Data on plasma levels of apolipoprotein E, correlations with lipids and lipoproteins stratified by APOE genotype, and risk of ischemic heart disease

Data on correlations of plasma apoE with levels of lipids and lipoproteins stratified by APOE genotypes as well as data exploring the association between plasma levels of apoE and risk of ischemic heart disease (IHD) are wanted. The present data on 91,695 individuals from the general population provides correlations between plasma levels of apoE and lipids and lipoproteins for the three APOE genotypes ε33, ε44 and ε22, representing each of the three apoE isoforms. Further, data on extreme groups of plasma apoE (highest 5%) versus lower levels of apoE at enrollment explores risk of IHD and myocardial infarction (MI) and is given as hazard ratios. In addition, IHD and MI as a function of apoE/high-density lipoprotein (HDL) cholesterol ratio, as well as data on lipids, lipoproteins and apolipoproteins are given as hazard ratios. Data is stratified by gender and presented for the Copenhagen General Population Study and the Copenhagen City Heart Study combined.

apolipoproteins are given as hazard ratios. Data is stratified by gender and presented for the Copenhagen General Population Study and the Copenhagen City Heart Study combined.
& 2016 Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

Subject area
Clinical Research -Epidemiology, Biomarkers, Nutrition More specific subject area Epidemiology, genetics, biomarkers, ischemic heart disease, myocardial infarction, apolipoprotein E, APOE, triglycerides, HDL. Type of data

Data accessibility
Data is within this article.

Value of the data
Data on correlations between plasma levels of apolipoprotein E (apoE) and lipids and lipoproteins for the three APOE genotypes, ε33, ε44 and ε22, provides value as isoform specific references.
These robust human isoform specific data may stimulate experimental research on structurefunction relationships.
The data suggests that triglyceride-mediated pathways may explain the associations between plasma levels of apoE and ischemic heart disease (IHD), and may stimulate the scientific society to explore triglyceride metabolism further.

Data
The present data in 91,695 individuals from the general population provides correlations between plasma levels of apoE and lipids and lipoproteins for the three APOE genotypes ε33, ε44 and ε22, representing each of the three apoE isoforms. Further, data in the form of hazard ratios for extreme groups of plasma apoE (highest 5%), tertiles of apoE, tertiles of apoE/HDL cholesterol ratio as well as tertiles of lipids, lipoproteins and apolipoproteins for risk of IHD and myocardial infarction (MI) is given. Additionally, data on characteristics of participants by apoE tertile is presented. Data is given as analyzed data (Figs. 1-8 and Table 1).

Experimental design, materials and methods
We used data from two similar studies of the Danish general population, the Copenhagen General Population Study (CGPS) and the Copenhagen City Heart Study (CCHS), with altogether 91,695    Hazard ratios were multifactorially adjusted for age, body mass index, hypertension, diabetes mellitus, smoking, alcohol consumption, physical inactivity, menopausal status and hormonal replacement therapy (only women), lipid-lowering therapy, education, and HDL cholesterol, and were stratified by sex. Tertiles of HDL cholesterol were used for adjustment for HDL cholesterol. We tested highest and middle versus lowest tertile of apoE. CI ¼ confidence interval. HDL ¼high-density lipoprotein. Fig. 4. Risk of ischemic heart disease (two left panels) and myocardial infarction (two right panels) as a function of plasma levels of apolipoprotein E in extreme groups in men (upper panels) and women (lower panels). Hazard ratios were multifactorially adjusted for age, body mass index, hypertension, diabetes mellitus, smoking, alcohol consumption, physical inactivity, menopausal status and hormonal replacement therapy (only women), lipid-lowering therapy, and education, and were stratified by sex. apoE ¼apolipoprotein. CI ¼ confidence interval. participants, of whom 4642 developed IHD [1][2][3]. Data was obtained from a questionnaire, a physical examination, and from blood samples including DNA extraction [1][2][3]. The CGPS is a prospective study of the Danish general population initiated in 2003 with ongoing enrollment, whereas the CCHS is a prospective study of the Danish general population initiated in 1976-78 with follow-up examinations in 1981-83, 1991-94, and 2001-03. Studies were approved by institutional review boards and Danish ethical committees, and were conducted according to the Declaration of Helsinki. Written informed consent was obtained from participants. All participants were white and of Danish descent. There was no overlap of individuals between the CGPS and the CCHS.  6. Risk of ischemic heart disease (two left panels) and myocardial infarction (two right panels) as a function of apoE/HDL cholesterol in tertiles, in men (upper panel) and women (lower panel). Hazard ratios were multifactorially adjusted for age, body mass index, hypertension, diabetes mellitus, smoking, alcohol consumption, physical inactivity, menopausal status and hormonal replacement therapy (only women), lipid-lowering therapy, and education, and were stratified by sex. Further adjustment included triglycerides in tertiles. apoE/HDLcholesterol ¼ ratio of apolipoprotein E relative to high-density lipoprotein cholesterol. We tested highest and middle versus lowest tertile. CI ¼ confidence interval. Fig. 7. Risk of ischemic heart disease (two left panels) and myocardial infarction (two right panels) as a function of apoE/HDL cholesterol in tertiles, in men (upper panel) and women (lower panel) in APOE genotype adjusted and ε33 stratified analyses. Hazard ratios were multifactorially adjusted for age, body mass index, hypertension, diabetes mellitus, smoking, alcohol consumption, physical inactivity, menopausal status and hormonal replacement therapy (only women), lipid-lowering therapy, and education, and were stratified by sex. Analyses were further adjusted for APOE genotype or analyzed in individuals with ε33 APOE genotype only. We tested highest and middle versus lowest tertile. apoE/HDL cholesterol ¼ ratio of apolipoprotein E relative to high-density lipoprotein cholesterol. CI ¼confidence interval. ε33¼APOE ε33 genotype. Biochemical and genetic analyses were similar to analyses provided by Rasmussen et al. [4,5].
For the statistical analyses we used Stata/S.E. version 12.0 (Stata Corp., College Station, Texas, USA). P-values o 0.0001 are given as powers of 10. Student's t-test and Pearson's χ 2 -test were used in comparisons of continuous and categorical variables, respectively. Spearman's rank correlation was used for the correlation of continuous values of lipids, lipoproteins, and apolipoproteins with continuous values of apoE, stratified by the homozygote APOE genotypes, ε33, ε44 and ε22, representing each of the three apoE isoforms. Missing data on categorical and continuous covariates (o 1.0%) were imputed from age, sex and population using multiple imputation with ten imputations. Multinomial logistic regression was applied for categorical variables and linear regression for continuous variables, and was performed using the "mi impute mlogit" and "mi impute chained (regress)" commands in Stata.
Cox proportional hazards regression models estimated hazard ratios for MI and IHD as a function of extreme groups and tertiles of plasma levels of apoE, tertiles of apoE/HDL cholesterol ratios, and tertiles of lipids, lipoproteins, and apolipoproteins. In the Cox models we adjusted for age (automatic adjustment as age is the time scale) and known risk factors as detailed in legend to Table 1. Further adjustment included adjustment for triglycerides in tertiles, HDL cholesterol in tertiles or APOE genotype. Further ε33 stratified analyses for apoE/HDL cholesterol ratios in tertiles were performed. As gender and apoE levels interacted in predicting IHD (p ¼0.04), the analyses were performed separately for each gender, and data is presented stratified by gender. Data is presented for the CGPS and the CCHS combined.