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

Atherosclerosis

Department of Preventive Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea; Jeonnam Regional Cancer Center, Chonnam National University Hwasun, Hwasun Hospital, Republic of Korea. Electronic address:

Published: January 2014

Objective: We evaluated the association between APOE polymorphism and carotid atherosclerosis in two large independent cohorts from South Korea.

Methods: The 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.

Results: In 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).

Conclusions: We 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.

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Source
http://dx.doi.org/10.1016/j.atherosclerosis.2013.11.027DOI Listing

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