spain; Department of Medicine, Autonomous University of Barcelona, Barcelona, Spain.
authors.forename: Elisabet
authors.initials: E
authors.lastname: Zamora
authors.affiliation: Biochemistry Department, Hospital Universitari Germans Trias i Pujol, Badalona, Spain.
authors.forename: Amparo
authors.initials: A
authors.lastname: Galán
authors.affiliation: Heart Failure Unit, Cardiology Department, Hospital Universitari Germans Trias i Pujol, Badalona, Spain.
authors.forename: Mar
authors.initials: M
authors.lastname: Domingo
authors.affiliation: Heart Failure Unit, Cardiology Department, Hospital Universitari Germans Trias i Pujol, Badalona, Spain; Department of Medicine, Autonomous University of Barcelona, Barcelona, Spain.
authors.forename: Agustín
authors.initials: A
authors.lastname: Urrutia
authors.affiliation: Heart Failure Unit, Cardiology Department, Hospital Universitari Germans Trias i Pujol, Badalona, Spain; Department of Medicine, Autonomous University of Barcelona, Barcelona, Spain.
authors.forename: Josep
authors.initials: J
authors.lastname: Lupón
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000453:epidemiology / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D015994:Incidence; D000072179:Interleukin-1 Receptor-Like 1 Protein; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010045:Outpatients; D010446:Peptide Fragments / Q000097:blood; D011379:Prognosis; D011446:Prospective Studies; D012372:ROC Curve; D011956:Receptors, Cell Surface / Q000378:metabolism*; D017472:Receptors, Interleukin-1; D018570:Risk Assessment; D015996:Survival Rate / Q000639:trends; D014481:United States / Q000453:epidemiology; D016277:Ventricular Function, Left
chemical_list: D015415:Biomarkers; C079241:IL1RL1 protein, human; D000072179:Interleukin-1 Receptor-Like 1 Protein; D010446:Peptide Fragments; D011956:Receptors, Cell Surface; D017472:Receptors, Interleukin-1; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain
keywords: Heart failure; biomarkers; prognosis