title: Oxidative stress and inflammatory response during and following coronary interventions for acute myocardial infarction.
abstract: BACKGROUND
  In acute myocardial infarction (AMI) treated with percutaneous coronary intervention (PCI), myocardial injury results from complex processes during both ischemia and reperfusion. Release of reactive oxygen species (ROS) may contribute to the accumulated myocardial damage.
  
  
  OBJECTIVE
  To examine by frequent sampling of peripheral blood oxidative stress and early inflammation in patients undergoing primary PCI for AMI. Secondly, to assess whether a correlation exists between these parameters and the extent of myocardial damage.
  
  
  METHODS
  Sixteen patients undergoing primary PCI within 6 h of AMI onset were included. Peripheral blood was sampled at start of procedure (t0) and repeatedly over 24 h following reperfusion. Main plasma analyses were: 8-iso-PGF2alpha (oxidative stress), 15-keto-dihydro-PGF2alpha (cyclooxygenase-mediated inflammation); and troponin-T (myocardial injury). Additional analyses included: total antioxidant status (TAS); vitamins; hsCRP and lipids.
  
  
  RESULTS
  8-Iso-PGF2alpha increased following restoration of blood flow, returned to t0 values after 3 h and was reduced below t0 the following day. TAS decreased significantly from t0 to the next day. There was no significant correlation between 8-iso-PGF2alpha and troponin T values. 15-Keto-dihydro-PGF2alpha was elevated during the first hour. There was a major rise in hsCRP after 24 h.
  
  
  CONCLUSIONS
  Following reperfusion by primary PCI in AMI, oxidative stress and an inflammatory response are induced immediately. A rise in 8-iso-PGF2a during ischemia indicate that ROS generation may also take place during severely reduced coronary blood flow and hypoxia. No direct relationship between 8-iso-PGF2alpha or 15-keto-dihydro-PGF2alpha and troponin T was evident. The present study adds to the increasingly complex pathophysiological roles of ROS acting both as signal molecules and as mediators of tissue injury.
authors.affiliation: Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway. kirsti.berg@medisin.ntnu.no
authors.forename: Kirsti
authors.initials: K
authors.lastname: Berg
authors.forename: Per
authors.initials: P
authors.lastname: Jynge
authors.forename: Kristian
authors.initials: K
authors.lastname: Bjerve
authors.forename: Sissel
authors.initials: S
authors.lastname: Skarra
authors.forename: Samar
authors.initials: S
authors.lastname: Basu
authors.forename: Rune
authors.initials: R
authors.lastname: Wiseth
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D003331:Coronary Vessels / Q000378:metabolism; D015237:Dinoprost / Q000737:chemistry / Q000378:metabolism; D005260:Female; D006801:Humans; D006900:Hydroxylation; D007249:Inflammation / Q000378:metabolism; D050356:Lipid Metabolism; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000378:metabolism* / Q000628:therapy*; D018384:Oxidative Stress; D012709:Serum Albumin / Q000378:metabolism; D020107:Troponin T / Q000378:metabolism
chemical_list: D012709:Serum Albumin; D020107:Troponin T; D015237:Dinoprost