A Description of the FINRISK 1992 and 1997 Cohorts

<p>Compared to FINRISK-92, the FINRISK-97 cohort includes an additional sample of individuals aged 65–74 y. Numbers for this additional sample are described at the right-hand side for each endpoint. Persons examined refers to cohort individuals for whom information on smoking, blood pressure, cholesterol, and DNA, as well as consent for the use of DNA to study CHD and stroke, were available. Subcohorts are stratified random samples of the original cohorts including also cases. Mortality cases show total mortality, including also those who died from CHD or stroke. Thus, numbers in the boxes of subcohorts and outcome events are not mutually exclusive (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020069#pgen-0020069-t001" target="_blank">Table 1</a>). F, females; M, males.</p

Association between LPA haplotypes and CHD in MORGAM.

<p>While MORGAM associations conditioned on a different allele set, haplotypic combinations are consistent with those reported in ref which are given here for comparison. Association was tested with a model adjusted for cohort and Framingham coefficients. Haplotypic ORs were used as coefficients for GRS1.</p

Addition of family history information to genetic risk scores.

<p>Reclassification results comparing a baseline model including family history (FH); to models including genetic risk scores for men aged 50–59.</p

Kaplan-Meier curves may better predict those with premature CHD.

<p>Survival curves assessing the time to incident CHD with increasing age across four GRS categories for GRS1 (A) and GRS2 (B). Survival probabilities are truncated from 0–0.4.</p

Schematic diagram of the case-cohort design in MORGAM.

<p>Outline of the selection of individuals in the MORGAM dataset. The subcohort and all CHD cases who were genotyped (N = 4818) were chosen from the full cohort. We restricted the validation analysis to 4209 men with complete genotype data for > = 11 SNPs with the remaining SNP data multiply imputed.</p

Background characteristics of the nine cohorts.

<p>Data are mean (SD) or number %. NA = not available, C = cohort. As ATBC and MONICA-KORA did not collect information on current drug therapy, these were considered as ‘no medication’ for the analysis.</p

Regional plots for the association of SNPs with MI in the region of <i>QKI</i>.

<p>Regional plots for the association of SNPs with MI in the region of <i>QKI</i>.</p

Study design for identification and validation of SNPs associated with MI and CHD.

<p>Study design for identification and validation of SNPs associated with MI and CHD.</p

Association of the known SNPs for coronary artery disease with incident MI and CHD in Stage I.

<p>Association of the known SNPs for coronary artery disease with incident MI and CHD in Stage I.</p

Association of the known SNPs for coronary artery disease with mortality after MI.

<p>Association of the known SNPs for coronary artery disease with mortality after MI.</p