The Association Between Cigarette Smoking and Carotid Intima–Media Thickness Is Influenced by the −930A/G CYBA Gene Polymorphism: The Cardiovascular Risk in Young Finns Study

Background Smoking-induced damage to the cardiovascular system has been shown in many studies; however, the degree of damage varies from individual to individual. We hypothesized that the −930A/G CYBA gene polymorphism in the NADPH oxidase influences the association between cigarette smoking and car...

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Published inAmerican journal of hypertension Vol. 22; no. 3; pp. 281 - 287
Main Authors Fan, M., Raitakari, O.T., Kähönen, M., Juonala, M., Hutri-Kähönen, N., Pörsti, I., Viikari, J., Lehtimäki, T.
Format Journal Article
LanguageEnglish
Published Basingstoke Oxford University Press 01.03.2009
Nature Publishing Group
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Online AccessGet full text
ISSN0895-7061
1941-7225
1941-7225
DOI10.1038/ajh.2008.349

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Abstract Background Smoking-induced damage to the cardiovascular system has been shown in many studies; however, the degree of damage varies from individual to individual. We hypothesized that the −930A/G CYBA gene polymorphism in the NADPH oxidase influences the association between cigarette smoking and carotid intima–media thickness (IMT) in young healthy adults. Methods Cross-sectional data obtained in 2001 for the Cardiovascular Risk in Young Finns Study were used. IMT was measured with ultrasound. The genotyping was performed using a 5′-nuclease assay. A linear regression model was used to test whether the interaction between smoking and the genotypes was associated with IMT. The magnitude of the interaction effect was further examined by performing a stratified analysis according to smoking habits. Results In the entire population, the mean and maxima IMT were higher in smokers than nonsmokers (P = 0.005 and 0.008, respectively). The differences were most significant in subjects with the GG genotype, borderline significant for the GA genotype, and nonsignificant for the AA genotype. The interaction of genotypes with smoking was associated with mean and maximal IMT (P = 0.042 and 0.022). Among smokers, subjects with the GG genotype had a higher mean and maximal IMT compared with carriers of the A allele (P = 0.021 and 0.012). In contrast, the mean and maximal IMT were lower for G allele carriers than subjects with the AA genotype among nonsmokers (P = 0.022 and 0.026). All results had been adjusted for potential risk factors related to IMT. Conclusion The −930A/G polymorphism modifies the association between cigarette smoking and IMT in young healthy adults. American Journal of Hypertension 2009; doi:10.1038/ajh.2008.349
AbstractList Background Smoking-induced damage to the cardiovascular system has been shown in many studies; however, the degree of damage varies from individual to individual. We hypothesized that the −930A/G CYBA gene polymorphism in the NADPH oxidase influences the association between cigarette smoking and carotid intima-media thickness (IMT) in young healthy adults. Methods Cross-sectional data obtained in 2001 for the Cardiovascular Risk in Young Finns Study were used. IMT was measured with ultrasound. The genotyping was performed using a 5′-nuclease assay. A linear regression model was used to test whether the interaction between smoking and the genotypes was associated with IMT. The magnitude of the interaction effect was further examined by performing a stratified analysis according to smoking habits. Results In the entire population, the mean and maxima IMT were higher in smokers than nonsmokers (P = 0.005 and 0.008, respectively). The differences were most significant in subjects with the GG genotype, borderline significant for the GA genotype, and nonsignificant for the AA genotype. The interaction of genotypes with smoking was associated with mean and maximal IMT (P = 0.042 and 0.022). Among smokers, subjects with the GG genotype had a higher mean and maximal IMT compared with carriers of the A allele (P = 0.021 and 0.012). In contrast, the mean and maximal IMT were lower for G allele carriers than subjects with the AA genotype among nonsmokers (P = 0.022 and 0.026). All results had been adjusted for potential risk factors related to IMT. Conclusion The −930A/G polymorphism modifies the association between cigarette smoking and IMT in young healthy adults. American Journal of Hypertension 2009; doi:10.1038/ajh.2008.349
Smoking-induced damage to the cardiovascular system has been shown in many studies; however, the degree of damage varies from individual to individual. We hypothesized that the -930A/G CYBA gene polymorphism in the NADPH oxidase influences the association between cigarette smoking and carotid intima-media thickness (IMT) in young healthy adults. Cross-sectional data obtained in 2001 for the Cardiovascular Risk in Young Finns Study were used. IMT was measured with ultrasound. The genotyping was performed using a 5'-nuclease assay. A linear regression model was used to test whether the interaction between smoking and the genotypes was associated with IMT. The magnitude of the interaction effect was further examined by performing a stratified analysis according to smoking habits. In the entire population, the mean and maxima IMT were higher in smokers than nonsmokers (P = 0.005 and 0.008, respectively). The differences were most significant in subjects with the GG genotype, borderline significant for the GA genotype, and nonsignificant for the AA genotype. The interaction of genotypes with smoking was associated with mean and maximal IMT (P = 0.042 and 0.022). Among smokers, subjects with the GG genotype had a higher mean and maximal IMT compared with carriers of the A allele (P = 0.021 and 0.012). In contrast, the mean and maximal IMT were lower for G allele carriers than subjects with the AA genotype among nonsmokers (P = 0.022 and 0.026). All results had been adjusted for potential risk factors related to IMT. The -930A/G polymorphism modifies the association between cigarette smoking and IMT in young healthy adults.
