title: Elevation of matrix metalloproteinases and interleukin-6 in the culprit coronary artery of myocardial infarction.
abstract: BACKGROUND
  Interleukin-6 (IL-6) and metalloproteinases (MMPs) are involved in the instability of vulnerable plaque associated with the induction of acute myocardial infarction (AMI). We examined the regional changes of cytokines, MMPs and adhesion molecules in patients with AMI to elucidate how these factors are involved in the onset of AMI.
  
  
  METHODS
  One hundred and twenty-two patients with AMI were included. Blood was aspirated from the culprit coronary artery with a thrombectomy catheter, and was also sampled from peripheral veins during the coronary intervention. Control samples were obtained from the peripheral blood of age-matched patients.
  
  
  RESULTS
  The serum levels of IL-6 (P < 0.05), tumour necrosis factor-alpha (P < 0.005), MMP-1 (P < 0.001), MMP-13 (P < 0.001), soluble intercellular adhesion molecule-1 (P < 0.005), and soluble vascular cellular adhesion molecule-1 (P < 0.05) in peripheral blood were significantly higher in the AMI group than in the controls. Aspirated serum contained significantly higher levels of IL-6 (P < 0.001), MMP-1 (P < 0.001), and MMP-13 (P < 0.05) compared to the peripheral blood of AMI. Serum IL-6 levels were significantly higher in the aspirated than in the peripheral blood in the patients hospitalized within 6 h and 6-12 h, but were similar in the aspirated and peripheral blood of the patients hospitalized 12-24 h after the onset of AMI. There were no differences between the aspirated serum and peripheral blood in the levels of interleukin-1beta and MMP-2.
  
  
  CONCLUSIONS
  The levels of MMP-1, MMP-13 and IL-6 were higher in the culprit coronary artery than in the peripheral blood. These factors appear to be involved in the early stage of AMI.
authors.affiliation: Third Department of Internal Medicine, Showa University School of Medicine, Hatanodai, Shinagawa-ku, Tokyo, Japan. hrsuzuki@med.showa-u.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: T
authors.initials: T
authors.lastname: Kusuyama
authors.forename: R
authors.initials: R
authors.lastname: Sato
authors.forename: Y
authors.initials: Y
authors.lastname: Yokota
authors.forename: F
authors.initials: F
authors.lastname: Tsunoda
authors.forename: T
authors.initials: T
authors.lastname: Sato
authors.forename: M
authors.initials: M
authors.lastname: Shoji
authors.forename: Y
authors.initials: Y
authors.lastname: Iso
authors.forename: S
authors.initials: S
authors.lastname: Koba
authors.forename: T
authors.initials: T
authors.lastname: Katagiri
mesh_terms: D000208:Acute Disease; D015415:Biomarkers / Q000097:blood*; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000378:metabolism*; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D020782:Matrix Metalloproteinases / Q000097:blood; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D020782:Matrix Metalloproteinases