Open AccessPolymorphism in the Cholesteryl Ester Transfer Protein Gene and the Risk of Early Onset Myocardial Infarction among Cigarette Smokers
Author(s) -
Goldenberg Ilan,
Moss Arthur J.,
Block Robert,
Ryan Daniel,
Corsetti James P.,
McNitt Scott,
Eberly Shirley W.,
Zareba Wojciech
Publication year - 2007
Publication title -
annals of noninvasive electrocardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.494
H-Index - 48
eISSN - 1542-474X
pISSN - 1082-720X
DOI - 10.1111/j.1542-474x.2007.00186.x
Subject(s) - taqi , medicine , cholesterylester transfer protein , myocardial infarction , genotype , allele , endocrinology , gastroenterology , polymorphism (computer science) , cholesterol , lipoprotein , genetics , gene , biology
Background: Cigarette smoking and the common B1 allele of the TaqI B polymorphism have both been reported to be associated with increased cholesteryl ester transfer protein (CETP) activity and altered lipoprotein levels. Thus, it is possible that the combined presence of these two respective environmental and genetic factors may enhance cardiovascular risk. We hypothesized that susceptibility to early onset myocardial infarction (MI) among cigarette smokers may be related to the presence of TaqI B polymorphism in the CETP gene. Methods: The age at onset of a first MI among current (n = 199), past (n = 345), and never (n = 270) smokers was related to the presence of the TaqI B1 and B2 alleles in a cohort of 814 first MI patients. Results: Multivariate regression analysis demonstrated that cigarette smoking was associated with a significant increase in the risk for early onset MI only among carriers of the TaqI B1 allele: current smokers with the B1B1 and B1B2 genotypes displayed a respective 9.4 (P < 0.001) and 8.4 (P < 0.001) year reduction in the age at onset of a first MI compared with never smokers, and past smokers with these genotypes exhibited a respective 3.8 (P = 0.003) and 3.7 (P = 0.01) year reduction. By contrast, current and past smoking was not associated with a significant increase in the risk for early onset MI among B2B2 homozygotes (3.0 [P = 0.28] and 0.2 [P = 0.93] year reduction, respectively). The smoking x genotype interaction was statistically significant (P = 0.04). Conclusions: The current findings suggest that genetic factors may modify susceptibility to early onset MI among cigarette smokers.