title: Hydroxyl radical generation, levels of tumor necrosis factor-alpha, and progression to heart failure after acute myocardial infarction.
abstract: OBJECTIVE
  We used acetylsalicylic acid (ASA) as a probing agent to quantify hydroxyl radical ((*)OH) in Controls and patients with coronary artery disease and to prospectively investigate (*)OH production in patients with myocardial infarction (MI) complicated by heart failure (HF).
  
  
  BACKGROUND
  Oxidative stress status (OSS) is a mechanism for transition to HF in experimental heart injury models, but evidence for its causal role in humans is still limited.
  
  
  METHODS
  Thirty healthy subjects (Controls), 12 patients with stable angina (Group 1), and 74 patients with ST-segment elevation MI (Group 2) were enrolled. A dose of 250 mg Flectadol was given intravenously before each blood collection to determine the 2,3-dihydroxybenzoic acid/salicylic acid (DHBA/SA) ratio. We also quantified vitamin E and coenzyme Q(10) to monitor antioxidant reserve, as well as tumor necrosis factor (TNF)-alpha, TNF-soluble receptors, interleukin (IL)-6, and IL-1ra to assess inflammatory status. All measurements were repeated at month 6 in Group 2.
  
  
  RESULTS
  There were no differences between Controls and Group 1. Group 2 showed increased (*)OH production, peaking at 24 h, whereas vitamin E and coenzyme Q(10) progressively declined. Group 2 patients developing HF during hospitalization (Group 2Bi) presented with an increase of both (*)OH production at discharge and inflammatory status, as compared with patients without HF (Group 2Ai), persisting at month 6 in post-MI patients with HF (Group 2Bii).
  
  
  CONCLUSIONS
  We found a distinct pattern of (*)OH generation in post-MI patients who show progression to HF. The interplay between OSS and inflammatory status should be targeted as a possible mechanism of progression to post-MI left ventricular dysfunction.
authors.affiliation: University of Ferrara, Ferrara, Italy. vlgmrc@unife.it
authors.forename: Marco
authors.initials: M
authors.lastname: Valgimigli
authors.forename: Elisa
authors.initials: E
authors.lastname: Merli
authors.forename: Patrizia
authors.initials: P
authors.lastname: Malagutti
authors.forename: Olga
authors.initials: O
authors.lastname: Soukhomovskaia
authors.forename: Giordano
authors.initials: G
authors.lastname: Cicchitelli
authors.forename: Alessandra
authors.initials: A
authors.lastname: Antelli
authors.forename: Donatella
authors.initials: D
authors.lastname: Canistro
authors.forename: Gloria
authors.initials: G
authors.lastname: Francolini
authors.forename: Gaetano
authors.initials: G
authors.lastname: Macrì
authors.forename: Francesca
authors.initials: F
authors.lastname: Mastrorilli
authors.forename: Moreno
authors.initials: M
authors.lastname: Paolini
authors.forename: Roberto
authors.initials: R
authors.lastname: Ferrari
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D018450:Disease Progression; D000068800:Etanercept; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000150:complications*; D006801:Humans; D017665:Hydroxyl Radical / Q000097:blood*; D007074:Immunoglobulin G / Q000097:blood; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D009203:Myocardial Infarction / Q000097:blood / Q000150:complications*; D011446:Prospective Studies; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D012795:Sialoglycoproteins / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: C507763:IL1RN protein, human; D007074:Immunoglobulin G; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6; D018124:Receptors, Tumor Necrosis Factor; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D017665:Hydroxyl Radical; D000068800:Etanercept