title: Dissociation of the Inflammatory Reaction following PCI for Acute Myocardial Infarction.
abstract: OBJECTIVE
  Neutrophils are activated and infiltrate the myocardium after ischemia and reperfusion. The involvement of neutrophils in irreversible reperfusion injury is suggested by numerous experimental studies. The aim of this study was to investigate markers of neutrophil activation following reperfusion of acute myocardial infarction (AMI) accomplished with percutaneous coronary intervention (PCI) and their relationship to markers of lipid peroxidation, cytokines and highly-sensitive C-reactive protein (hsCRP).
  
  
  METHODS
  Non-consecutive patients with their first myocardial infarction were evaluated. Setting. University hospital as primary referral center, single center.
  
  
  METHODS
  Forty-nine patients with AMI were evaluated. All were treated with primary PCI and infusion of abciximab. Reperfusion was verified by angiography. Blood samples for analyses of myeloperoxidase (MPO), neutrophil gelatinase-associated lipocalin (NGAL), matrix metalloproteinase-9 (MMP-9), malondialdehyde (MDA), 8-isoprostane-prostaglandin F2alpha (Iso-P), interleukin 6 (IL-6), interleukin 8 (IL-8), tumor necrosis factoralpha (TNFalpha), hsCRP, creatine kinase-monobasic fraction (CK-MB) and troponin-T (TnT) were obtained at baseline with the occluded coronary vessel, and subsequently after verified reperfusion at 1.5, 3 and 24 hours.
  
  
  RESULTS
  Significant increases in MMP-9, IL-6, IL-8, TNFalpha and hsCRP were observed, and a significant decrease in MPO and MDA was also observed over the same period. No significant changes in Iso-P and NGAL were found.
  
  
  CONCLUSIONS
  We found a dissociation of the inflammatory reaction after PCI for AMI: a decrease of markers of neutrophil activation and MDA, but an increase in cytokines and hsCRP. An antineutrophil effect of the PCI procedure including treatment with abciximab, an antiplatelet drug and a modulator of inflammation, is conceivable.
authors.affiliation: Department of Cardiology, Sahlgrenska University Hospital/S, SE 413 45, Goteborg, Sweden. karin.astrom-olsson@vgregion.se
authors.forename: Karin
authors.initials: K
authors.lastname: Aström-Olsson
authors.forename: Erik
authors.initials: E
authors.lastname: Hedström
authors.forename: Lillemor Mattsson
authors.initials: LM
authors.lastname: Hultén
authors.forename: Olov
authors.initials: O
authors.lastname: Wiklund
authors.forename: Håkan
authors.initials: H
authors.lastname: Arheden
authors.forename: Ann-Kristin
authors.initials: AK
authors.lastname: Ohlin
authors.forename: Anders
authors.initials: A
authors.lastname: Gottsäter
authors.forename: Hans
authors.initials: H
authors.lastname: Ohlin
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D016207:Cytokines / Q000097:blood; D005260:Female; D006801:Humans; D015227:Lipid Peroxidation / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000276:immunology* / Q000628:therapy*; D009504:Neutrophils / Q000276:immunology; D018384:Oxidative Stress / Q000276:immunology; D014657:Vasculitis / Q000209:etiology* / Q000276:immunology*
chemical_list: D015415:Biomarkers; D016207:Cytokines; D002097:C-Reactive Protein