title: Platelet activation, myocardial ischemic events and postoperative non-response to aspirin in patients undergoing major vascular surgery.
abstract: OBJECTIVE
  Myocardial ischemia is the leading cause of postoperative mortality and morbidity in patients undergoing major vascular surgery. Platelets have been implicated in the pathogenesis of acute thrombotic events. We hypothesized that platelet activity is increased following major vascular surgery and that this may predispose patients to myocardial ischemia.
  
  
  METHODS
  Platelet function in 136 patients undergoing elective surgery for subcritical limb ischemia or infrarenal abdominal aortic aneurysm repair was assessed by P-selectin expression and fibrinogen binding with and without adenosine diphosphate (ADP) stimulation, and aggregation mediated by thrombin receptor-activating peptide and arachidonic acid (AA). Cardiac troponin-I (cTnI) was performed.
  
  
  RESULTS
  P-selectin expression increased from days 1 to 3 after surgery [median increase from baseline on day 3: 53% (range: -28% to 212%, P < 0.01) for unstimulated and 12% (range: -9% to 45%, P < 0.01) for stimulated]. Fibrinogen binding increased in the immediate postoperative period [median increase from baseline: 34% (range: -46% to 155%, P < 0.05)] and decreased on postoperative day 3 (P < 0.05). ADP-stimulated fibrinogen binding increased on day1 (P < 0.05) and thereafter decreased. Platelet aggregation increased on days 1-5 (P < 0.05). Twenty-eight (21%) patients had a postoperative elevation (> 0.1 ng mL(-1)) of cTnI. They had significantly increased AA-stimulated platelet aggregation in the immediate postoperative period and on day 2 (P < 0.05), and non-response to aspirin (48% vs. 26%, P = 0.036).
  
  
  CONCLUSIONS
  This study has shown increased platelet activity and the existence of non-response to aspirin following major vascular surgery. Patients with elevated postoperative cTnI had significantly increased AA-mediated platelet aggregation and a higher incidence of non-response to aspirin compared with patients who did not.
authors.affiliation: Vascular Unit, Aberdeen Royal Infirmary, Aberdeen, UK.
authors.forename: S
authors.initials: S
authors.lastname: Rajagopalan
authors.forename: I
authors.initials: I
authors.lastname: Ford
authors.forename: P
authors.initials: P
authors.lastname: Bachoo
authors.forename: G S
authors.initials: GS
authors.lastname: Hillis
authors.forename: B
authors.initials: B
authors.lastname: Croal
authors.forename: M
authors.initials: M
authors.lastname: Greaves
authors.forename: J
authors.initials: J
authors.lastname: Brittenden
mesh_terms: D000244:Adenosine Diphosphate / Q000378:metabolism; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology*; D001792:Blood Platelets / Q000378:metabolism; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000473:pathology*; D019007:P-Selectin / Q000096:biosynthesis; D015539:Platelet Activation; D014656:Vascular Surgical Procedures / Q000009:adverse effects*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D019007:P-Selectin; D000244:Adenosine Diphosphate; D005340:Fibrinogen; D001241:Aspirin