Thromb Haemost 1997; 77(06): 1104-1108
DOI: 10.1055/s-0038-1656120
Clinical Studies
Schattauer GmbH Stuttgart

von Willebrand Factor and Factor VIII: C in Acute Cerebrovascular Disease

Relationship to Stroke Subtype and Mortality
Andrew J Catto
1   The Unit of Molecular Vascular Medicine, Research School of Medicine, University of Leeds, Leeds General Infirmary, Leeds, United Kingdom
,
Angela M Carter
1   The Unit of Molecular Vascular Medicine, Research School of Medicine, University of Leeds, Leeds General Infirmary, Leeds, United Kingdom
,
Jennifer H Barrett
1   The Unit of Molecular Vascular Medicine, Research School of Medicine, University of Leeds, Leeds General Infirmary, Leeds, United Kingdom
,
John Bamford
2   Department of Neurology, St James’s University Hospital, Leeds, United Kingdom
,
Penny J Rice
1   The Unit of Molecular Vascular Medicine, Research School of Medicine, University of Leeds, Leeds General Infirmary, Leeds, United Kingdom
,
Peter J Grant
1   The Unit of Molecular Vascular Medicine, Research School of Medicine, University of Leeds, Leeds General Infirmary, Leeds, United Kingdom
› Author Affiliations
Further Information

Publication History

Received 28 November 1996

Accepted after revision 26 February 1997

Publication Date:
12 July 2018 (online)

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.

 
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