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Updated: Oct 9, 2026
Isolation and Cannulation of Cerebral Parenchymal Arterioles
Published on: May 23, 2016
Association of resistance to activated protein C and dural arteriovenous fistulas
J A Kraus1, B K Stüper, P Berlit
1Department of Neurology, Alfried-Krupp Hospital, Essen, Germany.
Insights
The Factor V Leiden mutation, a common cause of blood clots, was found in three out of seven patients with dural arteriovenous fistulas (DAVFs). This suggests a potential link between this genetic mutation and the development of DAVFs.
Area of Science:
- Neuroscience
- Genetics
- Hematology
Background:
- Activated protein C resistance (APCR) is the most common genetic risk factor for venous thrombosis.
- FV Leiden mutation is the primary cause of APCR.
- Dural arteriovenous fistulas (DAVFs) are linked to cerebral venous thrombosis.
Purpose of the Study:
- To investigate the prevalence of the FV Leiden mutation in patients diagnosed with DAVFs.
- To explore the potential role of FV Leiden in the pathogenesis of DAVFs.
Main Methods:
- APCR ratio determination using standard procedures.
- Mutation analysis for FV Leiden via reverse hybridization assay in patients with pathological APCR ratios (less than 2.0).
Main Results:
- Three out of seven patients with DAVFs exhibited pathological APCR ratios.
- These three patients were found to be heterozygous for the FV Leiden mutation.
Conclusions:
- The study hypothesizes that the FV Leiden mutation may contribute to the development of DAVFs.
- Further research is warranted to confirm the association between FV Leiden and DAVF pathogenesis.
Abstract:
Resistance to activated protein C (APCR), shown to be the most common genetic risk factor for venous thrombosis, is mostly caused by a mutation in the factor V (FV) gene leading to FV Leiden. As dural arteriovenous fistulas (DAVFs) are associated with cerebral venous thrombosis, we looked for the FV Leiden mutation in seven patients with such fistulas. The APCR ratio was determined according to standard procedures. For APCR ratios considered pathological (less than 2.0), mutation analysis was done by a reverse hybridization assay. Three of the seven patients with DAVFs showed pathological APCR ratios and heterozygosity for FV Leiden mutation. Thus, it is hypothesized that FV Leiden might be involved in the pathogenesis of DAVFs.
