VON-WILLEBRAND-FACTOR AND FACTOR VIII-C IN ACUTE CEREBROVASCULAR-DISEASE - RELATIONSHIP TO STROKE SUBTYPE AND MORTALITY

Background. Elevated von Willebrand factor (vWF) is a risk factor in t he development of acute myocardial infarction. The importance of VWF a nd factor VIII:C in the pathogenesis of cerebrovascular disease (CVD) is poorly defined. Methods and results. We studied 208 cases of stroke whose pathological type was defined by cranial computed tomography. C erebral infarcts were grouped according to the Oxfordshire Community S troke Project (OCSP) clinical classification. The results in patients were compared with 184 healthy reference subjects. In patients, VWF an d FVIII:C levels were determined initially and after three months. Pat ients were followed prospectively for six months or until death. Level s 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 = 0.00 01). In the initial sample, vWF was associated with age (p = 0.01). FV III:C was related to age (p = 0.04), gender (p = 0.007 higher for fema les) and a history of diabetes mellitus (2.56 U/ml vs. 2.16 U/ml in no n-diabetics, p = 0.008). Initial vWF levels were higher in subjects wi th large vessel disease (TACI/PACI) group compared with the small vess el 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 fatalit y, VWF levels were associated with risk of death [p = 0.01, OR 1.73 (1 .12, 2.66) for an increase of 1 U/ml], even after allowing for stroke type. Conclusion. The relationship of vWF with stroke mortality has no t previously been described. Although we have not demonstrated a causa l role for vWF in the pathogenesis of CVD, elevated circulating levels of vWF may be associated with increased risk of death following strok e. A prospective study would be required to establish whether VWF is p redictive for the development of CVD.