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Ischemic stroke in the elderly. Role of the common factor V mutation causing resistance to activated protein C
1Department of Pathology, Oregon Health Sciences University, Portland 97201-3098, USA.
Insights
The factor V Arg 506 Gln mutation, linked to venous thrombosis, was not found to be a significant genetic risk factor for ischemic stroke in the elderly. Its prevalence in elderly stroke patients did not differ from controls.
Area of Science:
- Genetics
- Hematology
- Neurology
Background:
- A common missense mutation, factor V Arg 506 Gln, confers resistance to activated protein C.
- This mutation is associated with an increased risk of venous thrombosis.
Purpose of the Study:
- To investigate the correlation between the factor V Arg 506 Gln mutation and ischemic cerebrovascular disease.
- To compare the mutation's prevalence in stroke patients versus control groups.
Main Methods:
- A polymerase chain reaction (PCR)-based assay was used to detect the factor V Arg 506 Gln mutation.
- The study included 161 elderly ischemic stroke patients, 116 elderly controls with risk factors, 54 healthy elderly controls, and 287 younger controls.
Main Results:
- The prevalence of the heterozygous factor V Arg 506 Gln mutation was 2.5% in elderly stroke patients.
- No significant difference in mutation prevalence was observed between elderly stroke patients and age-matched controls (2%-4%).
- The mutation was significantly more prevalent in younger control groups (approx. 8%) compared to elderly stroke patients.
Conclusions:
- The factor V Arg 506 Gln mutation is not a significant genetic risk factor for ischemic stroke in the elderly population.
- Findings suggest that the hypercoagulable state associated with this mutation may not strongly influence ischemic stroke risk in older individuals.
Background And Purpose:
A common missense mutation in coagulation factor V (Arg 506 Gln) creates phenotypic resistance to the anticoagulant effects of activated protein C and predisposes carriers to venous thrombosis. To assess a correlation between this common hypercoagulable state and ischemic cerebrovascular disease, we have compared the prevalence of this mutation in a group of stroke patients with that in several control patient groups.
Methods:
The presence of the factor V Arg 506 Gln mutation was determined by a direct polymerase chain reaction-based assay on peripheral blood leukocytes from 161 elderly patients with acute ischemic stroke, 116 elderly patients with stroke risk factors but without acute stroke, 54 healthy elderly control subjects, and 287 younger control individuals (197 blood donors and 90 neonates).
Results:
The prevalence of the heterozygous Arg 506 Gln factor V mutation was not significantly different in the elderly stroke patients (2.5%) compared with either of the age-matched control groups (2% to 4%). The prevalence of this mutation was significantly higher in each of two younger control groups (approximately 8%) than in the elderly stroke patients (2.5%).
Conclusions:
The common factor V Arg 506 Gln mutation predisposing to venous thrombosis is not a significant genetic risk factor for ischemic stroke in the elderly.