Inhibition of systemic fibrinolysis is associated with myocardial injury in patients operated on for ruptured abdominal aortic aneurysm

Background: Previous work has demonstrated that ruptured abdominal aortic aneurysm (AAA) is associated with systemic thrombin generation and inhibition of systemic fibrinolysis. The procoagulant and hypofibrinolytic state associated with ruptured AAA predisposes to microvascular and macrovascular thrombosis and subsequent myocardial injury. The aim of this study was to determine the relationship between haemostatic derangement and biochemical evidence of myocardial injury in patients operated on for ruptured AAA. Methods: Ten patients undergoing repair of ruptured AAA were studied. Tissue plasminogen activator (tPA) activity, plasminogen activator inhibitor (PAI) activity, prothrombin fragment (PF) 1 + 2, D ‐dimer and fibrinogen levels were measured before operation, and immediately before and 5 min after aortic clamp release. Plasma levels of cardiac troponin (cTn) I were measured before operation, and 6 and 24 h after aortic clamp release. Results: There was no relationship between tPA activity, PF 1 + 2, D ‐dimer or fibrinogen and cTn‐I levels at any sampling point. There was, however, a significant positive correlation (Spearman rank test) between PAI activity immediately before (median 38·6 (range 13·0–39·4) units ml –1 ) and 5 min after (37·2 (10·6–39·4) units ml –1 ) aortic clamp release, and cTn‐I at 6 h (median 3·17 (range less than 0·5 to 71·1) ng ml –1 ) and 24 h (5·55 (range less than 0·5 to 110) ng ml –1 ) after aortic clamp release. Conclusion: These data strongly support the hypothesis that the inhibition of systemic fibrinolysis which occurs in response to ischaemia and reperfusion during ruptured AAA repair contributes to the development of subsequent myocardial injury. © 1999 British Journal of Surgery Society Ltd