Summary
Background. Elevated von Willebrand factor (vWF) is a risk factor in the development of acute
myocardial infarction. The importance of vWF and 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. 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 1 U/ml], even after allowing for
stroke type.
Conclusion. 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.
