title: Serum soluble ST2: a potential novel mediator in left ventricular and infarct remodeling after acute myocardial infarction.
abstract: OBJECTIVE
  This study sought to assess, for the first time, the relationship between serum concentrations of the soluble interleukin-1 receptor family member ST2 (sST2) and serial change in left ventricular (LV) function after acute myocardial infarction (AMI).
  
  
  BACKGROUND
  Serum sST2 levels are elevated early after AMI and are associated with lower pre-discharge LV ejection fraction and adverse cardiovascular outcomes.
  
  
  METHODS
  The sST2 levels were measured in 100 patients (mean age 58.9 +/- 12.0 years; 77% male), admitted with AMI with resultant LV systolic dysfunction, at baseline and at 12 and 24 weeks. Patients underwent cardiac magnetic resonance imaging and measurement of N-terminal pro-brain natriuretic peptide, norepinephrine, and aldosterone at each time point.
  
  
  RESULTS
  Median sST2 decreased from 263.3 pg/ml at baseline to 140.0 pg/ml at 24 weeks (p < 0.001). Serum sST2 correlated significantly with LV ejection fraction at baseline (r = -0.30, p = 0.002) and 24 weeks (r = -0.23, p = 0.026); change in sST2 correlated with change in LV end-diastolic volume index (r = -0.24, p = 0.023). Level of sST2 was positively associated with infarct volume index at baseline (r = 0.26, p = 0.005) and 24 weeks (r = 0.22, p = 0.037), and with change in infarct volume index (r = -0.28, p = 0.001). Level of sST2 was significantly higher in patients with greater infarct transmurality and endocardial extent, and in the presence of microvascular obstruction. Level of sST2 correlated significantly with norepinephrine and aldosterone, but not with N-terminal pro-brain natriuretic peptide.
  
  
  CONCLUSIONS
  Measurement of sST2 early after AMI assists in the prediction of medium-term LV functional recovery. Novel relationships were observed between sST2, infarct magnitude/evolution, and aldosterone. Serum sST2 may be of pathophysiological importance in ventricular and infarct remodeling after AMI. (Effects of Eplerenone on Left Ventricular Remodelling Following Heart Attack; NCT00132093).
authors.affiliation: Cardiology Department, Western Infirmary, Glasgow, Scotland, United Kingdom.
authors.forename: Robin A P
authors.initials: RA
authors.lastname: Weir
authors.forename: Ashley M
authors.initials: AM
authors.lastname: Miller
authors.forename: Grace E J
authors.initials: GE
authors.lastname: Murphy
authors.forename: Suzanne
authors.initials: S
authors.lastname: Clements
authors.forename: Tracey
authors.initials: T
authors.lastname: Steedman
authors.forename: John M C
authors.initials: JM
authors.lastname: Connell
authors.forename: Iain B
authors.initials: IB
authors.lastname: McInnes
authors.forename: Henry J
authors.initials: HJ
authors.lastname: Dargie
authors.forename: John J V
authors.initials: JJ
authors.lastname: McMurray
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D015331:Cohort Studies; D004311:Double-Blind Method; D000077545:Eplerenone; D005260:Female; D006801:Humans; D000072179:Interleukin-1 Receptor-Like 1 Protein; D008297:Male; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology; D011237:Predictive Value of Tests; D011956:Receptors, Cell Surface / Q000097:blood*; D013148:Spironolactone / Q000031:analogs & derivatives / Q000627:therapeutic use; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology*; D016896:Treatment Outcome; D020257:Ventricular Remodeling / Q000187:drug effects / Q000502:physiology*
chemical_list: D015415:Biomarkers; C079241:IL1RL1 protein, human; D000072179:Interleukin-1 Receptor-Like 1 Protein; D000451:Mineralocorticoid Receptor Antagonists; D011956:Receptors, Cell Surface; D013148:Spironolactone; D000077545:Eplerenone