Additional file 2 of DNA methylation biomarkers of myocardial infarction and cardiovascular disease

Additional file 2: Table S1. Discovery stage of the EWAS on acute myocardial infarction (REGICOR-1 sample). Model 1 was adjusted for estimated cell counts and two surrogate variables. Model 2 was further adjusted for smoking status. Model 3 was additionally adjusted for diabetes, hypercholesterolemia and hypertension. Coefficients, standard errors and p-values are given for each model before and after the correction of the inflation using the bacon R package. Suggestive significant associations (p-value<10-5) are in bold. The total number of suggestive significant associations in each model is given. Table S2. Meta-analyses of the results from the discovery (REGICOR-1) and the validation stage (REGICOR-2). Model 1 was adjusted for estimated cell counts and two surrogate variables. Model 2 was further adjusted for smoking status. Model 3 was additionally adjusted for diabetes, hypercholesterolemia and hypertension. Coefficients, standard errors and p-values of REGICOR-1 are those corrected with the bacon R package. Significant associations (p-value<6.17 × 10-8) are highlighted in bold. The total number of significant associations in each model is given. Table S3. Meta-analysis of the results from the follow-up association studies performed in the samples with incident cases of cardiovascular (CVD) and coronary heart disease (CHD). Model 1 was adjusted for age, estimated cell counts and two surrogate variables (plus ethnicity in WHI and sex in FOS). Model 2 was further adjusted for smoking status. Model 3 was additionally adjusted for diabetes, hypercholesterolaemia and hypertension. Significant associations (4.17 × 10-3) found in the fixed-effects meta-analysis are highlighted in bold. The total number of significant associations in each model is given. Table S4. Utility of the methylation risk scores (MRS): association with cardiovascular (CVD) or coronary (CHD) incidence and assessment of their predictive capacity. MRSs were based on the results from model 1 of incident CHD and CVD. Analyses of the association with the CVD or CHD incidence were adjusted for age, sex, total cholesterol and HDL-C levels, diabetes, smoking status, systolic blood pressure, and hypertensive treatment, which are the cardiovascular risk factors considered in the Framingham risk function. Analysis of the improvement in the predictive capacity of the Framingham function was performed with and without the corresponding MRS. Table S5. Results of the Wald ratio method applied to determine the causality between the identified CpGs and coronary heart disease or myocardial infarction.