Key result
Mutant CYP2A6 allele linked to ~20% higher severe coronary stenosis risk in male smokers.
Why the study?
CYP2A6 genetic polymorphism was suspected to explain the relationship between cigarette smoking and related diseases by altering nicotine metabolism, but its correlation with coronary atherosclerosis severity remained unconfirmed.
Does the CYP2A6 gene mutant allele correlate with increased severity of coronary atherosclerosis in male smokers with CAD?
Cross-Sectional (n=64)
No
Does the CYP2A6 gene mutant allele correlate with increased severity of coronary atherosclerosis in male smokers with CAD?
The CYP2A6 gene mutant allele is associated with a 1.2-fold increased risk of severe coronary stenosis in male smokers with CAD.
Answers are grounded in this paper and cite their sources.
Mutant CYP2A6 alleles associated with severe stenosis in male smokers; hypothesis-generating for genetic risk stratification pending larger studies.
Nicotine is a toxic alkaloid known to be responsible for the addictive feature of cigarettes. CYP2A6 genetic polymorphism among individuals was suspected to explain the relationship between cigarette smoking and related diseases. CYP2A6 works to slow nicotine metabolism and thus maintain a more prolonged nicotine concentration and increase nicotine exposure to the blood. We aimed to investigate the correlation between the CYP2A6 gene with the severity of coronary atherosclerosis. This cross-sectional study was conducted from April to July 2010 in Makassar Cardiac Centre, Dr Wahidin Sudirohusodo Hospital, Indonesia. Sixty-four male active smokers at the age of ≥45 years, diagnosed with coronary artery disease (CAD), were recruited and asked to smoke the usual number of cigarettes in the last 1 month prior to blood collection for CYP2A6 genotyping. Spearman correlation was performed to analyze the association between the allele variants and coronary stenosis degree, adjusted for CAD risk factors. Furthermore, we estimated the risk ratio to quantify the correlation. Of the 64 male smokers with CAD, the mean duration of smoking was 36.9 ± 8.6 years, and 49 (76.6%) were heavy smokers with >20 cigarettes per day. All 128 alleles were observed. Our results showed that all participants with CYP2A6 variants had a significant correlation with severe coronary artery stenosis (P = .006). Thus, this study suggests that the mutant CYP2A6 gene allele significantly increased the risk of having severe coronary stenosis 1.2 times higher compared to the wild type. This pilot study showed that CYP2A6 gene has an influential role in atherosclerotic development in male smokers. However, our findings should be confirmed with further more extensive studies.
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Mappangara et al. (2022) conducted a cross-sectional in Coronary artery disease (n=64). CYP2A6 gene variants vs. Wild type CYP2A6 was evaluated on Severe coronary artery stenosis (RR 1.2, p=.006). The mutant CYP2A6 gene allele significantly increased the risk of severe coronary stenosis by 1.2 times compared to the wild type in male smokers with coronary artery disease (P = .006).
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