Abstract
Coagulopathy is still a frequent complication in the surgical treatment of acute aortic dissection. However, the physiopathology of surgically induced coagulopathy has never been systematically and comprehensively studied in patients with acute aortic dissection. The aim of the present study was to describe the perioperative hemostatic system in patients with acute aortic dissection.The 87 patients who underwent aortic arch surgery for acute Stanford type A aortic dissection from January 2013 to September 2015 were enrolled in this study. The perioperative biomarkers of hemostatic system were evaluated using standard laboratory tests and enzyme-linked immunosorbent assays (ELISAs) at 5 time points: anesthesia induction (T1), lowest nasopharyngeal temperature (T2), protamine reversal (T3), 4 hours after surgery (T4), and 24 hours after surgery (T5).The ELISAs biomarkers revealed activation of coagulation (thrombin-antithrombin III complex [TAT] and prothrombin fragment 1 + 2 [F1 + 2] were elevated), suppression of anticoagulation (antithrombin III [AT III] levels were depressed), and activation of fibrinolysis (plasminogen was decreased and plasmin-antiplasmin complex [PAP] was elevated). The standard laboratory tests also demonstrated that surgery resulted in a significant reduction in platelet counts and fibrinogen concentration.Systemic activation of coagulation and fibrinolysis, and inhibition of anticoagulation were observed during the perioperative period in patients with acute aortic dissection. Indeed, these patients exhibited consumption coagulopathy and procoagulant state perioperatively. Therefore, we believe that this remarkable disseminated intravascular coagulation (DIC)-like coagulopathy has a high risk of bleeding and may influence postoperative outcome of patients with acute aortic dissection.