Abstract:
BACKGROUND:Activated protein C resistance due to factor V Leiden (FVL) is a common genetic risk factor for venous thrombosis in humans. Although the impact of FVL on the development of venous thrombosis is well established, its effect on arterial thrombosis and atherosclerosis is controversial. METHODS AND RESULTS:To determine the effect of the FVL mutation on arterial thrombosis in the mouse, wild-type (Fv+/+), heterozygous FVL (FvQ/+), and homozygous FVL (FvQ/Q) mice underwent photochemical carotid arterial injury to induce occlusive thrombosis. FvQ/Q mice formed occlusive thromboses 27+/-3 minutes (n=7) after the onset of injury, which was significantly shorter than that observed for Fv+/+ mice (56+/-7 minutes, n=9, P<0.01), whereas FvQ/+ mice (41+/-7 minutes, n=5) were intermediate (P=0.5, compared with Fv+/+). To determine the source of FVL relevant to the enhanced vascular thrombosis, bone marrow transplantation experiments were performed between Fv+/+ and FvQ/Q mice. FvQ/Q mice transplanted with Fv+/+ bone marrow formed occlusive thromboses at 35+/-5 minutes (n=7, P<0.05 compared with Fv+/+ mice), whereas Fv+/+ mice transplanted with FvQ/Q bone marrow occluded at 59+/-7 minutes (n=6, P<0.001 compared with FvQ/Q mice). To assess the effect of the FVL mutation on the development of atherosclerosis, FvQ/Q mice were crossed with the atherosclerosis-prone apolipoprotein E (ApoE)-deficient strain (ApoE-/-) to generate FvQ/Q,ApoE-/- mice. By 52 weeks of age, FvQ/Q,ApoE-/- mice (n=8) had developed more aortic atherosclerosis (40+/-6% lesion area) compared with Fv+/+,ApoE-/- mice (15+/-3% lesion area; n=12, P<0.02). CONCLUSIONS:In conclusion, homozygosity for the FVL mutation in mice leads to enhanced arterial thrombosis and atherosclerosis. The source of the FVL leading to accelerated thrombosis appears to be circulating, non-platelet-derived plasma FVL.
journal_name
Circulationjournal_title
Circulationauthors
Eitzman DT,Westrick RJ,Shen Y,Bodary PF,Gu S,Manning SL,Dobies SL,Ginsburg Ddoi
10.1161/01.CIR.0000160854.75779.E8subject
Has Abstractpub_date
2005-04-12 00:00:00pages
1822-5issue
14eissn
0009-7322issn
1524-4539pii
01.CIR.0000160854.75779.E8journal_volume
111pub_type
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