{'fraction_non_alphanumeric': 0.02809573361082206, 'fraction_numerical': 0.005549774540409296, 'mean_word_length': 5.408888888888889, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Fibrinolysis in patients with an abdominal aortic aneurysm with special emphasis on rupture and shock

Summary.  Background: A ruptured abdominal aortic aneurysm (AAA) is associated with high mortality. Postoperative complications such as hemorrhage, multiple organ failure, myocardial infarction, and thromboembolism are common. An active and balanced hemostatic system is essential to avoid bleeding as well as thrombosis. When these activities are not properly regulated the patient is at risk of developing either excessive bleeding or thrombosis‐related complications. Previous studies have shown a state of activated coagulation in patients with ruptured AAA. However, there are conflicting results regarding the fibrinolytic response. Objectives: The aim of the present study was to investigate the fibrinolytic state pre‐operatively in patients with ruptured and non‐ruptured AAA in relation to the clinical outcome with special regard to the influence of shock. Methods: A prospective study was performed on 95 patients who underwent surgery for a ruptured AAA with shock (n = 43), a ruptured AAA without shock (n = 12), and a non‐ruptured AAA (n = 40). Forty‐one controls without an aneurysm were matched to the AAA patients according to age, gender and smoking habits. Plasma levels of tissue plasminogen activator antigen (tPAag), and plasminogen activator inhibitor type‐1 (PAI‐1) were measured as markers of fibrinolytic activity. D‐dimer, a marker of fibrin turnover, was also measured. Results: D‐dimer was significantly higher in patients with a non‐ruptured AAA compared with controls without AAA. There were significantly higher levels of D‐dimer, tPAag, and PAI‐1 in patients operated for ruptured compared with non‐ruptured AAA. tPAag was also significantly higher in ruptured AAA patients with shock compared with without shock. No deaths occurred in patients operated on for a non‐ruptured AAA or ruptured AAA without shock. There were 12 deaths after repair of a ruptured AAA with shock, of which two patients died from bleeding and the remaining 10 from multiple organ failure and cardiac failure. Conclusion: Our results indicate a state of activated coagulation in patients with a non‐ruptured AAA, the state being intensified by rupture. The present data show normal fibrinolytic activities in patients with a non‐ruptured AAA, but increased systemic fibrinolysis, as demonstrated by elevated tPAag level, in patients with a ruptured AAA. The elevated PAI‐1 level indicates a simultaneous inhibition of the systemic fibrinolysis. Furthermore, the hyperfibrinolytic state was reinforced by shock in this study. However, the clinical outcome, with a relatively high incidence of thrombosis‐related deaths, indicate a prothrombotic state instead of a hyperfibrinolytic state as a major point of attention in patients with shock as a result of a ruptured AAA.