Please use this identifier to cite or link to this item: https://doi.org/10.4061/2011/424759
Title: Factor VII activating protease polymorphism (G534E) is associated with increased risk for stroke and mortality
Authors: Trompet, S
Pons, D
Kanse, S.M
De Craen, A.J.M
Ikram, M.A 
Verschuren, J.J.W
Zwinderman, A.H
Doevendans, P.A.F.M
Tio, R.A
De Winter, R.J
Slagboom, P.E
Westendorp, R.G.J
Jukema, J.W
Keywords: blood clotting factor 7
enzyme precursor
matrix metalloproteinase
placebo
pravastatin
proteinase
aged
article
controlled study
DNA polymorphism
female
genetic code
genetic polymorphism
genotype
hemostasis
human
human tissue
major clinical study
male
mortality
multicenter study
percutaneous coronary intervention
priority journal
randomized controlled trial
restenosis
risk assessment
stroke
vascular disease
Issue Date: 2011
Citation: Trompet, S, Pons, D, Kanse, S.M, De Craen, A.J.M, Ikram, M.A, Verschuren, J.J.W, Zwinderman, A.H, Doevendans, P.A.F.M, Tio, R.A, De Winter, R.J, Slagboom, P.E, Westendorp, R.G.J, Jukema, J.W (2011). Factor VII activating protease polymorphism (G534E) is associated with increased risk for stroke and mortality. Stroke Research and Treatment : 424759. ScholarBank@NUS Repository. https://doi.org/10.4061/2011/424759
Rights: Attribution 4.0 International
Abstract: Introduction: The FSAP-Marburg I polymorphism (1704GA), which reduces FSAP activity, is associated with late complications of carotid stenosis in humans. Therefore, this study examines the influence of the Marburg I polymorphism and the closely linked Marburg II polymorphism (1280GC) on various cardiovascular outcomes in two large independent study populations. Methods. The two Marburg polymorphisms in the HABP2 gene encoding FSAP were genotyped in a large population of elderly patients at risk for vascular disease (the PROSPER-study, n=5804) and in a study population treated with a percutaneous coronary intervention (the GENDER-study, n=3104). Results. In the PROSPER study, the Marburg I polymorphism was associated with an increased risk of clinical stroke (HR: 1.60, 95 CI: 1.13-2.28) and all-cause mortality (HR: 1.33, 95 CI: 1.04-1.71). In the GENDER study carriers of this variant seemed at lower risk of developing restenosis (HR: 0.59, 95 CI: 0.34-1.01). The Marburg II polymorphism showed similar but weaker results. Conclusion. The increase in stroke risk in Marburg I carriers could be due to differential effects on smooth muscle cells and on matrix metalloproteinases, thereby influencing plaque stability. The possible protective effect on restenosis could be the result of reduced activation of zymogens, which are involved in hemostasis and matrix remodeling. Copyright © 2011 Stella Trompet et al.
Source Title: Stroke Research and Treatment
URI: https://scholarbank.nus.edu.sg/handle/10635/183252
ISSN: 20420056
DOI: 10.4061/2011/424759
Rights: Attribution 4.0 International
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