{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T06:19:41Z","timestamp":1792131581726,"version":"4.4.0"},"reference-count":37,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2013,9,10]]},"abstract":"<jats:sec>\n            <jats:title>Background\u2014<\/jats:title>\n            <jats:p>Chemically measured high-density lipoprotein cholesterol (HDL-C) may not be the best clinical measure of HDL. Little is known about alternative HDL measures such as HDL size or particle number (HDL-P) as determinants of residual risk after potent statin therapy.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods and Results\u2014<\/jats:title>\n            <jats:p>\n              In Justification for the Use of statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER), HDL size and HDL-P were measured by nuclear magnetic resonance spectroscopy, and HDL-C and apolipoprotein A-I (apoA-I) were chemically assayed in 10 886 participants without cardiovascular disease (CVD) before and after random allocation to rosuvastatin 20 mg\/d or placebo. Levels were examined with first CVD (n=234). HDL-P correlated better with apoA-I (Spearman\n              <jats:italic>r<\/jats:italic>\n              =0.69,\n              <jats:italic>P<\/jats:italic>\n              &lt;0.0001) than with HDL-C (\n              <jats:italic>r<\/jats:italic>\n              =0.55,\n              <jats:italic>P<\/jats:italic>\n              &lt;0.0001). Rosuvastatin lowered low-density lipoprotein cholesterol (49%) and raised HDL-C (6.1%), apoA-I (2.1%), HDL-P (3.8%), and HDL size (1.2%); all\n              <jats:italic>P<\/jats:italic>\n              &lt;0.0001. Among placebo-allocated individuals, on-treatment HDL-C, apoA-I, and HDL-P had similar inverse associations with CVD (risk factor\u2013adjusted hazard ratio and 95% confidence interval per 1 standard deviation: 0.79 [0.63\u20130.98], 0.75 [0.62\u20130.92], and 0.81 [0.67\u20130.97], respectively). Among rosuvastatin-allocated individuals, on-treatment HDL-P had a statistically significant and somewhat stronger association with CVD (0.73, 0.57\u20130.93,\n              <jats:italic>P<\/jats:italic>\n              =0.01) than HDL-C (0.82, 0.63\u20131.08,\n              <jats:italic>P<\/jats:italic>\n              =0.16) or apoA-I (0.86, 0.67\u20131.10,\n              <jats:italic>P<\/jats:italic>\n              =0.22). Among rosuvastatin-allocated individuals, on-treatment HDL-P remained significant (0.72, 0.53\u20130.97,\n              <jats:italic>P<\/jats:italic>\n              =0.03) after additionally adjusting for HDL-C. In risk factor\u2013adjusted models, HDL size showed no significant association with CVD.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>In the setting of potent statin therapy, HDL particle number may be a better marker of residual risk than chemically measured HDL-C or apoA-I. This has potential implications for evaluating novel therapies targeting HDL.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Clinical Trial Registration\u2014<\/jats:title>\n            <jats:p>\n              URL:\n              <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"http:\/\/www.clinicaltrials.gov\">http:\/\/www.clinicaltrials.gov<\/jats:ext-link>\n              . Unique identifier: NCT00239681.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circulationaha.113.002671","type":"journal-article","created":{"date-parts":[[2013,9,4]],"date-time":"2013-09-04T03:53:13Z","timestamp":1378266793000},"page":"1189-1197","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":210,"title":["High-Density Lipoprotein Cholesterol, Size, Particle Number, and Residual Vascular Risk After Potent Statin Therapy"],"prefix":"10.1161","volume":"128","author":[{"given":"Samia","family":"Mora","sequence":"first","affiliation":[{"name":"From the Center for Cardiovascular Disease Prevention, Division of Preventive Medicine (S.M., R.J.G., P.MR.) and Division of Cardiovascular Medicine (S.M., P.MR.), Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, MA; and Department of Biostatistics, Harvard School of Public Health, Boston, MA (R.J.G.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert J.","family":"Glynn","sequence":"additional","affiliation":[{"name":"From the Center for Cardiovascular Disease Prevention, Division of Preventive Medicine (S.M., R.J.G., P.MR.) and Division of Cardiovascular Medicine (S.M., P.MR.), Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, MA; and Department of Biostatistics, Harvard School of Public Health, Boston, MA (R.J.G.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul M","family":"Ridker","sequence":"additional","affiliation":[{"name":"From the Center for Cardiovascular Disease Prevention, Division of Preventive Medicine (S.M., R.J.G., P.MR.) and Division of Cardiovascular Medicine (S.M., P.MR.), Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, MA; and Department of Biostatistics, Harvard School of Public Health, Boston, MA 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