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Thrombus stability explains the factor V Leiden paradox: a mouse model.

S A Shaya^1,2, R J Westrick³, P L Gross^1,2,4

¹Thrombosis and Atherosclerosis Research Institute and.

|November 8, 2019

Summary

Factor V Leiden (FVL) mutation increases venous thrombosis risk. In mice, FVL variants showed larger, more stable deep vein thrombi (DVT) with less embolization, explaining the FVL paradox.

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Area of Science:

Biomedical Science
Hematology
Thrombosis Research

Background:

Factor V Leiden (FVL) variant carriers have a fivefold higher risk of venous thrombosis.
A paradox exists where deep vein thrombosis (DVT) incidence is disproportionately higher than pulmonary embolism (PE) in FVL carriers.

Purpose of the Study:

To investigate the hypothesis that FVL carriers develop more stable thrombi, leading to clinically significant DVTs more frequently than non-carriers.
To elucidate the mechanisms behind the FVL paradox by comparing thrombus stability and embolization in FVL and wild-type models.

Main Methods:

Induced femoral vein thrombi in wild-type (WT), heterozygous (F5L/+), and homozygous (F5L/L) mice.
Utilized intravital microscopy to visualize thrombus size and embolization.
Quantified emboli in the lungs to assess pulmonary embolism (PE) burden.

Main Results:

Femoral vein thrombi were larger and embolized less in FVL (F5L/+) and homozygous (F5L/L) mice compared to WT mice.
Homozygous FVL (F5L/L) mice exhibited significantly decreased total and large embolic events and reduced PE burden.
The percentage of thrombus that embolized was significantly lower in FVL mice.

Conclusions:

FVL variant leads to more stable thrombi with reduced embolization, contributing to a higher incidence of symptomatic DVT.
Less embolization in FVL carriers allows thrombi to grow, potentially causing symptomatic DVT, whereas in non-carriers, embolization may prevent small thrombi from becoming clinically significant.