Coagulation and fibrinolysis in patients undergoing operation for rupturedand nonruptured infrarenal abdominal aortic aneurysms

Purpose: Hemorrhage and thrombosis predisposing to myocardial infarction, m ultiple organ failure, and thromboembolism account for the majority of the morbidity and mortality associated with repair of ruptured and nonruptured abdominal aortic aneurysms (AAAs). The aim of this study was to examine coa gulation and fibrinolysis in patients operated on for ruptured and nonruptu red infrarenal AAAs. Methods: Ten patients operated on for ruptured and 9 patients operated on f or nonruptured AAAs were studied. Tissue plasminogen activator (t-PA) antig en, thrombin-antithrombin (TAT), and D-dimer were measured before induction of anesthesia. Plasminogen activator inhibitor (PAI) activity, t-PA activi ty, and prothrombin fragment (PE) 1+2 were measured before induction of ane sthesia, immediately before aortic clamp release, and 5 minutes and 24 hour s after aortic clamp release. Results: Preoperatively, ruptured AAA was associated with significantly ele vated t-PA antigen (median 15.7 ng/mL, range 9.0 to 22.1 ng/mL versus nonru pture: median 6.6 ng/mL, range 4.7 to 16.4 ng/mL; P < .01, Mann-Whitney tes t), increased PAT activity (median 36.5 arbitrary units/mL, range 20.6 to 3 8.8 arbitrary units/mL versus nonrupture: median 8.2 arbitrary units/mL, ra nge 3.2 to 21.7 arbitrary units/mL; P < .001), reduced t-PA activity (media n 0.12 IU/mL, range 0.06 to 0.4 IU/mL versus nonrupture: median 0.49 IU/mL, range 0.14 to 3.2 IU/mL; P < .01), elevated TAT (median 135.5 mu g/L, rang e 61.2 to 209.4 mu g/L versus nonrupture: median 21.6 mu g/L, range 6.6 to 180.4 mu g/L; P < .02) and elevated PF 1+2 (median 9.0 nmol/L, range 5.4 to 11.6 nmol/L versus nonrupture: median 2.2 nmol/L, range 0.7 to 7.1 nmol/L, P < .001). There was no significant difference in preoperative D-dimer lev els (median 3460 ng/mL, range 1236 to 7860 ng/mL versus nonrupture: median 1642 ng/mL, range 728 to 5334 ng/mL; P = .07). The differences in PAI activ ity, t-PA activity, and PP 1+2 persisted throughout the course of surgery, but there was no significant difference between the groups at 24 hours. Conclusion: These novel data demonstrate that ruptured AAA repair is associ ated with inhibition of systemic fibrinolysis and intense thrombin generati on. Similar changes are seen in nonruptured AAA but are of a lesser magnitu de. This procoagulant state may contribute to the microvascular and macrova scular thrombosis that leads to myocardial infarction, multiple organ failu re, and thromboembolism.