title: Association of the fibrinolytic system and hemorheology with symptoms in patients with carotid occlusive disease.
abstract: OBJECTIVE
  The risk of stroke caused by a symptomatic high-grade carotid stenosis (CS) is high. Disturbed balance between the procoagulant and fibrinolytic activity in blood associated with unfavorable hemorheology could render CS symptomatic. We wanted to assess whether hemostatic and fibrinolytic plasma markers as well as basic indicators of hemorheology differentiate asymptomatic and symptomatic patients with a high-grade CS and whether they are associated with the macroscopic appearance of the plaque and the rate of microembolization.
  
  
  METHODS
  We recruited 92 consecutive consenting patients referred to the neurological or the surgical department of our university teaching hospital for treatment of their high-grade CS. Blood samples were collected before surgery for determination of prothrombin fragments F1 and 2, thrombin-antithrombin complex, tissue-type plasminogen activator (tPA) activity and antigen, plasminogen activator inhibitor-1 (PAI-1) activity and antigen, D-dimer, homocysteine, fibrinogen, in plasma, and hematocrit in blood, and the patients underwent transcranial Doppler ultrasonology for evaluation of microembolic signals (MES).
  
  
  RESULTS
  Patients with symptomatic plaques had higher hematocrit levels (p = 0.04), as well as trends for higher tPA antigen and MES rate (p = 0.07). Hematocrit, tPA antigen, and PAI-1 antigen and activity were positively correlated with the degree of stenosis. Ulceration was more common in symptomatic plaques but did not reflect variables of hemostasis or fibrinolysis. In multivariate analysis, tPA antigen and hematocrit were risk factors for a symptomatic high-grade stenosis.
  
  
  CONCLUSIONS
  Mediators of fibrinolysis and unfavorable hemorheology may contribute to the development of a symptomatic disease in patients with a high-grade CS.
authors.affiliation: Department of Neurology, Helsinki University Central Hospital, Helsinki, Finland. lauri.soinne@hus.fi
authors.forename: Lauri
authors.initials: L
authors.lastname: Soinne
authors.forename: Eija
authors.initials: E
authors.lastname: Saimanen
authors.forename: Kirsi
authors.initials: K
authors.lastname: Malmberg-Céder
authors.forename: Petri
authors.initials: P
authors.lastname: Kovanen
authors.forename: Perttu J
authors.initials: PJ
authors.lastname: Lindsberg
authors.forename: Markku
authors.initials: M
authors.lastname: Kaste
authors.forename: Riitta
authors.initials: R
authors.lastname: Lassila
mesh_terms: D000368:Aged; D001779:Blood Coagulation Factors / Q000378:metabolism*; D016893:Carotid Stenosis / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D016022:Case-Control Studies; D002560:Cerebrovascular Circulation / Q000502:physiology; D005260:Female; D005342:Fibrinolysis / Q000502:physiology*; D018056:Hemorheology; D006801:Humans; D020766:Intracranial Embolism / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology; D002546:Ischemic Attack, Transient / Q000097:blood* / Q000209:etiology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D015843:Serpins / Q000097:blood*; D020521:Stroke / Q000097:blood* / Q000209:etiology / Q000503:physiopathology; D014463:Ultrasonography
chemical_list: D001779:Blood Coagulation Factors; D015843:Serpins