Journal
JOURNAL OF THROMBOSIS AND HAEMOSTASIS
Volume 9, Issue 5, Pages 899-908Publisher
WILEY
DOI: 10.1111/j.1538-7836.2011.04243.x
Keywords
cardiovascular disease; genetics; ischemic stroke; myocardial infarction; von Willebrand factor
Categories
Funding
- Erasmus University Medical Center
- Netherlands Heart Foundation [2007B159]
Ask authors/readers for more resources
It is well established that high plasma von Willebrand factor (VWF) levels are associated with an increased risk of arterial thrombosis, including myocardial infarction and ischemic stroke. As plasma VWF levels are, to a large extent, genetically determined, numerous association studies have been performed to assess the effect of genetic variability in the VWF gene (VWF) on VWF antigen and activity levels, and on the risk of arterial thrombosis. Genetic variations in other regulators of VWF, including the ABO blood group, ADAM-TS-13, thrombospondin-1 and the recently identified SNARE protein genes, have also been investigated. In this article, we review the current literature as exploring the associations between genetic variations and the risk of arterial thrombosis may help elucidate the role of VWF in the pathogenesis of arterial thrombosis. However, as studies frequently differ in design, population and endpoint, and are often underpowered, it remains unclear whether VWF is causally related to the occurrence of arterial thrombosis or primarily mirrors endothelial dysfunction, which predisposes to atherosclerosis and subsequent arterial thrombosis. Nevertheless, current studies provide interesting results that do not exclude the possibility of VWF as causal mediator and justify further research into the relationship between VWF and arterial thrombosis. Large prospective studies are required to further establish the role of VWF in the occurrence of arterial thrombosis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available