{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T02:28:46Z","timestamp":1768789726818,"version":"3.49.0"},"reference-count":30,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2017,8,2]]},"abstract":"\n Background<\/jats:title>\n \n The contribution of apolipoprotein A\u2010I (apoA\u2010I) to coronary heart disease (\n CHD<\/jats:styled-content>\n ) risk stratification over and above high\u2010density lipoprotein cholesterol (\n HDL<\/jats:styled-content>\n \u2010C) is unclear. We studied the associations between plasma levels of\n HDL<\/jats:styled-content>\n \u2010C and apoA\u2010I, either alone or combined, with risk of\n CHD<\/jats:styled-content>\n events and cardiovascular risk factors among apparently healthy men and women.\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n HDL<\/jats:styled-content>\n \u2010C and apoA\u2010I levels were measured among 17\u00a0661 participants of the\n EPIC<\/jats:styled-content>\n (European Prospective Investigation into Cancer)\u2010Norfolk prospective population study. Hazard ratios for\n CHD<\/jats:styled-content>\n events and distributions of risk factors were calculated by quartiles of\n HDL<\/jats:styled-content>\n \u2010C and apoA\u2010I. Results were validated using data from the\n ARIC<\/jats:styled-content>\n (Atherosclerosis Risk in Communities) and\n WHS<\/jats:styled-content>\n (Women's Health Study) cohorts, comprising 15\u00a0494 and 27\u00a0552 individuals, respectively. In\n EPIC<\/jats:styled-content>\n \u2010Norfolk, both\n HDL<\/jats:styled-content>\n \u2010C and apoA\u2010I quartiles were strongly and inversely associated with\n CHD<\/jats:styled-content>\n risk. Within\n HDL<\/jats:styled-content>\n \u2010C quartiles, higher apoA\u2010I levels were not associated with lower\n CHD<\/jats:styled-content>\n risk; in fact,\n CHD<\/jats:styled-content>\n risk was higher within some\n HDL<\/jats:styled-content>\n \u2010C quartiles. ApoA\u2010I levels were associated with higher levels of\n CHD<\/jats:styled-content>\n risk factors: higher body mass index, HbA1c, non\u2010\n HDL<\/jats:styled-content>\n \u2010C, triglycerides, apolipoprotein B, systolic blood pressure, and C\u2010reactive protein, within fixed\n HDL<\/jats:styled-content>\n \u2010C quartiles. In contrast,\n HDL<\/jats:styled-content>\n \u2010C levels were consistently inversely associated with overall\n CHD<\/jats:styled-content>\n risk and\n CHD<\/jats:styled-content>\n risk factors within apoA\u2010I quartiles (\n P<\/jats:italic>\n <0.001). These findings were validated in the\n ARIC<\/jats:styled-content>\n and\n WHS<\/jats:styled-content>\n cohorts.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Our findings demonstrate that apoA\u2010I levels do not offer predictive information over and above\n HDL<\/jats:styled-content>\n \u2010C. In fact, within some\n HDL<\/jats:styled-content>\n \u2010C quartiles, higher apoA\u2010I levels were associated with higher risk of\n CHD<\/jats:styled-content>\n events, possibly because of the unexpected higher prevalence of cardiovascular risk factors in association with higher apoA\u2010I levels.\n <\/jats:p>\n <\/jats:sec>\n \n Clinical Trial Registration<\/jats:title>\n \n URL<\/jats:styled-content>\n :\n https:\/\/www.clinicaltrials.gov<\/jats:ext-link>\n . Unique identifier:\n NCT<\/jats:styled-content>\n 00000479.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.117.006636","type":"journal-article","created":{"date-parts":[[2017,8,4]],"date-time":"2017-08-04T00:10:09Z","timestamp":1501805409000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":13,"title":["Association of High\u2010Density Lipoprotein\u2010Cholesterol Versus Apolipoprotein A\u2010I With Risk of Coronary Heart Disease: The European Prospective Investigation Into Cancer\u2010Norfolk Prospective Population Study, the Atherosclerosis Risk in Communities Study, and the Women's Health Study"],"prefix":"10.1161","volume":"6","author":[{"given":"Julian C.","family":"van Capelleveen","sequence":"first","affiliation":[{"name":"Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrea E.","family":"Bochem","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Academic Medical Center, Amsterdam, The Netherlands"},{"name":"Department of Medicine, Columbia University, New York, NY"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S. Matthijs","family":"Boekholdt","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Academic Medical Center, Amsterdam, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Samia","family":"Mora","sequence":"additional","affiliation":[{"name":"Brigham and Women's Hospital, Harvard Medical School, Boston, MA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ron C.","family":"Hoogeveen","sequence":"additional","affiliation":[{"name":"Department of Medicine, Baylor College of Medicine, Houston, TX"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christie M.","family":"Ballantyne","sequence":"additional","affiliation":[{"name":"Department of Medicine, Baylor College of Medicine, Houston, TX"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul M","family":"Ridker","sequence":"additional","affiliation":[{"name":"Brigham and Women's Hospital, Harvard Medical School, Boston, MA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wensheng","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Medicine, Baylor College of Medicine, Houston, TX"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Philip J.","family":"Barter","sequence":"additional","affiliation":[{"name":"School of Medical Sciences, University of New South Wales, Sydney, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alan R.","family":"Tall","sequence":"additional","affiliation":[{"name":"Department of Medicine, Columbia University, New York, NY"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aeilko H.","family":"Zwinderman","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Academic Medical Center, Amsterdam, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John J. 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