{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T21:18:05Z","timestamp":1792444685189,"version":"4.5.0"},"reference-count":48,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2019,8,20]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>DNA methylation is implicated in coronary heart disease (CHD), but current evidence is based on small, cross-sectional studies. We examined blood DNA methylation in relation to incident CHD across multiple prospective cohorts.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Nine population-based cohorts from the United States and Europe profiled epigenome-wide blood leukocyte DNA methylation using the Illumina Infinium 450k microarray, and prospectively ascertained CHD events including coronary insufficiency\/unstable angina, recognized myocardial infarction, coronary revascularization, and coronary death. Cohorts conducted race-specific analyses adjusted for age, sex, smoking, education, body mass index, blood cell type proportions, and technical variables. We conducted fixed-effect meta-analyses across cohorts.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>Among 11\u2009461 individuals (mean age 64 years, 67% women, 35% African American) free of CHD at baseline, 1895 developed CHD during a mean follow-up of 11.2 years. Methylation levels at 52 CpG (cytosine-phosphate-guanine) sites were associated with incident CHD or myocardial infarction (false discovery rate&lt;0.05). These CpGs map to genes with key roles in calcium regulation (ATP2B2, CASR, GUCA1B, HPCAL1), and genes identified in genome- and epigenome-wide studies of serum calcium (CASR), serum calcium-related risk of CHD (CASR), coronary artery calcified plaque (PTPRN2), and kidney function (CDH23, HPCAL1), among others. Mendelian randomization analyses supported a causal effect of DNA methylation on incident CHD; these CpGs map to active regulatory regions proximal to long non-coding RNA transcripts.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>Methylation of blood-derived DNA is associated with risk of future CHD across diverse populations and may serve as an informative tool for gaining further insight on the development of CHD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circulationaha.118.039357","type":"journal-article","created":{"date-parts":[[2019,8,19]],"date-time":"2019-08-19T14:00:21Z","timestamp":1566223221000},"page":"645-657","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":211,"title":["Blood Leukocyte DNA Methylation Predicts Risk of Future Myocardial Infarction and Coronary Heart Disease"],"prefix":"10.1161","volume":"140","author":[{"given":"Golareh","family":"Agha","sequence":"first","affiliation":[{"name":"Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York (G.A., A.A.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael M.","family":"Mendelson","sequence":"additional","affiliation":[{"name":"Population Sciences Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD (M.M.M., D.L., R.J.)."},{"name":"Framingham Heart Study, MA (M.M.M., D.L.)."},{"name":"Department of Cardiology, Boston Children\u2019s Hospital, MA (M.M.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cavin K.","family":"Ward-Caviness","sequence":"additional","affiliation":[{"name":"National Health and Environmental Effects Research Laboratory, Environmental Public Health Division, Chapel Hill, NC (C.K.W.C.)."},{"name":"Institute of Epidemiology II, Helmholtz Institute, Ingolstaedter Landstrasse 1, Neuherberg, Germany (C.K.W.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roby","family":"Joehanes","sequence":"additional","affiliation":[{"name":"Population Sciences Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD (M.M.M., D.L., R.J.)."},{"name":"Hebrew SeniorLife, Harvard Medical School, Boston, MA (R.J.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"TianXiao","family":"Huan","sequence":"additional","affiliation":[{"name":"The Population Sciences Branch, Division of Intramural Research, National Heart, Lung and Blood Institute, Bethesda, MD (T.X.H.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rahul","family":"Gondalia","sequence":"additional","affiliation":[{"name":"Department of Epidemiology (R.G.), University of North Carolina, Chapel 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