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Published on: December 22, 2017
Arterial thrombosis in mice with factor V Leiden mutation
Ellis S Sampram1, Yasser Saad, Kenneth Ouriel
1Department of Vascular Surgery, The Cleveland Clinic, Cleveland, OH, USA. esampram@gmail.com
Vascular
|February 9, 2008
Summary
The factor V Leiden (FVL) mutation increases arterial thrombosis risk. Homozygous FVL mice showed the shortest time to occlusion, indicating higher thrombogenicity compared to heterozygous and wild-type mice.
Area of Science:
- Cardiovascular Research
- Hematology
- Genetics
Background:
- The factor V Leiden (FVL) mutation is a known risk factor for venous thrombosis.
- Its role in arterial thrombosis remains debated due to variability in clinical studies.
Purpose of the Study:
- To investigate the association between the FVL mutation and arterial thrombosis using a controlled mouse model.
- To compare thrombotic propensity in homozygous FVL, heterozygous FVL, and wild-type mice.
Main Methods:
- Developed a mouse model with three genotypes: wild-type, heterozygous FVL, and homozygous FVL.
- Induced arterial injury in the carotid artery using ferric chloride.
- Assessed arterial thrombosis by measuring time to occlusion (TTO) with an ultrasonic flow probe.
Main Results:
- A statistically significant relationship was found between FVL genotype and TTO (p = .002).
- Wild-type mice had the longest TTO, while homozygous FVL mice exhibited the shortest TTO.
- Arterial occlusion occurred in 97.3% of animals within 60 minutes.
Conclusions:
- The FVL mutation is associated with increased arterial thrombogenicity in mice.
- Thrombotic risk is dose-dependent, with homozygotes showing greater susceptibility than heterozygotes.
- Findings support clinical observations linking FVL mutation to increased arterial event risk.
