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Updated: May 30, 2026
13:08
Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
Published on: September 9, 2012
Factor VII Activating Protease Polymorphism (G534E) Is Associated with Increased Risk for Stroke and Mortality
Stella Trompet1, Douwe Pons, Sandip M Kanse
1Department of Cardiology, Leiden University Medical Center, C5-P, P.O. Box 9600, 2300 RC Leiden, The Netherlands.
Stroke Research and Treatment
|July 27, 2011
Summary
The FSAP-Marburg I polymorphism increases stroke risk and all-cause mortality but may reduce restenosis risk. This genetic variant influences cardiovascular disease outcomes, impacting plaque stability and hemostasis.
Area of Science:
- Genetics and Cardiovascular Disease
- Molecular Biology and Vascular Health
Background:
- The FSAP-Marburg I polymorphism (1704G>A) is linked to reduced FSAP activity and carotid stenosis complications.
- Understanding genetic influences on cardiovascular disease is crucial for risk stratification and treatment.
Purpose of the Study:
- To investigate the impact of FSAP-Marburg I and Marburg II polymorphisms on cardiovascular outcomes.
- To analyze these genetic variants in large, independent elderly and interventional study populations.
Main Methods:
- Genotyping of Marburg I and II polymorphisms in the HABP2 gene (encoding FSAP).
- Analysis of data from the PROSPER study (n=5804, elderly at risk) and the GENDER study (n=3104, post-PCI).
Main Results:
- In PROSPER, Marburg I was associated with increased stroke risk (HR: 1.60) and mortality (HR: 1.33).
- In GENDER, Marburg I carriers showed a trend towards lower restenosis risk (HR: 0.59).
- Marburg II polymorphism exhibited similar, but less pronounced, associations.
Conclusions:
- Marburg I polymorphism may increase stroke risk via effects on smooth muscle cells and matrix metalloproteinases, affecting plaque stability.
- A potential protective effect against restenosis might stem from reduced zymogen activation, influencing hemostasis and matrix remodeling.
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