title: Depletion of antioxidants is associated with no-reflow phenomenon in acute myocardial infarction.
abstract: BACKGROUND
  No-reflow phenomenon is observed in approximately one-third of patients after percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI), and is associated with poor functional and clinical outcomes. On the other hand, the formation of free radicals in vasculature exerts deleterious effects on coronary microcirculation.
  
  
  OBJECTIVE
  We hypothesized that redox state in coronary circulation may play a crucial role in no-reflow phenomenon in AMI.
  
  
  METHODS
  Consecutive 26 patients with first AMI who underwent primary PCI < 24 h after onset were enrolled. Before PCI, blood samples were obtained from coronary sinus to measure plasma or serum antioxidative vitamins (vitamin C, vitamin E, and beta-carotene) and antioxidative enzymes (extracellular glutathione peroxidase [GPX], superoxide dismutase, and catalase). After PCI, the corrected Thrombolysis In Myocardial Infarction (TIMI) frame count (CTFC) was measured in the target vessel. Patients with TIMI < or = 2 flow despite an optimal PCI result were designated as no-reflow group (Group NR, n = 6) and the others as reflow group (Group R, n = 20).
  
  
  RESULTS
  Levels of vitamin C, vitamin E, and GPX before PCI were significantly lower in Group NR than in Group R. The CTFC correlated inversely with levels of vitamin C, vitamin E, and GPX (p < 0.05).
  
  
  CONCLUSIONS
  Depletion of antioxidants is associated with no-reflow phenomenon in AMI. These findings strongly suggest that the redox state in coronary circulation plays an important role in the pathogenesis of no-reflow phenomenon.
authors.affiliation: Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
authors.forename: Hidenari
authors.initials: H
authors.lastname: Matsumoto
authors.forename: Nobutaka
authors.initials: N
authors.lastname: Inoue
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Takaoka
authors.forename: Katsuya
authors.initials: K
authors.lastname: Hata
authors.forename: Toshiro
authors.initials: T
authors.lastname: Shinke
authors.forename: Ryohei
authors.initials: R
authors.lastname: Yoshikawa
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Masai
authors.forename: Satoshi
authors.initials: S
authors.lastname: Watanabe
authors.forename: Toru
authors.initials: T
authors.lastname: Ozawa
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Yokoyama
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000097:blood*; D002374:Catalase / Q000097:blood; D003326:Coronary Circulation / Q000502:physiology*; D005260:Female; D005979:Glutathione Peroxidase / Q000097:blood*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D015425:Myocardial Reperfusion; D010084:Oxidation-Reduction; D018709:Statistics, Nonparametric; D013482:Superoxide Dismutase / Q000097:blood; D014810:Vitamin E / Q000097:blood*; D019207:beta Carotene / Q000097:blood
chemical_list: D000975:Antioxidants; D019207:beta Carotene; D014810:Vitamin E; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D001205:Ascorbic Acid