{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T13:24:10Z","timestamp":1789133050285,"version":"build-2803163510"},"reference-count":41,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2019,8,13]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Total cholesterol and high-density lipoprotein cholesterol (HDL-C) measurements are central to cardiovascular disease (CVD) risk assessment, but there is continuing debate around the utility of other lipids for risk prediction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Participants from UK Biobank without baseline CVD and not taking statins, with relevant lipid measurements (n=346 686), were included in the primary analysis. An incident fatal or nonfatal CVD event occurred in 6216 participants (1656 fatal) over a median of 8.9 years. Associations of nonfasting lipid measurements (total cholesterol, HDL-C, non\u2013HDL-C, direct and calculated low-density lipoprotein cholesterol [LDL-C], and apolipoproteins [Apo] A1 and B) with CVD were compared using Cox models adjusting for classical risk factors, and predictive utility was determined by the C-index and net reclassification index. Prediction was also tested in 68 649 participants taking a statin with or without baseline CVD (3515 CVD events).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      ApoB, LDL-C, and non\u2013HDL-C were highly correlated (\n                      <jats:italic>r<\/jats:italic>\n                      &gt;0.90), while HDL-C was strongly correlated with ApoA1 (\n                      <jats:italic>r<\/jats:italic>\n                      =0.92). After adjustment for classical risk factors, 1 SD increase in ApoB, direct LDL-C, and non\u2013HDL-C had similar associations with composite fatal\/nonfatal CVD events (hazard ratio, 1.23, 1.20, 1.21, respectively). Associations for 1 SD increase in HDL-C and ApoA1 were also similar (hazard ratios, 0.81 [both]). Adding either total cholesterol and HDL-C, or ApoB and ApoA, to a CVD risk prediction model (C-index, 0.7378) yielded similar improvement in discrimination (C-index change, 0.0084; 95% CI, 0.0065, 0.0104, and 0.0089; 95% CI, 0.0069, 0.0109, respectively). Once total and HDL-C were in the model, no further substantive improvement was achieved with the addition of ApoB (C-index change, 0.0004; 95% CI, 0.0000, 0.0008) or any measure of LDL-C. Results for predictive utility were similar for a fatal CVD outcome, and in a discordance analysis. In participants taking a statin, classical risk factors (C-index, 0.7118) were improved by non\u2013HDL-C (C-index change, 0.0030; 95% CI, 0.0012, 0.0048) or ApoB (C-index change, 0.0030; 95% CI, 0.0011, 0.0048). However, adding ApoB or LDL-C to a model already containing non\u2013HDL-C did not further improve discrimination.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>Measurement of total cholesterol and HDL-C in the nonfasted state is sufficient to capture the lipid-associated risk in CVD prediction, with no meaningful improvement from addition of apolipoproteins, direct or calculated LDL-C.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circulationaha.119.041149","type":"journal-article","created":{"date-parts":[[2019,6,20]],"date-time":"2019-06-20T05:02:37Z","timestamp":1561006957000},"page":"542-552","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":177,"title":["Comparison of Conventional Lipoprotein Tests and Apolipoproteins in the Prediction of Cardiovascular Disease"],"prefix":"10.1161","volume":"140","author":[{"given":"Claire","family":"Welsh","sequence":"first","affiliation":[{"name":"Institute of Cardiovascular and Medical Sciences (C.W., C.A.C.-M., R.B., P.B.M., S.R.G., L.D.F., P.S.J., J.M.R.G., N.S., P.W.), University of Glasgow, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carlos A.","family":"Celis-Morales","sequence":"additional","affiliation":[{"name":"Institute of Cardiovascular and Medical Sciences (C.W., C.A.C.-M., R.B., P.B.M., S.R.G., L.D.F., P.S.J., J.M.R.G., N.S., P.W.), University of Glasgow, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rosemary","family":"Brown","sequence":"additional","affiliation":[{"name":"Institute of Cardiovascular and Medical Sciences (C.W., C.A.C.-M., R.B., P.B.M., S.R.G., L.D.F., P.S.J., J.M.R.G., N.S., P.W.), University of Glasgow, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel 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