{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T16:14:49Z","timestamp":1767888889146,"version":"3.49.0"},"reference-count":49,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2014,5,22]]},"abstract":"\n Background<\/jats:title>\n \n Recent data suggest that high\u2010density lipoprotein cholesterol (\n HDL<\/jats:styled-content>\n \u2010C) levels are likely not in the causative pathway of atheroprotection, shifting focus from\n HDL<\/jats:styled-content>\n \u2010C to its subfractions and associated proteins. This study's goal was to determine which\n HDL<\/jats:styled-content>\n phenotype was the better predictor of carotid artery disease (\n CAAD<\/jats:styled-content>\n ).\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n HDL<\/jats:styled-content>\n \u20102 and\n HDL<\/jats:styled-content>\n \u20103 were measured in 1725 participants of European ancestry in a prevalent case\u2010control cohort study of\n CAAD<\/jats:styled-content>\n . Stratified analyses were conducted for men (n=1201) and women (n=524). Stepwise linear regression was used to determine whether\n HDL<\/jats:styled-content>\n \u2010C,\n HDL<\/jats:styled-content>\n \u20102,\n HDL<\/jats:styled-content>\n \u20103, or apolipoprotein A1 was the best predictor of\n CAAD<\/jats:styled-content>\n , while adjusting for the confounders of censored age, diabetes, and current smoking status. In both men and women,\n HDL<\/jats:styled-content>\n \u20103 was negatively associated with\n CAAD<\/jats:styled-content>\n (\n P<\/jats:italic>\n =0.0011 and 0.033 for men and women, respectively); once\n HDL<\/jats:styled-content>\n \u20103 was included in the model, no other\n HDL<\/jats:styled-content>\n phenotype was significantly associated with\n CAAD<\/jats:styled-content>\n . Addition of paraoxonase 1 activity to the aforementioned regression model showed a significant and independent (of\n HDL<\/jats:styled-content>\n \u20103) association with\n CAAD<\/jats:styled-content>\n in men (\n P<\/jats:italic>\n =0.001) but not in the smaller female subgroup.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n This study is the first to contrast the associations of\n HDL<\/jats:styled-content>\n \u20102 and\n HDL<\/jats:styled-content>\n \u20103 with\n CAAD<\/jats:styled-content>\n . We found that\n HDL<\/jats:styled-content>\n \u20103 levels were more predictive of\n CAAD<\/jats:styled-content>\n status than\n HDL<\/jats:styled-content>\n \u20102,\n HDL<\/jats:styled-content>\n \u2010C, or apolipoprotein A1. In addition, for men, paraoxonase 1 activity improved the overall model prediction for\n CAAD<\/jats:styled-content>\n independently and additively with\n HDL<\/jats:styled-content>\n \u20103 levels. Further investigation into the molecular mechanisms through which\n HDL<\/jats:styled-content>\n \u20103 is associated with protection from\n CAAD<\/jats:styled-content>\n is warranted.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.114.000902","type":"journal-article","created":{"date-parts":[[2014,6,26]],"date-time":"2014-06-26T05:50:30Z","timestamp":1403761830000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":37,"title":["HDL\u20103 is a Superior Predictor of Carotid Artery Disease in a Case\u2010Control Cohort of 1725 Participants"],"prefix":"10.1161","volume":"3","author":[{"given":"Daniel Seung","family":"Kim","sequence":"first","affiliation":[{"name":"Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA"},{"name":"Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Amber A.","family":"Burt","sequence":"additional","affiliation":[{"name":"Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elisabeth A.","family":"Rosenthal","sequence":"additional","affiliation":[{"name":"Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jane E.","family":"Ranchalis","sequence":"additional","affiliation":[{"name":"Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jason F.","family":"Eintracht","sequence":"additional","affiliation":[{"name":"Department of General Medicine, Virginia Mason Medical Center, Seattle, WA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas S.","family":"Hatsukami","sequence":"additional","affiliation":[{"name":"Division of Vascular Surgery, Department of Surgery, University of Washington School of Medicine, Seattle, WA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Clement E.","family":"Furlong","sequence":"additional","affiliation":[{"name":"Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA"},{"name":"Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Santica","family":"Marcovina","sequence":"additional","affiliation":[{"name":"Northwest Lipid Metabolism and Diabetes Research Laboratories, Seattle, WA"},{"name":"Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John J.","family":"Albers","sequence":"additional","affiliation":[{"name":"Northwest Lipid Metabolism and Diabetes Research Laboratories, Seattle, WA"},{"name":"Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gail P.","family":"Jarvik","sequence":"additional","affiliation":[{"name":"Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA"},{"name":"Department of Genome Sciences, University of Washington School of Medicine, Seattle, 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