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A systematic review and meta-analysis of 130,000 individuals shows smoking does not modify the association of APOE genotype on risk of coronary heart disease
MV. Holmes, R. Frikke-Schmidt, D. Melis, R. Luben, FW. Asselbergs, JM. Boer, J. Cooper, J. Palmen, P. Horvat, J. Engmann, KW. Li, NC. Onland-Moret, MH. Hofker, M. Kumari, BJ. Keating, JA. Hubacek, V. Adamkova, R. Kubinova, M. Bobak, KT. Khaw, BG....
Jazyk angličtina Země Irsko
Typ dokumentu časopisecké články, metaanalýza, Research Support, N.I.H., Extramural, práce podpořená grantem, přehledy
- MeSH
- alely MeSH
- apolipoprotein E4 genetika MeSH
- dospělí MeSH
- genotyp * MeSH
- heterozygot MeSH
- interakce genů a prostředí MeSH
- kohortové studie MeSH
- koronární nemoc genetika MeSH
- kouření škodlivé účinky MeSH
- lidé středního věku MeSH
- lidé MeSH
- rizikové faktory MeSH
- senioři MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- metaanalýza MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Research Support, N.I.H., Extramural MeSH
BACKGROUND: Conflicting evidence exists on whether smoking acts as an effect modifier of the association between APOE genotype and risk of coronary heart disease (CHD). METHODS AND RESULTS: We searched PubMed and EMBASE to June 11, 2013 for published studies reporting APOE genotype, smoking status and CHD events and added unpublished data from population cohorts. We tested for presence of effect modification by smoking status in the relationship between APOE genotype and risk of CHD using likelihood ratio test. In total 13 studies (including unpublished data from eight cohorts) with 10,134 CHD events in 130,004 individuals of European descent were identified. The odds ratio (OR) for CHD risk from APOE genotype (ε4 carriers versus non-carriers) was 1.06 (95% confidence interval (CI): 1.01, 1.12) and for smoking (present vs. past/never smokers) was OR 2.05 (95%CI: 1.95, 2.14). When the association between APOE genotype and CHD was stratified by smoking status, compared to non-ε4 carriers, ε4 carriers had an OR of 1.11 (95%CI: 1.02, 1.21) in 28,789 present smokers and an OR of 1.04 (95%CI 0.98, 1.10) in 101,215 previous/never smokers, with no evidence of effect modification (P-value for heterogeneity = 0.19). Analysis of pack years in individual participant data of >60,000 with adjustment for cardiovascular traits also failed to identify evidence of effect modification. CONCLUSIONS: In the largest analysis to date, we identified no evidence for effect modification by smoking status in the association between APOE genotype and risk of CHD.
Department of Cardiology Division Heart and Lungs University Medical Center Utrecht The Netherlands
Department of Clinical Biochemistry Rigshospitalet Copenhagen University Hospital Copenhagen Denmark
Department of Epidemiology and Public Health University College London London UK
Department of Public Health and Primary Care University of Cambridge Cambridge UK
Durrer Center for Cardiogenetic Research ICIN Netherlands Heart Institute Utrecht The Netherlands
Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark
Julius Center for Health Sciences and Primary Care University Medical Center Utrecht The Netherlands
MRC Epidemiology Unit Institute of Metabolic Science University of Cambridge UK
National Institute of Public Health Srobarova 48 10042 Prague Czech Republic
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- $a 10.1016/j.atherosclerosis.2014.07.038 $2 doi
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- $a Holmes, Michael V $u Department of Surgery, Division of Transplantation, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Department of Epidemiology & Public Health, University College London, London, UK. Electronic address: mvholmes@gmail.com.
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- $a A systematic review and meta-analysis of 130,000 individuals shows smoking does not modify the association of APOE genotype on risk of coronary heart disease / $c MV. Holmes, R. Frikke-Schmidt, D. Melis, R. Luben, FW. Asselbergs, JM. Boer, J. Cooper, J. Palmen, P. Horvat, J. Engmann, KW. Li, NC. Onland-Moret, MH. Hofker, M. Kumari, BJ. Keating, JA. Hubacek, V. Adamkova, R. Kubinova, M. Bobak, KT. Khaw, BG. Nordestgaard, N. Wareham, SE. Humphries, C. Langenberg, A. Tybjaerg-Hansen, PJ. Talmud,
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- $a BACKGROUND: Conflicting evidence exists on whether smoking acts as an effect modifier of the association between APOE genotype and risk of coronary heart disease (CHD). METHODS AND RESULTS: We searched PubMed and EMBASE to June 11, 2013 for published studies reporting APOE genotype, smoking status and CHD events and added unpublished data from population cohorts. We tested for presence of effect modification by smoking status in the relationship between APOE genotype and risk of CHD using likelihood ratio test. In total 13 studies (including unpublished data from eight cohorts) with 10,134 CHD events in 130,004 individuals of European descent were identified. The odds ratio (OR) for CHD risk from APOE genotype (ε4 carriers versus non-carriers) was 1.06 (95% confidence interval (CI): 1.01, 1.12) and for smoking (present vs. past/never smokers) was OR 2.05 (95%CI: 1.95, 2.14). When the association between APOE genotype and CHD was stratified by smoking status, compared to non-ε4 carriers, ε4 carriers had an OR of 1.11 (95%CI: 1.02, 1.21) in 28,789 present smokers and an OR of 1.04 (95%CI 0.98, 1.10) in 101,215 previous/never smokers, with no evidence of effect modification (P-value for heterogeneity = 0.19). Analysis of pack years in individual participant data of >60,000 with adjustment for cardiovascular traits also failed to identify evidence of effect modification. CONCLUSIONS: In the largest analysis to date, we identified no evidence for effect modification by smoking status in the association between APOE genotype and risk of CHD.
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