Faculty of Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, London, UK.
Int J Epidemiol. 2013 Apr;42(2):475-92. doi: 10.1093/ije/dyt034.
At the APOE gene, encoding apolipoprotein E, genotypes of the ε2/ε3/ε4 alleles associated with higher LDL-cholesterol (LDL-C) levels are also associated with higher coronary risk. However, the association of APOE genotype with other cardiovascular biomarkers and risk of ischaemic stroke is less clear. We evaluated the association of APOE genotype with risk of ischaemic stroke and assessed whether the observed effect was consistent with the effects of APOE genotype on LDL-C or other lipids and biomarkers of cardiovascular risk.
We conducted a systematic review of published and unpublished studies reporting on APOE genotype and ischaemic stroke. We pooled 41 studies (with a total of 9027 cases and 61,730 controls) using a Bayesian meta-analysis to calculate the odds ratios (ORs) for ischaemic stroke with APOE genotype. To better evaluate potential mechanisms for any observed effect, we also conducted a pooled analysis of primary data using 16 studies (up to 60,883 individuals) of European ancestry. We evaluated the association of APOE genotype with lipids, other circulating biomarkers of cardiovascular risk and carotid intima-media thickness (C-IMT).
The ORs for association of APOE genotypes with ischaemic stroke were: 1.09 (95% credible intervals (CrI): 0.84-1.43) for ε2/ε2; 0.85 (95% CrI: 0.78-0.92) for ε2/ε3; 1.05 (95% CrI: 0.89-1.24) for ε2/ε4; 1.05 (95% CrI: 0.99-1.12) for ε3/ε4; and 1.12 (95% CrI: 0.94-1.33) for ε4/ε4 using the ε3/ε3 genotype as the reference group. A regression analysis that investigated the effect of LDL-C (using APOE as the instrument) on ischaemic stroke showed a positive dose-response association with an OR of 1.33 (95% CrI: 1.17, 1.52) per 1 mmol/l increase in LDL-C. In the separate pooled analysis, APOE genotype was linearly and positively associated with levels of LDL-C (P-trend: 2 × 10(-152)), apolipoprotein B (P-trend: 8.7 × 10(-06)) and C-IMT (P-trend: 0.001), and negatively and linearly associated with apolipoprotein E (P-trend: 6 × 10(-26)) and HDL-C (P-trend: 1.6 × 10(-12)). Associations with lipoprotein(a), C-reactive protein and triglycerides were non-linear.
In people of European ancestry, APOE genotype showed a positive dose-response association with LDL-C, C-IMT and ischaemic stroke. However, the association of APOE ε2/ε2 genotype with ischaemic stroke requires further investigation. This cross-domain concordance supports a causal role of LDL-C on ischaemic stroke.
在 APOE 基因中,编码载脂蛋白 E 的等位基因 ε2/ε3/ε4 与 LDL 胆固醇(LDL-C)水平升高相关,也与更高的冠状动脉风险相关。然而,APOE 基因型与其他心血管生物标志物和缺血性中风风险的关联则不太明确。我们评估了 APOE 基因型与缺血性中风风险的关联,并评估了观察到的效应是否与 APOE 基因型对 LDL-C 或其他脂质和心血管风险的生物标志物的影响一致。
我们对已发表和未发表的研究报告 APOE 基因型和缺血性中风的文献进行了系统回顾。我们使用贝叶斯荟萃分析汇总了 41 项研究(总共有 9027 例病例和 61730 例对照),以计算 APOE 基因型与缺血性中风的比值比(OR)。为了更好地评估任何观察到的效应的潜在机制,我们还使用来自欧洲血统的 16 项研究(最多 60883 人)的原始数据进行了汇总分析。我们评估了 APOE 基因型与脂质、其他心血管风险的循环生物标志物和颈动脉内膜中层厚度(C-IMT)的关联。
APOE 基因型与缺血性中风的关联的 OR 为:ε2/ε2 为 1.09(95%可信区间(CrI):0.84-1.43);ε2/ε3 为 0.85(95% CrI:0.78-0.92);ε2/ε4 为 1.05(95% CrI:0.89-1.24);ε3/ε4 为 1.05(95% CrI:0.99-1.12);ε4/ε4 为 1.12(95% CrI:0.94-1.33),以 ε3/ε3 基因型作为参考组。一项使用 LDL-C(APOE 作为工具)对缺血性中风影响的回归分析显示,LDL-C 每增加 1mmol/L,OR 为 1.33(95% CrI:1.17,1.52),呈正剂量反应关系。在单独的汇总分析中,APOE 基因型与 LDL-C(P 趋势:2×10^(-152))、载脂蛋白 B(P 趋势:8.7×10^(-06))和 C-IMT(P 趋势:0.001)呈线性正相关,与载脂蛋白 E(P 趋势:6×10^(-26))和高密度脂蛋白胆固醇(P 趋势:1.6×10^(-12))呈线性负相关。与脂蛋白(a)、C 反应蛋白和甘油三酯的关联是非线性的。
在欧洲血统的人群中,APOE 基因型与 LDL-C、C-IMT 和缺血性中风呈正剂量反应关联。然而,APOE ε2/ε2 基因型与缺血性中风的关联需要进一步研究。这种跨领域的一致性支持 LDL-C 对缺血性中风的因果作用。