Signe Voigt Lauridsen

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

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No hyperfibrinolysis following subarachnoid or intracerebral haemorrhage: A prospective cohort study. / Lauridsen, Signe V.; Hvas, Christine L.; Sandgaard, Emilie et al.
In: Blood Coagulation and Fibrinolysis, Vol. 30, No. 7, 01.01.2019, p. 341-349.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

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Lauridsen SV, Hvas CL, Sandgaard E, Gyldenholm T, Tønnesen EK, Hvas AM. No hyperfibrinolysis following subarachnoid or intracerebral haemorrhage: A prospective cohort study. Blood Coagulation and Fibrinolysis. 2019 Jan 1;30(7):341-349. doi: 10.1097/MBC.0000000000000845

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Lauridsen, Signe V. ; Hvas, Christine L. ; Sandgaard, Emilie et al. / No hyperfibrinolysis following subarachnoid or intracerebral haemorrhage : A prospective cohort study. In: Blood Coagulation and Fibrinolysis. 2019 ; Vol. 30, No. 7. pp. 341-349.

Bibtex

@article{17a93d2ec46749bba16c6b767d7a0719,
title = "No hyperfibrinolysis following subarachnoid or intracerebral haemorrhage: A prospective cohort study",
abstract = "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.",
keywords = "factor XIII, fibrinolysis, intracerebral haemorrhage, plasminogen activator inhibitor 1, subarachnoid haemorrhage",
author = "Lauridsen, {Signe V.} and Hvas, {Christine L.} and Emilie Sandgaard and Tua Gyldenholm and T{\o}nnesen, {Else K.} and Hvas, {Anne Mette}",
year = "2019",
month = jan,
day = "1",
doi = "10.1097/MBC.0000000000000845",
language = "English",
volume = "30",
pages = "341--349",
journal = "Blood Coagulation and Fibrinolysis",
issn = "0957-5235",
publisher = "LIPPINCOTT WILLIAMS & WILKINS",
number = "7",

}

RIS

TY - JOUR

T1 - No hyperfibrinolysis following subarachnoid or intracerebral haemorrhage

T2 - A prospective cohort study

AU - Lauridsen, Signe V.

AU - Hvas, Christine L.

AU - Sandgaard, Emilie

AU - Gyldenholm, Tua

AU - Tønnesen, Else K.

AU - Hvas, Anne Mette

PY - 2019/1/1

Y1 - 2019/1/1

N2 - 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.

AB - 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.

KW - factor XIII

KW - fibrinolysis

KW - intracerebral haemorrhage

KW - plasminogen activator inhibitor 1

KW - subarachnoid haemorrhage

UR - http://www.scopus.com/inward/record.url?scp=85073183748&partnerID=8YFLogxK

U2 - 10.1097/MBC.0000000000000845

DO - 10.1097/MBC.0000000000000845

M3 - Journal article

C2 - 31592776

AN - SCOPUS:85073183748

VL - 30

SP - 341

EP - 349

JO - Blood Coagulation and Fibrinolysis

JF - Blood Coagulation and Fibrinolysis

SN - 0957-5235

IS - 7

ER -