Apolipoprotein E polymorphism affects carotid artery atherosclerosis in smoking hypertensive men

• Published in: Journal of hypertension Vol. 20; no. 12; p. 2371
• Main Authors: Karvonen, Jarkko, Kauma, Heikki, Kervinen, Kari, Ukkola, Olavi, Rantala, Maire, Päivänsalo, Markku, Savolainen, Markku J, Kesäniemi, Y Antero
• Format: Journal Article
• Language: English
• Published: England 01.12.2002
• Subjects: Adult; Apolipoprotein E4; Apolipoproteins E - genetics; Carotid Artery Diseases - etiology; Case-Control Studies; Cross-Sectional Studies; Genetic Predisposition to Disease; Heterozygote; Humans; Hypertension - diagnostic imaging; Hypertension - genetics; Intracranial Arteriosclerosis - etiology; Male; Middle Aged; Polymorphism, Genetic; Smoking - adverse effects; Tunica Intima - diagnostic imaging; Tunica Media - diagnostic imaging; Ultrasonography
• ISSN: 0263-6352
• DOI: 10.1097/00004872-200212000-00015

Smoking is a risk factor for increased carotid artery intima-media thickness (IMT). The apolipoprotein E (apoE) 4 allele has been associated with cardiovascular diseases, but the role of apoE in regard to intima-media thickness (IMT) has remained controversial. The objective was to investigate whether there is some gene-environment interaction between smoking and apoE polymorphism. DESIGN Cross-sectional case-control study. IMTs of 511 hypertensive and control men were measured ultrasonographically and the apoE genotypes were determined. Genotypes with the 4 allele were pooled into one group and the genotypes without it into another. A significant interaction between the 4 allele and smoking affecting IMT was observed among the hypertensive smokers, as assessed by analysis of covariance. The mean carotid IMT was significantly greater (1.01 versus 0.90 mm, P = 0.003) in the 4 carriers than in the subjects without 4 among the hypertensive smokers. The number of plaques was also significantly higher. No differences were found in the other subjects (hypertensive non-smokers or controls). Linear regression analysis indicated that the 4 allele was an independent determinant of IMT in the hypertensive smokers but not in the other subjects. The estimated average effect of the 4 allele on the mean IMT in the hypertensive smokers was 0.088 mm (P < 0.001). In the oldest age group, the interaction of smoking and 4 was also seen in the control subjects. The findings suggest that the 4 carriers are particularly susceptible to the atherogenic effects of smoking. This interaction is particularly clear in hypertensive subjects.