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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.

Holmes MV, Frikke-Schmidt R, Melis D, Luben R, Asselbergs FW, Boer JM, Cooper J, Palmen J, Horvat P, Engmann J, Li KW, Onland-Moret NC, Hofker MH, Kumari M, Keating BJ, Hubacek JA, Adamkova V, Kubinova R, Bobak M, Khaw KT, Nordestgaard BG, Wareham N, Humphries SE, Langenberg C, Tybjaerg-Hansen A, Talmud PJ - Atherosclerosis (2014)

Bottom Line: In total 13 studies (including unpublished data from eight cohorts) with 10,134 CHD events in 130,004 individuals of European descent were identified.When the association between APOE genotype and CHD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.

View Article: PubMed Central - PubMed

Affiliation: 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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Detailed association between APOE genotype and CHD overall (left) and stratified by smoking status (right).
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fig3: Detailed association between APOE genotype and CHD overall (left) and stratified by smoking status (right).

Mentions: When we investigated the association between APOE genotype status and CHD regardless of smoking status, we found strong evidence for a linear association between APOE genotype and CHD status when individuals were arranged in the following order: ε2/ε2, ε2/ε3, ε3/ε3, ε3/ε4 or ε4/ε4 with the log odds of CHD increasing by 0.046 (SE 0.019; P = 0.017) for each incremental increase in APOE genotype status (Fig. 3).


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.

Holmes MV, Frikke-Schmidt R, Melis D, Luben R, Asselbergs FW, Boer JM, Cooper J, Palmen J, Horvat P, Engmann J, Li KW, Onland-Moret NC, Hofker MH, Kumari M, Keating BJ, Hubacek JA, Adamkova V, Kubinova R, Bobak M, Khaw KT, Nordestgaard BG, Wareham N, Humphries SE, Langenberg C, Tybjaerg-Hansen A, Talmud PJ - Atherosclerosis (2014)

Detailed association between APOE genotype and CHD overall (left) and stratified by smoking status (right).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4232362&req=5

fig3: Detailed association between APOE genotype and CHD overall (left) and stratified by smoking status (right).
Mentions: When we investigated the association between APOE genotype status and CHD regardless of smoking status, we found strong evidence for a linear association between APOE genotype and CHD status when individuals were arranged in the following order: ε2/ε2, ε2/ε3, ε3/ε3, ε3/ε4 or ε4/ε4 with the log odds of CHD increasing by 0.046 (SE 0.019; P = 0.017) for each incremental increase in APOE genotype status (Fig. 3).

Bottom Line: In total 13 studies (including unpublished data from eight cohorts) with 10,134 CHD events in 130,004 individuals of European descent were identified.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.

View Article: PubMed Central - PubMed

Affiliation: 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.

Show MeSH
Related in: MedlinePlus