Background Smoking-induced damage to the cardiovascular system has been shown in many studies; however, the degree of damage varies from individual to individual. We hypothesized that the −930A/G CYBA gene polymorphism in the NADPH oxidase influences the association between cigarette smoking and carotid intima–media thickness (IMT) in young healthy adults. Methods Cross-sectional data obtained in 2001 for the Cardiovascular Risk in Young Finns Study were used. IMT was measured with ultrasound. The genotyping was performed using a 5′-nuclease assay. A linear regression model was used to test whether the interaction between smoking and the genotypes was associated with IMT. The magnitude of the interaction effect was further examined by performing a stratified analysis according to smoking habits. Results In the entire population, the mean and maxima IMT were higher in smokers than nonsmokers (P = 0.005 and 0.008, respectively). The differences were most significant in subjects with the GG genotype, borderline significant for the GA genotype, and nonsignificant for the AA genotype. The interaction of genotypes with smoking was associated with mean and maximal IMT (P = 0.042 and 0.022). Among smokers, subjects with the GG genotype had a higher mean and maximal IMT compared with carriers of the A allele (P = 0.021 and 0.012). In contrast, the mean and maximal IMT were lower for G allele carriers than subjects with the AA genotype among nonsmokers (P = 0.022 and 0.026). All results had been adjusted for potential risk factors related to IMT. Conclusion The −930A/G polymorphism modifies the association between cigarette smoking and IMT in young healthy adults. American Journal of Hypertension 2009; doi:10.1038/ajh.2008.349
Smoking-induced damage to the cardiovascular system has been shown in many studies; however, the degree of damage varies from individual to individual. We hypothesized that the -930A/G CYBA gene polymorphism in the NADPH oxidase influences the association between cigarette smoking and carotid intima-media thickness (IMT) in young healthy adults. Cross-sectional data obtained in 2001 for the Cardiovascular Risk in Young Finns Study were used. IMT was measured with ultrasound. The genotyping was performed using a 5'-nuclease assay. A linear regression model was used to test whether the interaction between smoking and the genotypes was associated with IMT. The magnitude of the interaction effect was further examined by performing a stratified analysis according to smoking habits. In the entire population, the mean and maxima IMT were higher in smokers than nonsmokers (P = 0.005 and 0.008, respectively). The differences were most significant in subjects with the GG genotype, borderline significant for the GA genotype, and nonsignificant for the AA genotype. The interaction of genotypes with smoking was associated with mean and maximal IMT (P = 0.042 and 0.022). Among smokers, subjects with the GG genotype had a higher mean and maximal IMT compared with carriers of the A allele (P = 0.021 and 0.012). In contrast, the mean and maximal IMT were lower for G allele carriers than subjects with the AA genotype among nonsmokers (P = 0.022 and 0.026). All results had been adjusted for potential risk factors related to IMT. The -930A/G polymorphism modifies the association between cigarette smoking and IMT in young healthy adults.
