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Mild hyperhomocyst(e)inemia: a possible risk factor for cervical artery dissection
V Gallai1, V Caso, M Paciaroni
1Neuroscience Department, University of Perugia, Perugia, Italy. neurol@unipg.it
Stroke
|March 10, 2001
Summary
Mild hyperhomocysteinemia (hyperH(e)) may be a risk factor for cervical artery dissection (CAD). The 5,10-methylenetetrahydrofolate reductase (MTHFR) gene mutation was not significantly associated with CAD in this study.
Area of Science:
- Neurology
- Vascular Biology
- Genetics
Background:
- Cervical artery dissection (CAD) pathogenesis is largely unknown.
- Hyperhomocysteinemia (hyperH(e)) is a known risk factor for cerebrovascular disease.
- Endothelial cell damage is induced by hyperH(e) in animal models.
Purpose of the Study:
- To investigate the role of homocyst(e)ine levels and MTHFR genotype in CAD.
- To compare serum homocyst(e)ine levels and MTHFR genotypes between CAD patients and controls.
Main Methods:
- Study included 26 CAD patients and age-matched controls.
- Blood samples analyzed for homocyst(e)ine levels and MTHFR genotype.
- Vascular imaging included duplex ultrasound, MR angiography, and/or conventional angiography.
Main Results:
- CAD patients had significantly higher mean plasma homocyst(e)ine levels (17.88 µmol/L) compared to controls (6.0 µmol/L).
- MTHFR thermolabile mutation heterozygosity was 54% in CAD patients vs. 40% in controls (P=0.4).
- MTHFR thermolabile mutation homozygosity was 27% in CAD patients vs. 10% in controls (P=0.1).
Conclusions:
- Mild hyperH(e) may be a risk factor for cervical artery dissection.
- MTHFR gene mutation is not significantly associated with CAD.
- Complex interactions between genetic and environmental factors likely contribute to arterial wall damage in CAD.