Reduced clot-stability during the first 6 hours after aneurysmal subarachnoid haemorrhage--a prospective case-control study |
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Authors: | Larsen Carl C Sørensen Benny Nielsen Jørn D Astrup Jens |
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Affiliation: | a Department of Neurosurgery, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmarkb Haemostasis Research Unit, Centre for Haemostasis & Thrombosis, St Thomas’ Hospital , Westminster Bridge Road, London SE1 7EH, UKc Thrombosis & Haemostasis Unit, University Hospital of Copenhagen, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmarkd Department of Neurosurgery, Glostrup University Hospital, Nordre Ringvej 57, DK-2600 Glostrup, Denmark |
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Abstract: | IntroductionEarly rebleeding is an important cause of death and disability following aneurysmal subarachnoid haemorrhage (SAH). Recent studies have shown that 50-90% of the rebleedings occurred within the first 6 hours after the primary bleeding. The mechanism leading to rebleeding remains to be established. In the present prospective case-control study we hypothesize that patients with SAH develop a coagulopathy characterized by reduced clot stability during the early period after the initial bleeding.MethodsPatients with aneurysmal SAH was studied with a dynamic clot lysis assay and markers of fibrinolysis and clot stabilizers in blood samples taken within and after 6 hours after onset of bleeding. Results were compared with blood samples from age and gender matched healthy controls.Results36 patients were enrolled, 26 patients had blood samples collected within 6 hours after the initial bleeding whereas 10 patients had blood samples taken later than 6 hours after the initial bleeding. Patients demonstrated significantly reduced clot stability during the first 6 hours after initial bleeding. Fibrinolytic activity was increased during the first 6 hours along with the inhibitors of fibrinolysis whereas the modulators of fibrinolysis were reduced or inactivated.ConclusionDuring the first 6 hours after SAH patients exhibit reduced clot-stability. Probably a consequence of activated fibrinolysis in combination with reduced or inactivated factor XIII and thrombin-activable fibrinolysis inhibitor. |
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Keywords: | AUC, area under the clot lysis curve CT, computed tomography ELISA, enzyme-linked immunosorbent assays MRI, magnetic resonance imaging PAI-1, plasminogen activator inhibitor 1 PAP, plasmin-antiplasmin SAH, subarachnoid haemorrhage t-PA, tissue plasminogen activator TAFI, thrombin-activatable fibrinolysis inhibitor TAT, thrombin-antithrombin TXA, tranexamic acid |
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