title: Myocardial injury and systemic fibrinolysis in patients undergoing repair of ruptured abdominal aortic aneurysm: a preliminary report.
abstract: BACKGROUND
  ruptured abdominal aortic aneurysm (AAA) is associated with inhibition of systemic fibrinolysis. Hypofibrinolysis is a risk factor for ischaemic myocardial injury, one of the commonest complications of ruptured AAA repair. Cardiac troponin I (cTnI) is one of the most sensitive and specific marker of myocardial injury currently available.
  
  
  OBJECTIVE
  To examine, for the first time, the relationship between fibrinolytic activity and myocardial injury in patients operated for ruptured AAA.
  
  
  METHODS
  Twenty patients (18 men and 2 women of median age 74, range 65-86 years) undergoing repair of ruptured AAA were prospectively studied. Plasma tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1) activity were measured pre-operatively, immediately before and five minutes following aortic clamp release. Serum cTnI was measured pre-operatively, 6 and 24 h following clamp release. Results cTnI was detectable at one or more sample points in 13 (65%) patients, and in 7 out of 8 patients who suffered major cardiac complications. There was a significant negative correlation between pre-operative t-PA activity and cTnI before operation (r =-0.55, p = 0.01) and 6 h ( r =-0.51, p =0.02) after clamp release. There was a significant positive correlation between pre-operative PAI activity and cTnI before operation (r =+0.50, p =0.03), 6 h ( r =+0.47, p =0.04) and 24 h ( r =+0.50, p =0.03) after clamp release. There was no correlation between pre- and intra-operative hypotension or blood transfusion requirement and cTnI release.
  
  
  CONCLUSIONS
  Hypofibrinolysis during ruptured AAA repair is associated with the development of peri-operative myocardial injury. The causal mechanisms underlying this state are not clear but treatment of this prothrombotic/hypofibrinolytic diathesis may help to limit myocardial cell necrosis.
authors.affiliation: University Department of Vascular Surgery, Birmingham Heartlands & Solihull NHS Trust, Birmingham, UK.
authors.forename: P C
authors.initials: PC
authors.lastname: Haggart
authors.forename: D J
authors.initials: DJ
authors.lastname: Adam
authors.forename: P F
authors.initials: PF
authors.lastname: Ludman
authors.forename: C A
authors.initials: CA
authors.lastname: Ludman
authors.forename: A W
authors.initials: AW
authors.lastname: Bradbury
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D017544:Aortic Aneurysm, Abdominal / Q000601:surgery*; D001019:Aortic Rupture / Q000601:surgery*; D015415:Biomarkers; D005260:Female; D005342:Fibrinolysis; D006801:Humans; D008297:Male; D017202:Myocardial Ischemia / Q000097:blood / Q000175:diagnosis / Q000503:physiopathology*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011183:Postoperative Complications / Q000097:blood / Q000175:diagnosis / Q000503:physiopathology*; D011446:Prospective Studies; D018709:Statistics, Nonparametric; D010959:Tissue Plasminogen Activator / Q000097:blood; D019210:Troponin I / Q000097:blood
chemical_list: D015415:Biomarkers; D017395:Plasminogen Activator Inhibitor 1; D019210:Troponin I; D010959:Tissue Plasminogen Activator