Dataset Information

Determination of genetic correlation between tobacco smoking and coronary artery disease.

ABSTRACT:

Backgrounds

Tobacco smoking is an important risk factor for coronary artery disease (CAD), but the genetic mechanisms linking smoking to CAD remain largely unknown.

Methods

We analyzed summary data from the genome-wide association study (GWAS) of the UK Biobank for CAD, plasma lipid concentrations (n = 184,305), and smoking (n = 337,030) using different biostatistical methods, which included LD score regression and Mendelian randomization (MR).

Results

We identified SNPs shared by CAD and at least one smoking behavior, the genes where these SNPs are located were found to be significantly enriched in the processes related to lipoprotein metabolic, chylomicron-mediated lipid transport, lipid digestion, mobilization, and transport. The MR analysis revealed a positive correlation between smoking cessation and decreased risk for CAD when smoking cessation was considered as exposure (p = 0.001), and a negative correlation between the increased risk for CAD and smoking cessation when CAD was considered as exposure (p = 2.95E-08). This analysis further indicated that genetic liability for smoking cessation increased the risk of CAD.

Conclusion

These findings inform the concomitant conditions of CAD and smoking and support the idea that genetic liabilities for smoking behaviors are strongly associated with the risk of CAD.

SUBMITTER: Zhu Z

PROVIDER: S-EPMC10562694 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature

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Publications

Determination of genetic correlation between tobacco smoking and coronary artery disease.

Zhu Zhouhai Z Liu Qiang Q Li Meng M Yao Yinghao Y Qi Feiyan F Xu Yi Y Lu Sheming S Yang Zhongli Z Guan Ying Y Li Ming D MD Yao Jianhua J

Frontiers in psychiatry 20230926

<h4>Backgrounds</h4>Tobacco smoking is an important risk factor for coronary artery disease (CAD), but the genetic mechanisms linking smoking to CAD remain largely unknown.<h4>Methods</h4>We analyzed summary data from the genome-wide association study (GWAS) of the UK Biobank for CAD, plasma lipid concentrations (<i>n</i> = 184,305), and smoking (<i>n</i> = 337,030) using different biostatistical methods, which included LD score regression and Mendelian randomization (MR).<h4>Results</h4>We iden ...[more]

PMID: 37822793

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Project description:BackgroundElevated lipoprotein(a) (Lp[a]) is a risk factor for first atherosclerotic thrombosis events, but the role of elevated Lp(a) in secondary prevention is controversial. This study aimed to retrospectively investigate the influence of elevated Lp(a) levels on the prognosis of patients with coronary artery disease.MethodsThe team collected and compared clinical information of patients hospitalized during percutaneous coronary intervention (PCI). This study used a multivariate logistic regression model to evaluate the relationships between Lp(a) levels, cardiovascular risk factors, and the prognosis of coronary artery disease in patients undergoing PCI.ResultsThere were no statistically significant differences between patients grouped according to Lp(a) level in terms of sex; age; body mass index and obesity; hyperuricemia; smoking; cardiac insufficiency; acute myocardial infarction; multivessel lesion; in-stent restenosis; secondary PCI; apolipoprotein AI level; incidence of high total cholesterol or high low-density lipoprotein cholesterol; or family history of hypertension, diabetes, or coronary artery disease. The average Lp(a) concentration did not statistically significantly decrease after 1 year of statin treatment after PCI. One year after patients began statins, there were no significant differences between Lp(a) groups in the incidence of high triglycerides (P = .13), high total cholesterol (P = .52), or high low-density lipoprotein cholesterol (P = .051). Multivariate logistic regression analysis indicated that diabetes (P = .02) was associated with in-stent restenosis, whereas diabetes (P = .02) and multivessel lesions (P < .001) were associated with secondary PCI in patients who underwent coronary angiography 1 year after PCI. Compared with normal Lp(a) levels, high Lp(a) levels did not significantly increase the incidence of in-stent restenosis or secondary PCI in patients who underwent coronary angiography 1 year after PCI.ConclusionSustained high concentrations of Lp(a) did not significantly increase the incidence of in-stent restenosis or secondary PCI in patients who underwent coronary angiography 1 year after PCI.

Dataset Information

Determination of genetic correlation between tobacco smoking and coronary artery disease.

Backgrounds

Methods

Results

Conclusion

Publications

Determination of genetic correlation between tobacco smoking and coronary artery disease.

Similar Datasets

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