title: Acetylsalicylic acid treatment until surgery reduces oxidative stress and inflammation in patients undergoing coronary artery bypass grafting.
abstract: OBJECTIVE
  Acetylsalicylic acid (ASA) is a cornerstone in the treatment of coronary artery disease (CAD) due to its antiplatelet effect. Cessation of aspirin before coronary artery bypass grafting (CABG) is often recommended to avoid bleeding, but the practice is controversial because it is suggested to worsen the underlying CAD. The aims of the present prospective, randomized study were to assess if ASA administration until the day before CABG decreases the oxidative load through a reduction of inflammation and myocardial damage, compared with patients with preoperative discontinuation of ASA.
  
  
  METHODS
  Twenty patients scheduled for CABG were randomly assigned to either routine ASA-treatment (160 mg daily) until the time of surgery (ASA), or to ASA-withdrawal 7 days before surgery (No-ASA). Blood-samples were taken from a radial artery and coronary sinus, during and after surgery and analysed for 8-iso-prostaglandin (PG) F2α; a major F2-isoprostane, high-sensitivity C-reactive protein (hs-CRP), cytokines and troponin T. Left ventricle Tru-Cut biopsies were taken from viable myocardium close to the left anterior descending artery just after connection to cardiopulmonary bypass, and before cardioplegia were established for gene analysis (Illumina HT-12) and immunohistochemistry (CD45).
  
  
  RESULTS
  8-Iso-PGF2α at baseline (t1) were 111 (277) pmol/l and 221 (490) pmol/l for ASA and No-ASA, respectively (P = 0.065). Area under the curve showed a significantly lower level in plasma concentration of 8-iso-PGF2α and hsCRP in the ASA group compared with the No-ASA group with (158 pM vs 297 pM, P = 0.035) and hsCRP (8.4 mg/l vs 10.1 mg/l, P = 0.013). All cytokines increased during surgery, but no significant differences between the two groups were observed. Nine genes (10 transcripts) were found with a false discovery rate (FDR) <0.1 between the ASA and No-ASA groups.
  
  
  CONCLUSIONS
  Continued ASA treatment until the time of CABG reduced oxidative and inflammatory responses. Also, a likely beneficial effect upon myocardial injury was noticed. Although none of the genes known to be involved in oxidative stress or inflammation took a different expression in myocardial tissue, the genetic analysis showed interesting differences in the mRNA level. Further research in this field is necessary to understand the role of the genes.
authors.affiliation: Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway. kirsti.berg@ntnu.no
authors.forename: Kirsti
authors.initials: K
authors.lastname: Berg
authors.forename: Mette
authors.initials: M
authors.lastname: Langaas
authors.forename: Madelene
authors.initials: M
authors.lastname: Ericsson
authors.forename: Hilde
authors.initials: H
authors.lastname: Pleym
authors.forename: Samar
authors.initials: S
authors.lastname: Basu
authors.forename: Ivar Skjåk
authors.initials: IS
authors.lastname: Nordrum
authors.forename: Nicola
authors.initials: N
authors.lastname: Vitale
authors.forename: Rune
authors.initials: R
authors.lastname: Haaverstad
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001241:Aspirin / Q000008:administration & dosage*; D002097:C-Reactive Protein / Q000378:metabolism; D001026:Coronary Artery Bypass / Q000379:methods*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D004334:Drug Administration Schedule; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects*; D019106:Postoperative Hemorrhage; D011446:Prospective Studies; D020107:Troponin T / Q000097:blood
chemical_list: D020107:Troponin T; C075750:8-epi-prostaglandin F2alpha; D002097:C-Reactive Protein; D015237:Dinoprost; D001241:Aspirin