doi: 10.1161/hs0901.095377
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(Stroke. 2001;32:1947.)
© 2001 American Heart Association, Inc.
Original Contributions |
Apolipoprotein E and Carotid Artery Atherosclerosis
The Rotterdam Study
From the Department of Epidemiology and Biostatistics, Erasmus Medical Center, Rotterdam, Netherlands (A.J.C.S., M.L.B., A.I. del S., D.E.G., A.H., J.C.M.W., C.M. van D.); TNO Prevention and Health, Gaubius Laboratory and Department of Cardiology and Internal Medicine, University Hospital Leiden, Leiden, Netherlands (L.M.H.); Julius Center for Patient Oriented Research (M.L.B., D.E.G.) and Department of Neurology (A.J.C.S.), University Medical Center, Utrecht, Netherlands; and Molecular Genetics Laboratory, Flanders Interuniversity Institute for Biotechnology, Born-Bunge Foundation, Department of Biochemistry, University of Antwerpen, Antwerp, Belgium (M.C., C. Van B.).
Reprint requests to Professor C.M. van Duijn, Department of Epidemiology and Biostatistics, Erasmus Medical Center, Dr Molewaterplein 50, PO Box 1738, 3000 DR Rotterdam, Netherlands. E-mail vanduijn{at}epib.fgg.eur.nl
Background and Purpose—— Carotid artery atherosclerosis is a strong predictor for future stroke. It is yet unclear whether the apolipoprotein E polymorphism (APOE) is related to atherosclerosis in the carotid arteries. The aim of the present study was to investigate the role of APOE in carotid artery atherosclerosis.
Methods—— A population-based cross-sectional study was performed on 5401 subjects. Atherosclerosis was noninvasively assessed by the common carotid artery intima-media wall thickness and the presence of plaques in the carotid arteries. The relationship of the 6 APOE genotypes with these 2 indicators was studied with linear and logistic regression analysis, respectively, with adjustments for age and sex.
Results—— Carriers of the E2E3 genotype had a thinner intima-media wall thickness (mean difference, -0.02 mm; 95% CI, -0.03 to -0.01 mm) and fewer plaques (odds ratio for >3 plaques at 6 sites, 0.6; 95% CI, 0.4 to 0.8) than the most common group, E3E3. The E4E4 group had slightly more atherosclerosis, but this was not statistically significant. Adjusting for the level of the apolipoprotein E protein (apoE) in serum or total or HDL cholesterol did not essentially change these findings.
Conclusions—— Our results suggest that APOE*4 is not an important risk factor for carotid artery atherosclerosis. The inverse relationship of E2E3 with carotid artery atherosclerosis seems to be independent of serum apoE and total and HDL cholesterol levels. However, the low frequency, together with the small effects, implies that any protective effect of E2E3 on carotid artery atherosclerosis is limited.
Key Words: apolipoproteins • atherosclerosis • carotid arteries • genetics • polymorphism (genetics)
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