No hyperfibrinolysis following subarachnoid or intracerebral haemorrhage: A prospective cohort study

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Changes in fibrinolysis following subarachnoid haemorrhage (SAH) and intracerebral haemorrhage (ICH) are sparsely investigated. To investigate fibrinolysis in the acute phase in SAH and ICH patients compared with healthy individuals, fibrinolysis after 24h in ICH patients and the in-vivo effect of tranexamic acid (TXA) on fibrinolysis in SAH patients. Further, ex-vivo studies were performed by addition of several haemostatic agents to blood samples obtained at admission. Blood was sampled from 46 SAH and 41 ICH patients upon admission. In ICH patients, a second blood sample was obtained 24h after symptom onset, and in SAH patients after TXA treatment. A sex-matched healthy control group was used for comparison. Fibrinolysis and clot stability were assessed by a dynamic fibrin clot lysis assay, and measurements of plasminogen activator inhibitor I, tissue plasminogen activator and coagulation factor XIII were performed. On admission, no difference in lysis time was found in SAH or ICH patients compared with healthy controls (all P values >0.15). For SAH and ICH patients, median plasminogen activator inhibitor I, tissue plasminogen activator and factor XIII levels were within the reference intervals. In ICH patients, lysis time remained within 24h after symptom onset (P=0.63). In SAH patients, the clot lysis curve showed a complete block of fibrinolysis after TXA administration. Ex-vivo addition of solulin and prothrombin complex concentrate reduced fibrinolysis (P<0.001). SAH and ICH patients showed no hyperfibrinolysis on admission. Fibrinolysis remained normal in ICH patients, and TXA treatment obliterated fibrinolysis in SAH patients.

Original languageEnglish
JournalBlood Coagulation and Fibrinolysis
Volume30
Issue7
Pages (from-to)341-349
Number of pages9
ISSN0957-5235
DOIs
Publication statusPublished - 1 Jan 2019

    Research areas

  • factor XIII, fibrinolysis, intracerebral haemorrhage, plasminogen activator inhibitor 1, subarachnoid haemorrhage

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