Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3030132 | Thrombosis Research | 2007 | 5 Pages |
BackgroundDeep vein thrombosis (DVT) occurs with high prevalence in association with the Factor V Leiden (R506Q) mutation, whereas most evidence suggests no correlation with clinical arterial thrombosis.ObjectiveThis study compared arterial to venous thrombosis in the mutationally analogous Factor V Leiden mouse.MethodsThree separate vascular thrombosis models were evaluated in Fv+/+ (wild-type), FvQ/+ (heterozygous) and FvQ/Q (homozygous) Factor V Leiden mice.ResultsIn a FeCl3-induced arterial thrombosis model, no statistical differences among the three genotypes were found in the time to thrombotic occlusion. In contrast, FvQ/+ and FvQ/Q mice demonstrated larger femoral vein thrombi at 30 and 60 min compared to wild-types, with FvQ/Q mice having statistically larger thrombi than both wild-type and FvQ/+ mice at 10 and 60 min and 24 h (p < 0.05). In a model of thrombotic occlusion following arterial and venous anastomotic repair, both FvQ/+ and FvQ/Q mice had higher rates of venous thrombosis than wild-types, but only FvQ/Q homozygotes showed a statistically greater arterial occlusion rate than wild-types.ConclusionThe Factor V Leiden mouse demonstrated a greater propensity for venous vs. arterial thrombosis, paralleling clinical epidemiologic findings and supporting its use for research on deep vein thrombosis.