Mild hyperhomocyst(e)inemia - A possible risk factor for cervical artery dissection

Background and Purpose-The pathogenesis of cervical artery dissection (CAD) remains unknown in most cases. Hyperhomocyst(e)inemia [hyperH(e)], an inde pendent risk factor for cerebrovascular disease, induces damage in endothel ial cells in animal cell culture. Consecutive patients with CAD and age-mat ched control subjects have been studied by serum levels of homocyst(e)ine a nd the genotype of 5,10-methylenetetrahydrofolate reductase (MTHFR). Methods-Twenty-six patients with CAD, admitted to our Stroke Unit (15 men a nd 11 women; 16 vertebral arteries, 10 internal carotid arteries), were com pared with age-matched control subjects. All patients underwent duplex ultr asound, MR angiography, and/or conventional angiography, Results-Mean plasma homocyst(e)ine level was 17.88 mu mol/L (range 5.95 to 40.0 mu mol/L) for patients with CAD and 6.0+/-0.99 mu mol/L for controls ( P<0.001). The genetic analysis for the thermolabile form of MTHFR in CAD pa tients showed heterozygosity in 54% and homozygosity in 27%; comparable fig ures for controls were 40% (P=0.4) and 10% (P=0.1), respectively. Conclusions-Mild hyperH(e) might represent a risk factor for cervical arter y 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.