APOE polymorphism and carotid atherosclerosis in Korean population: The Dong-gu Study and the Namwon Study

- The APOE polymorphism is associated with carotid atherosclerosis.
- E2E2 and E2E3 genotypes had lower carotid IMT compared with E3E3 genotype.
- E2E3 genotype had a lower risk of carotid plaque compared with E3E3 genotype.
- E3E4 genotype had a higher risk of carotid plaque compared with E3E3 genotype.
- These associations were partly mediated through blood lipids.

ObjectiveWe evaluated the association between APOE polymorphism and carotid atherosclerosis in two large independent cohorts from South Korea.MethodsThe datasets were from the Dong-gu Study (N = 9056) and the Namwon Study (N = 10,158). Carotid ultrasonography was performed to measure carotid intima-media thickness (IMT) and the presence of carotid plaques. The APOE polymorphism was determined by PCR-RFLP. We performed combined and separate analyses for the two datasets.ResultsIn the combined analysis, individuals with E2E2 or E2E3 genotype had a lower common carotid IMT compared with individuals with E3E3 genotype (0.684 mm vs. 0.736 mm, p = 0.007; 0.718 mm vs. 0.736 mm, p < 0.001, respectively). This association was very slightly attenuated but remained statistically significant after adjustment for blood lipids (0.690 mm vs. 0.736 mm, p = 0.033; 0.725 mm vs. 0.736 mm, p = 0.005, respectively). Compared with individuals with E3E3 genotype, individuals with E2E3 genotype had lower risk for carotid plaque (odds ratio (OR) = 0.83, 95% confidence interval (CI) = 0.75-0.93), while individuals with E3E4 genotype had a higher risk for carotid plaque (OR = 1.09, 95% CI = 1.00-1.20). After adjustment for blood lipids, ORs of E2E3 genotype for carotid plaque was slightly attenuated but remained significant (OR = 0.87 95% CI = 0.78-0.97), while OR of E3E4 genotype were slightly attenuated and not significant (OR = 1.08, 95% CI, 0.99-1.18).ConclusionsWe found that APOE polymorphism is associated with carotid atherosclerosis and this association was partly mediated through blood lipid. Our results suggest that APOE polymorphism may influence atherosclerosis through non-lipid pathways.