{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T02:44:02Z","timestamp":1790304242764,"version":"4.1.0"},"reference-count":23,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2013,9,26]]},"abstract":"\n Background<\/jats:title>\n \n Lipoprotein\u2010associated phospholipase A2 (Lp\u2010\n PLA<\/jats:styled-content>\n 2<\/jats:sub>\n ) levels are associated with coronary heart disease (\n CHD<\/jats:styled-content>\n ) in healthy individuals and in patients who have had ischemic events.\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n The Long\u2010term Intervention with Pravastatin in Ischemic Disease (\n LIPID<\/jats:styled-content>\n ) study randomized 9014 patients with cholesterol levels of 4.0 to 7.0\u00a0mmol\/L to placebo or pravastatin 3 to 36\u00a0months after myocardial infarction or unstable angina and showed a reduction in\n CHD<\/jats:styled-content>\n and total mortality. We assessed the value of baseline and change in Lp\u2010\n PLA<\/jats:styled-content>\n 2<\/jats:sub>\n activity to predict outcomes over a 6\u2010year follow\u2010up, the effect of pravastatin on Lp\u2010\n PLA<\/jats:styled-content>\n 2<\/jats:sub>\n levels, and whether pravastatin treatment effect was related to Lp\u2010\n PLA<\/jats:styled-content>\n 2<\/jats:sub>\n activity change. Lp\u2010\n PLA<\/jats:styled-content>\n 2<\/jats:sub>\n was measured at randomization and 1\u00a0year, and levels were grouped as quartiles. The prespecified end point was\n CHD<\/jats:styled-content>\n death or nonfatal myocardial infarction. Baseline Lp\u2010\n PLA<\/jats:styled-content>\n 2<\/jats:sub>\n activity was positively associated with\n CHD<\/jats:styled-content>\n events (\n P<\/jats:italic>\n <0.001) but not after adjustment for 23 baseline factors (\n P<\/jats:italic>\n =0.66). In 6518 patients who were event free at 1\u00a0year, change in Lp\u2010\n PLA<\/jats:styled-content>\n 2<\/jats:sub>\n was a significant independent predictor of subsequent\n CHD<\/jats:styled-content>\n events after adjustment for these risk factors, including\n LDL<\/jats:styled-content>\n cholesterol and\n LDL<\/jats:styled-content>\n cholesterol changes (\n P<\/jats:italic>\n <0.001). Pravastatin reduced Lp\u2010\n PLA<\/jats:styled-content>\n 2<\/jats:sub>\n by 16% compared with placebo (\n P<\/jats:italic>\n <0.001). After adjustment for Lp\u2010\n PLA<\/jats:styled-content>\n 2<\/jats:sub>\n change, the pravastatin treatment effect was reduced from 23% to 10% (\n P<\/jats:italic>\n =0.26), with 59% of the treatment effect accounted for by changes in Lp\u2010\n PLA<\/jats:styled-content>\n 2<\/jats:sub>\n . Similar reductions in treatment effect were seen after adjustment for\n LDL<\/jats:styled-content>\n cholesterol change.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n \n Reduction in Lp\u2010\n PLA<\/jats:styled-content>\n 2<\/jats:sub>\n activity during the first year was a highly significant predictor of\n CHD<\/jats:styled-content>\n events, independent of change in\n LDL<\/jats:styled-content>\n cholesterol, and may account for over half of the benefits of pravastatin in the\n LIPID<\/jats:styled-content>\n study.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.113.000360","type":"journal-article","created":{"date-parts":[[2013,10,24]],"date-time":"2013-10-24T03:08:36Z","timestamp":1382584116000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":39,"title":["Changes in Lipoprotein\u2010Associated Phospholipase A2 Activity Predict Coronary Events and Partly Account for the Treatment Effect of Pravastatin: Results From the Long\u2010term Intervention with Pravastatin in Ischemic Disease Study"],"prefix":"10.1161","volume":"2","author":[{"given":"Harvey D.","family":"White","sequence":"first","affiliation":[{"name":"Green Lane Cardiovascular Service, Auckland City Hospital, Auckland, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John","family":"Simes","sequence":"additional","affiliation":[{"name":"NHMRC Clinical Trials Centre, University of Sydney, Sydney, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ralph A. H.","family":"Stewart","sequence":"additional","affiliation":[{"name":"Green Lane Cardiovascular Service, Auckland City Hospital, Auckland, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"Blankenberg","sequence":"additional","affiliation":[{"name":"University Heart Centre Hamburg, Hamburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth H.","family":"Barnes","sequence":"additional","affiliation":[{"name":"NHMRC Clinical Trials Centre, University of Sydney, Sydney, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian C.","family":"Marschner","sequence":"additional","affiliation":[{"name":"NHMRC Clinical Trials Centre, University of Sydney, Sydney, Australia"},{"name":"Department of Statistics, Macquarie University, Sydney, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Thompson","sequence":"additional","affiliation":[{"name":"University of Western Australia, Perth, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Malcolm","family":"West","sequence":"additional","affiliation":[{"name":"University of Queensland, Brisbane, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tanja","family":"Zeller","sequence":"additional","affiliation":[{"name":"University Heart Centre Hamburg, Hamburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David M.","family":"Colquhoun","sequence":"additional","affiliation":[{"name":"Greenslopes Hospital, Greenslopes, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Nestel","sequence":"additional","affiliation":[{"name":"Baker IDI Heart and Diabetes Institute, Melbourne, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anthony C.","family":"Keech","sequence":"additional","affiliation":[{"name":"NHMRC Clinical Trials Centre, University of Sydney, Sydney, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David R.","family":"Sullivan","sequence":"additional","affiliation":[{"name":"Royal Prince Alfred Hospital, Camperdown, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Hunt","sequence":"additional","affiliation":[{"name":"Department of Cardiology and University of Melbourne, Melbourne, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"Tonkin","sequence":"additional","affiliation":[{"name":"Monash University, Melbourne, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"name":"The LIPID Study 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