{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T14:35:13Z","timestamp":1790087713289,"version":"4.0.1"},"reference-count":37,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2019,6]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>\n              Inflammation is a causal risk factor for cardiovascular disease (CVD). sPLA\n              <jats:sub>2<\/jats:sub>\n              -IIA (group IIA secretory phospholipase A\n              <jats:sub>2<\/jats:sub>\n              ) plays an integral role in regulating vascular inflammation. Although studies investigated sPLA\n              <jats:sub>2<\/jats:sub>\n              -IIA in secondary prevention, we prospectively evaluated sPLA\n              <jats:sub>2<\/jats:sub>\n              -IIA mass and genetic variants with CVD events in a primary prevention population with chronic inflammation.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>\n              The JUPITER trial (Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin) randomized participants with LDL (low-density lipoprotein) &lt;130 mg\/dL and hsCRP (high-sensitivity C-reactive protein) \u22652 mg\/L to high-intensity rosuvastatin versus placebo. Baseline and 1-year plasma sPLA\n              <jats:sub>2<\/jats:sub>\n              -IIA mass was measured (N=11\u2009269 baseline; N=9620 1 year). We also identified genetic variants influencing sPLA\n              <jats:sub>2<\/jats:sub>\n              -IIA using genome-wide association and examined them with CVD. Three hundred thirteen incident CVD events occurred during follow-up. Baseline sPLA\n              <jats:sub>2<\/jats:sub>\n              -IIA mass (median, 25th\u201375th percentile: 3.81, 2.49\u20136.03 ng\/mL) was associated with increased risk of CVD: risk factor\u2013adjusted hazard ratio (95% CI;\n              <jats:italic>P<\/jats:italic>\n              ) per SD increment: 1.22 (1.08\u20131.38;\n              <jats:italic>P<\/jats:italic>\n              =0.002). This remained significant (1.18; 1.04\u20131.35;\n              <jats:italic>P<\/jats:italic>\n              =0.01) after incrementally adjusting for hsCRP. Similar estimates were observed in rosuvastatin and placebo groups (\n              <jats:italic>P<\/jats:italic>\n              treatment interaction&gt;0.05). The rs11573156C variant in\n              <jats:italic>PLA2G2A<\/jats:italic>\n              (encoding sPLA\n              <jats:sub>2<\/jats:sub>\n              -IIA) had the strongest effect on sPLA\n              <jats:sub>2<\/jats:sub>\n              -II: median (25th\u201375th percentile, ng\/mL) for CC and GG genotypes: 2.79 (1.97\u20134.01) and 7.38 (5.38\u201310.19), respectively; and had nonsignificant trend for higher CVD risk (hazard ratio, 1.11; 95% CI, 0.89\u20131.38;\n              <jats:italic>P<\/jats:italic>\n              =0.34).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>\n              In the JUPITER population recruited on chronic inflammation, sPLA\n              <jats:sub>2<\/jats:sub>\n              -IIA mass was associated with CVD risk relating to vascular inflammation not fully reflected by hsCRP. Additional studies, including larger functional genetic and clinical studies, are needed to determine whether sPLA\n              <jats:sub>2<\/jats:sub>\n              -IIA may be a potential pharmacological target for primary prevention of CVD.\n            <\/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\/atvbaha.118.311894","type":"journal-article","created":{"date-parts":[[2019,4,11]],"date-time":"2019-04-11T10:37:25Z","timestamp":1554979045000},"page":"1182-1190","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":36,"title":["Group IIA Secretory Phospholipase A\n            <sub>2<\/sub>\n            , Vascular Inflammation, and Incident Cardiovascular Disease"],"prefix":"10.1161","volume":"39","author":[{"given":"Akintunde O.","family":"Akinkuolie","sequence":"first","affiliation":[{"name":"From the Center for Lipid Metabolomics, Division of Preventive Medicine (A.O.A., P.R.L., R.J.G., P.M.R., D.I.C., S.M.), Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA"},{"name":"Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston (A.O.A.)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick R.","family":"Lawler","sequence":"additional","affiliation":[{"name":"From the Center for Lipid Metabolomics, Division of Preventive Medicine (A.O.A., P.R.L., R.J.G., P.M.R., D.I.C., S.M.), Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA"},{"name":"Peter Munk Cardiac Centre, Toronto General Hospital, ON, Canada (P.R.L.)"},{"name":"Heart and Stroke\/Richard Lewar Centre for Excellence in Cardiovascular Research, University of Toronto, ON, Canada (P.R.L.)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Audrey Y.","family":"Chu","sequence":"additional","affiliation":[{"name":"Merck Research Laboratories, Boston, MA (A.Y.C.)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Caulfield","sequence":"additional","affiliation":[{"name":"Department of Endocrinology &amp; CVD, Quest Diagnostics Nichols Institute, San Juan Capistrano, CA (M.C., J.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianying","family":"Mu","sequence":"additional","affiliation":[{"name":"Department of Endocrinology &amp; CVD, Quest Diagnostics Nichols Institute, San Juan Capistrano, CA (M.C., J.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bo","family":"Ding","sequence":"additional","affiliation":[{"name":"Medical Evidence &amp; Observational Research, Global Medical Affairs (B.D., F.N.), AstraZeneca R&amp;D, M\u00f6lndal, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fredrik","family":"Nyberg","sequence":"additional","affiliation":[{"name":"Medical Evidence &amp; Observational Research, Global Medical Affairs (B.D., F.N.), AstraZeneca R&amp;D, M\u00f6lndal, Sweden"},{"name":"Occupational and Environmental Medicine, Sahlgrenska Academy, University of Gothenburg, Sweden (F.N.)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert J.","family":"Glynn","sequence":"additional","affiliation":[{"name":"From the Center for Lipid Metabolomics, Division of Preventive Medicine (A.O.A., P.R.L., R.J.G., P.M.R., D.I.C., S.M.), Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA"},{"name":"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 Lipid Metabolomics, Division of Preventive Medicine (A.O.A., P.R.L., R.J.G., P.M.R., D.I.C., S.M.), Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA"},{"name":"Cardiovascular Medicine (P.M.R., S.M.), Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eva","family":"Hurt-Camejo","sequence":"additional","affiliation":[{"name":"Cardiovascular &amp; Metabolic Diseases, Innovative Medicines (E.H.-C.), AstraZeneca R&amp;D, M\u00f6lndal, Sweden"},{"name":"Division of Clinical Chemistry, Department of Laboratory Medicine, Karolinska Institute, Stockholm, Sweden (E.H.-C.)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel I.","family":"Chasman","sequence":"additional","affiliation":[{"name":"From the Center for Lipid Metabolomics, Division of Preventive Medicine (A.O.A., P.R.L., R.J.G., P.M.R., D.I.C., S.M.), Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samia","family":"Mora","sequence":"additional","affiliation":[{"name":"From the Center for Lipid Metabolomics, Division of Preventive Medicine (A.O.A., P.R.L., R.J.G., P.M.R., D.I.C., S.M.), Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA"},{"name":"Cardiovascular Medicine (P.M.R., S.M.), Department of Medicine, Brigham and Women\u2019s Hospital, Boston, 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