title: Neurohormonal activation in acute heart failure: results from VERITAS.
abstract: OBJECTIVE
  Recent heart failure studies have suggested that inflammatory and immune system activation are associated with increased levels of cytokines, chemokines and inflammatory proteins during acutely decompensated heart failure. The objectives of this substudy were to evaluate the role of neurohormonal and inflammatory activation in the pathogenesis and outcome of acute heart failure (AHF) and the correlation between biomarker levels and clinical outcomes.
  
  
  METHODS
  Serum levels of B-type natriuretic peptide-32 (BNP-32), endothelin-1 (ET-1), norepinephrine, troponins I and T, C-reactive protein (CRP), von Willebrand factor, plasminogen activator inhibitor-1, interleukin-6 (IL-6) and tissue plasminogen activator (TPA) were measured at baseline, 24 and 48 h and 7 and 30 days in 112 patients with AHF recruited to the Value of Endothelin Receptor Inhibition with Tezosentan in Acute Heart Failure Study neurohormonal substudy.
  
  
  RESULTS
  On univariable analysis, CRP, BNP and ET-1 were predictive of worsening heart failure by day 30; when considered together, only CRP and BNP were significantly associated with this outcome. On adjustment for age, baseline blood pressure, serum sodium and serum creatinine, only age and BNP remained significant. CRP, IL-6 and TPA levels were significantly correlated with 180-day mortality on univariable analysis.
  
  
  CONCLUSIONS
  Circulating markers of inflammation may be useful in gauging prognosis in patients with AHF.
authors.affiliation: Momentum Research Inc., Durham, NC 27707,USA. olgacotter@momentum-research.com
authors.forename: Olga
authors.initials: O
authors.lastname: Milo-Cotter
authors.forename: Beth
authors.initials: B
authors.lastname: Cotter-Davison
authors.forename: Carlo
authors.initials: C
authors.lastname: Lombardi
authors.forename: Hengrui
authors.initials: H
authors.lastname: Sun
authors.forename: Luca
authors.initials: L
authors.lastname: Bettari
authors.forename: Silvia
authors.initials: S
authors.lastname: Bugatti
authors.forename: Michele
authors.initials: M
authors.lastname: Rund
authors.forename: Marco
authors.initials: M
authors.lastname: Metra
authors.forename: Edo
authors.initials: E
authors.lastname: Kaluski
authors.forename: Isaac
authors.initials: I
authors.lastname: Kobrin
authors.forename: Aline
authors.initials: A
authors.lastname: Frey
authors.forename: Maurizio
authors.initials: M
authors.lastname: Rainisio
authors.forename: John J V
authors.initials: JJ
authors.lastname: McMurray
authors.forename: John R
authors.initials: JR
authors.lastname: Teerlink
authors.forename: Gad
authors.initials: G
authors.lastname: Cotter-Davison
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000032:analysis; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000209:etiology; D006801:Humans; D007118:Immunoassay; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D018377:Neurotransmitter Agents / Q000097:blood*; D009638:Norepinephrine / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011379:Prognosis; D016016:Proportional Hazards Models; D016032:Randomized Controlled Trials as Topic; D010959:Tissue Plasminogen Activator / Q000097:blood; D019210:Troponin I / Q000097:blood; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D018377:Neurotransmitter Agents; D017395:Plasminogen Activator Inhibitor 1; D019210:Troponin I; D014841:von Willebrand Factor; D020097:Natriuretic Peptide, Brain; D002097:C-Reactive Protein; D010959:Tissue Plasminogen Activator; D009638:Norepinephrine