Genetics
Smoking advances first heart attack by up to 9 years in CETP TaqIB B1 carriers, but not in B2B2 homozygotes (Ann Noninvasive Electrocardiol 2007)
Original title: Polymorphism in the cholesteryl ester transfer protein gene and the risk of early onset myocardial infarction among cigarette smokers
Since both cigarette smoking and the common CETP TaqIB B1 allele have been separately linked to increased CETP activity and altered lipoproteins, this study tested whether TaqIB genotype modifies smoking-related susceptibility to early-onset myocardial infarction (MI), relating age at first MI among current (n=199), past (n=345), and never smokers (n=270) to TaqIB genotype in a cohort of 814 first-MI patients. Cigarette smoking significantly increased risk for early-onset MI only among B1 allele carriers: current smokers with B1B1 and B1B2 genotypes had their first MI 9.4 and 8.4 years earlier respectively than never-smokers (both P less than 0.001), and past smokers with these genotypes had it 3.8 and 3.7 years earlier (P=0.003 and P=0.01). In contrast, current and past smoking showed no significant association with earlier MI onset among B2B2 homozygotes. The smoking-by-genotype interaction was statistically significant (P=0.04).
Original abstract
Background: Cigarette smoking and the common B1 allele of the TaqIB 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 TaqIB 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 TaqIB1 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 TaqIB1 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.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.