title: Myeloperoxidase may contribute to the no-reflow phenomenon in patients with acute myocardial infarction.
abstract: BACKGROUND
  The no-reflow phenomenon is a deteriorating factor for prognosis of acute myocardial infarction (AMI). Leukocyte enzymes may be involved in developing the no-reflow phenomenon. The aim of this study was to clarify the association of myeloperoxidase, a leukocyte enzyme, with the no-reflow phenomenon in patients with AMI after percutaneous coronary inetervention (PCI).
  
  
  METHODS
  We enrolled 50 patients with AMI whose infarct-related coronary arteries were rescued by thrombectomy devices. Blood samples were collected from peripheral vein (PV), ostium and culprit lesion of infarct-related coronary artery. Myeloperoxidase, elastase and interleukin (IL)-8 were measured by ELISA. Antegrade blood flow in the infarct-related coronary artery and myocardial perfusion were evaluated according to the corrected TIMI frame counts (cTFC) and the myocardial blush grade (MBG).
  
  
  RESULTS
  Plasma myeloperoxidase and IL-8 levels at the ostium and the culprit lesion of infarct-related coronary artery were significantly greater than those in PV. No-reflow was found in 10 patients (20%). Plasma levels of myeloperoxidase at the culprit lesion of infarct-related coronary artery were significantly greater in the patients with no-reflow than those without no-reflow. Plasma myeloperoxidase levels at the culprit lesion of infarct-related coronary artery positively correlated with the cTFC. Also, plasma myeloperoxidase levels were significantly higher in the patients with MBG 0-1 than those with MBG 2-3.
  
  
  CONCLUSIONS
  The present findings indicate that local myeloperoxidase levels in the culprit coronary artery may contribute to the no-reflow phenomenon in the patients with AMI.
authors.affiliation: Department of Medicine, Jichi Medical University Saitama Medical Center, 1-847 Amanuma Omiya-ku, Saitama, Saitama 330-8503 Japan. funahiro@omiya.jichi.ac.jp
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Funayama
authors.forename: San-e
authors.initials: SE
authors.lastname: Ishikawa
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Sugawara
authors.forename: Norifumi
authors.initials: N
authors.lastname: Kubo
authors.forename: Shin-ichi
authors.initials: S
authors.lastname: Momomura
authors.forename: Masanobu
authors.initials: M
authors.lastname: Kawakami
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary; D017023:Coronary Angiography; D003326:Coronary Circulation / Q000502:physiology*; D005260:Female; D006801:Humans; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000628:therapy*; D010196:Pancreatic Elastase / Q000097:blood; D009195:Peroxidase / Q000097:blood*; D017211:Treatment Failure
chemical_list: D016209:Interleukin-8; D009195:Peroxidase; D010196:Pancreatic Elastase