title: Serum soluble E-selectin and NT-proBNP levels additively predict mortality in diabetic patients with chronic heart failure.
abstract: BACKGROUND
  Neuroendocrine activation with endothelial dysfunction is a key pathophysiological process in chronic heart failure (CHF). Although increased soluble E-selectin (sE-selectin) levels predict adverse events in several forms of cardiovascular disease, there are only scarce data on its predictive value in CHF. The aim of our study was to investigate whether sE-selectin is a useful predictor of mortality in CHF patients and whether its predictive power is additive to that of NT-proBNP.
  
  
  METHODS
  Plasma levels of sE-selectin were measured by ELISA in 192 CHF patients with clinical systolic heart failure. The study population was followed up for 14.9 months on average; 46 patients died during this period.
  
  
  RESULTS
  Levels of sE-selectin were significantly higher in non-surviving patients than in survivors (p = 0.005) and significantly correlated with the following inflammatory markers: CRP (r = 0.242, p = 0.001), TNF-α (r = 0.201, p = 0.005), TNF-RII (r = 0.207, p = 0.004), and IL-6 (r = 0.339, p < 0.0001). According to Cox regression analysis of the prediction power of sE-selectin for all-cause mortality, high sE-selectin levels independently and significantly predicted short-term mortality in CHF (HR 1.47, 95% CI 1.103-1.956). Furthermore, sE-selectin predicted mortality in CHF patients with concomitant diabetes mellitus, as well as simultaneously elevated sE-selectin and NT-proBNP levels additively predicted mortality.
  
  
  CONCLUSIONS
  This study demonstrated a weak correlation of sE-selectin level with inflammatory markers and prediction of short-term mortality in diabetic CHF patients. Elevated serum sE-selectin levels and concomitantly increased NT-proBNP concentrations have additive predictive power in CHF. This suggests that parallel activation of various pathophysiological pathways confers increased risk of adverse outcome in CHF.
authors.affiliation: Research Laboratory, 3rd Department of Internal Medicine, Szentágothai Knowledge Center, Semmelweis University, Budapest, Hungary. czucz@kut.sote.hu
authors.forename: Judit
authors.initials: J
authors.lastname: Czúcz
authors.forename: László
authors.initials: L
authors.lastname: Cervenak
authors.forename: Zsolt
authors.initials: Z
authors.lastname: Förhécz
authors.forename: Tímea
authors.initials: T
authors.lastname: Gombos
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Pozsonyi
authors.forename: Jan
authors.initials: J
authors.lastname: Kunde
authors.forename: István
authors.initials: I
authors.lastname: Karádi
authors.forename: Lívia
authors.initials: L
authors.lastname: Jánoskuti
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Prohászka
mesh_terms: D000368:Aged; D002908:Chronic Disease; D015331:Cohort Studies; D016207:Cytokines / Q000097:blood; D048909:Diabetes Complications / Q000097:blood* / Q000401:mortality*; D019040:E-Selectin / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000150:complications / Q000401:mortality*; D006801:Humans; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D010446:Peptide Fragments / Q000097:blood*; D011379:Prognosis; D011446:Prospective Studies
chemical_list: D016207:Cytokines; D019040:E-Selectin; D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain