(Stroke. 2001;32:714.)
© 2001 American Heart Association, Inc.
Original Contributions |
Mild Hyperhomocyst(e)inemia
A Possible Risk Factor for Cervical Artery Dissection
From the Neuroscience Department, University of Perugia, Perugia, Italy (V.G, V.C., M.P., G.C., L.P.), and Institute of Metabolic Disease, Baylor University Medical Center, Dallas, Tex (E.A., T.B.).
Correspondence to Prof Virgilio Gallai, Department of Neuroscience, University of Perugia, Via Enrico dal Pozzo, 06126 Perugia, Italy. E-mail neurol{at}unipg.it
Background and Purpose—The pathogenesis of cervical artery dissection (CAD) remains unknown in most cases. Hyperhomocyst(e)inemia [hyperH(e)], an independent risk factor for cerebrovascular disease, induces damage in endothelial cells in animal cell culture. Consecutive patients with CAD and age-matched control subjects have been studied by serum levels of homocyst(e)ine and the genotype of 5,10-methylenetetrahydrofolate reductase (MTHFR).
Methods—Twenty-six patients with CAD, admitted to our Stroke Unit (15 men and 11 women; 16 vertebral arteries, 10 internal carotid arteries), were compared with age-matched control subjects. All patients underwent duplex ultrasound, MR angiography, and/or conventional angiography.
Results—Mean plasma homocyst(e)ine level was 17.88 µmol/L (range 5.95 to 40.0 µmol/L) for patients with CAD and 6.0±0.99 µmol/L for controls (P<0.001). The genetic analysis for the thermolabile form of MTHFR in CAD patients showed heterozygosity in 54% and homozygosity in 27%; comparable figures for controls were 40% (P=0.4) and 10% (P=0.1), respectively.
Conclusions—Mild hyperH(e) might represent a risk factor for cervical artery dissection. The MTHFR mutation is not significantly associated with CAD. An interaction between different genetic and environmental factors probably takes place in the cascade of pathogenetic events leading to arterial wall damage.
Key Words: amine oxidoreductases • dissection • homocyst(e)ine • stroke • ultrasonography
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