{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T21:21:56Z","timestamp":1790803316949,"version":"4.1.0"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2016,11]]},"abstract":"<jats:sec>\n            <jats:title>Objectives\u2014<\/jats:title>\n            <jats:p>Non\u2013high-density lipoprotein cholesterol (non-HDLC) levels reflect the full burden of cholesterol transported in atherogenic lipoproteins. Genetic studies suggest a causal association between elevated triglycerides (TGs)-rich lipoproteins and atherosclerosis. We evaluated associations between achieved non-HDLC and TG levels on changes in coronary atheroma volume.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>\n              Data were analyzed from 9 clinical trials involving 4957 patients with coronary disease undergoing serial intravascular ultrasonography to assess changes in percent atheroma volume (\u0394PAV) and were evaluated against on-treatment non-HDLC and TG levels. The effects of lower (&lt;100 mg\/dL) versus higher (\u2265100 mg\/dL) achieved non-HDLC levels and lower (&lt;200 mg\/dL) versus higher (\u2265200 mg\/dL) achieved TG levels were evaluated in populations with variable on-treatment low-density lipoprotein cholesterol (LDLC) &lt;\/\u226570 mg\/dL and C-reactive protein &lt;\/\u22652 mg\/L and in patients with or without diabetes mellitus. On-treatment non-HDLC levels linearly associated with \u0394PAV. Overt PAV progression (\u0394PAV&gt;0) was associated with achieved TG levels &gt;200 mg\/dL, respectively. Lower on-treatment non-HDLC and TG levels associated with significant PAV regression compared with higher non-HDLC and TG levels across all levels of LDLC and C-reactive protein and irrespective of diabetic status (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001 across all comparisons). \u0394PAV were more strongly influenced by changes in non-HDLC (\u03b2=0.62;\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001) compared with changes in LDLC (\u03b2=0.51;\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001). Kaplan\u2013Meier sensitivity analyses demonstrated significantly greater major adverse cardiovascular event rates in those with higher versus lower non-HDLC and TG levels, with an earlier separation of the non-HDLC compared with the LDLC curve.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>Achieved non-HDLC levels seem more closely associated with coronary atheroma progression than LDLC. Plaque progression associates with achieved TGs, but only above levels of 200 mg\/dL. These observations support a more prominent role for non-HDLC (and possibly TG) lowering in combating residual cardiovascular risk.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.116.307601","type":"journal-article","created":{"date-parts":[[2016,8,12]],"date-time":"2016-08-12T03:28:56Z","timestamp":1470972536000},"page":"2220-2228","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":134,"title":["Non-HDL Cholesterol and Triglycerides"],"prefix":"10.1161","volume":"36","author":[{"given":"Rishi","family":"Puri","sequence":"first","affiliation":[{"name":"From the Cleveland Clinic Coordinating Center for Clinical Research (C5R) (R.P., S.E.N., M.S.), and Department of Cardiovascular Medicine (R.P., S.E.N., M.B.E., S.R.K., E.M.T.), Cleveland Clinic, OH; Department of Medicine, University of Adelaide, Australia (R.P., S.J.N.); and South Australian Health and Medical Research Institute, Adelaide, Australia (Y.K., S.J.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven E.","family":"Nissen","sequence":"additional","affiliation":[{"name":"From the Cleveland Clinic Coordinating Center for Clinical Research (C5R) (R.P., S.E.N., M.S.), and Department of Cardiovascular Medicine (R.P., S.E.N., M.B.E., S.R.K., E.M.T.), Cleveland Clinic, OH; Department of Medicine, University of Adelaide, Australia (R.P., S.J.N.); and South Australian Health and Medical Research Institute, Adelaide, Australia (Y.K., S.J.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mingyuan","family":"Shao","sequence":"additional","affiliation":[{"name":"From the Cleveland Clinic Coordinating Center for Clinical Research (C5R) (R.P., S.E.N., M.S.), and Department of Cardiovascular Medicine (R.P., S.E.N., M.B.E., S.R.K., E.M.T.), Cleveland Clinic, OH; Department of Medicine, University of Adelaide, Australia (R.P., S.J.N.); and South Australian Health and Medical Research Institute, Adelaide, Australia (Y.K., S.J.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamed B.","family":"Elshazly","sequence":"additional","affiliation":[{"name":"From the Cleveland Clinic Coordinating Center for Clinical Research (C5R) (R.P., S.E.N., M.S.), and Department of Cardiovascular Medicine (R.P., S.E.N., M.B.E., S.R.K., E.M.T.), Cleveland Clinic, OH; Department of Medicine, University of Adelaide, Australia (R.P., S.J.N.); and South Australian Health and Medical Research Institute, Adelaide, Australia (Y.K., S.J.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Kataoka","sequence":"additional","affiliation":[{"name":"From the Cleveland Clinic Coordinating Center for Clinical Research (C5R) (R.P., S.E.N., M.S.), and Department of Cardiovascular Medicine (R.P., S.E.N., M.B.E., S.R.K., E.M.T.), Cleveland Clinic, OH; Department of Medicine, University of Adelaide, Australia (R.P., S.J.N.); and South Australian Health and Medical Research Institute, Adelaide, Australia (Y.K., S.J.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samir R.","family":"Kapadia","sequence":"additional","affiliation":[{"name":"From the Cleveland Clinic Coordinating Center for Clinical Research (C5R) (R.P., S.E.N., M.S.), and Department of Cardiovascular Medicine (R.P., S.E.N., M.B.E., S.R.K., E.M.T.), Cleveland Clinic, OH; Department of Medicine, University of Adelaide, Australia (R.P., S.J.N.); and South Australian Health and Medical Research Institute, Adelaide, Australia (Y.K., S.J.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E. Murat","family":"Tuzcu","sequence":"additional","affiliation":[{"name":"From the Cleveland Clinic Coordinating Center for Clinical Research (C5R) (R.P., S.E.N., M.S.), and Department of Cardiovascular Medicine (R.P., S.E.N., M.B.E., S.R.K., E.M.T.), Cleveland Clinic, OH; Department of Medicine, University of Adelaide, Australia (R.P., S.J.N.); and South Australian Health and Medical Research Institute, Adelaide, Australia (Y.K., S.J.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen J.","family":"Nicholls","sequence":"additional","affiliation":[{"name":"From the Cleveland Clinic Coordinating Center for Clinical Research (C5R) (R.P., S.E.N., M.S.), and Department of Cardiovascular Medicine (R.P., S.E.N., M.B.E., S.R.K., E.M.T.), Cleveland Clinic, OH; Department of Medicine, University of Adelaide, Australia (R.P., S.J.N.); and South Australian Health and Medical Research Institute, Adelaide, Australia (Y.K., 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