title: von Willebrand factor and factor VIII: C in acute cerebrovascular disease. Relationship to stroke subtype and mortality.
abstract: BACKGROUND
  Elevated von Willebrand factor (vWF) is a risk factor in the development of acute myocardial infarction. The importance of vWF and factor VII:C in the pathogenesis of cerebrovascular disease (CVD) is poorly defined.
  
  
  RESULTS
  We studied 208 cases of stroke whose pathological type was defined by cranial computed tomography. Cerebral infarcts were grouped according to the Oxfordshire Community Stroke Project (OCSP) clinical classification. The results in patients were compared with 184 healthy reference subjects. In patients, vWF and FVIII:C levels were determined initially and after three months. Patients were followed prospectively for six months or until death. Levels of vWF and FVIII:C were elevated initially (1.86 IU/ml and 2.20 U/ml respectively) and after 3 months (1.51 IU/ml and 1.90 U/ml) compared with a healthy reference population (1.26 IU/ml and 1.49 U/ml p = 0.0001). In the initial sample, vWF was associated with age (p = 0.01). FVIII:C was related to age (p = 0.04), gender (p = 0.007 higher for females) and a history of diabetes mellitus (2.56 U/ml vs. 2.16 U/ml in non-diabetics, p = 0.008). Initial vWF levels were higher in subjects with large vessel disease (TACI/PACI) group compared with the small vessel disease (LACI) group [2.12 IU/ml, (n = 112) vs. 1.48 IU/ml (n = 59) respectively, p = 0.0001] and similarly in initial FVIII:C levels (2.43 U/ml vs. 1.87 U/ml, p = 0.0001). Analysis of six-month case fatality, vWF levels were associated with risk of death [p = 0.01, OR 1.73 (1.12, 2.66) for an increase of I U/ml], even after allowing for stroke type.
  
  
  CONCLUSIONS
  The relationship of vWF with stroke mortality has not previously been described. Although we have not demonstrated a causal role for vWF in the pathogenesis of CVD, elevated circulating levels of vWF may be associated with increased risk of death following stroke. A prospective study would be required to establish whether vWF is predictive for the development of CVD.
authors.affiliation: Unit of Molecular Vascular Medicine, Research School of Medicine, University of Leeds, Leeds General Infirmary, United Kingdom.
authors.forename: A J
authors.initials: AJ
authors.lastname: Catto
authors.forename: A M
authors.initials: AM
authors.lastname: Carter
authors.forename: J H
authors.initials: JH
authors.lastname: Barrett
authors.forename: J
authors.initials: J
authors.lastname: Bamford
authors.forename: P J
authors.initials: PJ
authors.lastname: Rice
authors.forename: P J
authors.initials: PJ
authors.lastname: Grant
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002561:Cerebrovascular Disorders / Q000097:blood* / Q000401:mortality / Q000503:physiopathology; D005169:Factor VIII / Q000032:analysis*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D014841:von Willebrand Factor / Q000032:analysis*
chemical_list: D014841:von Willebrand Factor; D005169:Factor VIII