Smoking-induced damage to the cardiovascular system has been shown in many studies; however, the degree of damage varies from individual to individual. We hypothesized that the -930A/G CYBA gene polymorphism in the NADPH oxidase influences the association between cigarette smoking and carotid intima-media thickness (IMT) in young healthy adults.BACKGROUNDSmoking-induced damage to the cardiovascular system has been shown in many studies; however, the degree of damage varies from individual to individual. We hypothesized that the -930A/G CYBA gene polymorphism in the NADPH oxidase influences the association between cigarette smoking and carotid intima-media thickness (IMT) in young healthy adults.Cross-sectional data obtained in 2001 for the Cardiovascular Risk in Young Finns Study were used. IMT was measured with ultrasound. The genotyping was performed using a 5'-nuclease assay. A linear regression model was used to test whether the interaction between smoking and the genotypes was associated with IMT. The magnitude of the interaction effect was further examined by performing a stratified analysis according to smoking habits.METHODSCross-sectional data obtained in 2001 for the Cardiovascular Risk in Young Finns Study were used. IMT was measured with ultrasound. The genotyping was performed using a 5'-nuclease assay. A linear regression model was used to test whether the interaction between smoking and the genotypes was associated with IMT. The magnitude of the interaction effect was further examined by performing a stratified analysis according to smoking habits.In the entire population, the mean and maxima IMT were higher in smokers than nonsmokers (P = 0.005 and 0.008, respectively). The differences were most significant in subjects with the GG genotype, borderline significant for the GA genotype, and nonsignificant for the AA genotype. The interaction of genotypes with smoking was associated with mean and maximal IMT (P = 0.042 and 0.022). Among smokers, subjects with the GG genotype had a higher mean and maximal IMT compared with carriers of the A allele (P = 0.021 and 0.012). In contrast, the mean and maximal IMT were lower for G allele carriers than subjects with the AA genotype among nonsmokers (P = 0.022 and 0.026). All results had been adjusted for potential risk factors related to IMT.RESULTSIn the entire population, the mean and maxima IMT were higher in smokers than nonsmokers (P = 0.005 and 0.008, respectively). The differences were most significant in subjects with the GG genotype, borderline significant for the GA genotype, and nonsignificant for the AA genotype. The interaction of genotypes with smoking was associated with mean and maximal IMT (P = 0.042 and 0.022). Among smokers, subjects with the GG genotype had a higher mean and maximal IMT compared with carriers of the A allele (P = 0.021 and 0.012). In contrast, the mean and maximal IMT were lower for G allele carriers than subjects with the AA genotype among nonsmokers (P = 0.022 and 0.026). All results had been adjusted for potential risk factors related to IMT.The -930A/G polymorphism modifies the association between cigarette smoking and IMT in young healthy adults.CONCLUSIONThe -930A/G polymorphism modifies the association between cigarette smoking and IMT in young healthy adults.
Author Pörsti, I.
Fan, M.
Kähönen, M.
Raitakari, O.T.
Viikari, J.
Lehtimäki, T.
Juonala, M.
Hutri-Kähönen, N.
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Carotid
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Snippet Background Smoking-induced damage to the cardiovascular system has been shown in many studies; however, the degree of damage varies from individual to...
Background Smoking-induced damage to the cardiovascular system has been shown in many studies; however, the degree of damage varies from individual to...
Smoking-induced damage to the cardiovascular system has been shown in many studies; however, the degree of damage varies from individual to individual. We...
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SubjectTerms Adult
Arterial hypertension. Arterial hypotension
Atherosclerosis - genetics
Atherosclerosis - pathology
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Cardiovascular Diseases - epidemiology
Cardiovascular Diseases - genetics
Cardiovascular Diseases - pathology
Carotid Arteries - pathology
Clinical manifestations. Epidemiology. Investigative techniques. Etiology
DNA - genetics
DNA - isolation & purification
Female
Finland - epidemiology
Gene Frequency
Genotype
Humans
Male
Medical sciences
NADPH Oxidases - genetics
Polymorphism, Genetic - genetics
Risk Factors
Smoking - epidemiology
Smoking - genetics
Smoking - pathology
Young Adult
Title The Association Between Cigarette Smoking and Carotid Intima–Media Thickness Is Influenced by the −930A/G CYBA Gene Polymorphism: The Cardiovascular Risk in Young Finns Study
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