title: Hemostatic activation in acute ischemic stroke.
abstract: OBJECTIVE
  The purpose of this study was to examine the association between hemostatic activation and stroke severity, and to provide data on hemostatic variables in acute ischemic stroke.
  
  
  METHODS
  The patient material comprised 76 consecutive patients with acute ischemic stroke (median 16 h, interquartile range 3-48). Levels of hemostatic variables were determined in blood samples collected on the day of hospitalization. Stroke severity was assessed on admission by the Oxfordshire Community Stroke Project (OCSP) classification, and on discharge (median 9 days, interquartile range 6-14) by Barthel Index (BI, scores 0-50, 55-90, or 95-100) and modified Rankin Scale (mRS, scores 0-1 or 2-6). Associations were assessed by multiple linear regression analyses.
  
  
  RESULTS
  Levels of the fibrin degradation product D-Dimer and the activation peptide prothrombin fragment 1 + 2 (F1 + 2) were linearly related to stroke severity, whether assessed on admission (P = .001 and.03, respectively, for the OCSP classification), or on discharge (P = .009 and.43, respectively, for BI; and.001 and.05, respectively, for mRS). High levels of D-Dimer and F(1 + 2), as well as low levels of antithrombin and protein C were also present in patients with a presumed embolic source, and low antithrombin or protein C was borderline significantly associated with atrial fibrillation (P = .072 and.058, respectively). Low levels of protein C or protein S, and the presence of antiphospholipid antibodies, including lupus anticoagulant (LA), was detected in 13/73 (18%) and 15/70 (21%) of the patients, respectively.
  
  
  CONCLUSIONS
  Activation of the hemostatic system is independently related to acute stroke severity and short-term outcome. Low levels of coagulation inhibitors or presence of antiphospholipid antibodies is a relatively frequent finding in unselected patients with acute ischemic stroke, but a causative role cannot be inferred from our study.
authors.affiliation: Hematological Research Laboratory, Department of Hematology, Ullevål University Hospital, N-0407, Oslo, Norway. eivind.berge@ulleval.no
authors.forename: E
authors.initials: E
authors.lastname: Berge
authors.forename: P
authors.initials: P
authors.lastname: Friis
authors.forename: P M
authors.initials: PM
authors.lastname: Sandset
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000925:Anticoagulants / Q000097:blood; D000991:Antithrombins / Q000378:metabolism; D001281:Atrial Fibrillation / Q000150:complications; D002545:Brain Ischemia / Q000097:blood* / Q000150:complications; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D006490:Hemostatics / Q000097:blood*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000378:metabolism; D011486:Protein C / Q000378:metabolism; D011516:Prothrombin / Q000378:metabolism; D012044:Regression Analysis; D012720:Severity of Illness Index; D020521:Stroke / Q000097:blood* / Q000150:complications
chemical_list: D000925:Anticoagulants; D000991:Antithrombins; D005338:Fibrin Fibrinogen Degradation Products; D006490:Hemostatics; D010446:Peptide Fragments; D011486:Protein C; C036309:fibrin fragment D; C045879:prothrombin fragment 1.2; D011516:Prothrombin