{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T10:57:44Z","timestamp":1774609064707,"version":"3.50.1"},"reference-count":16,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2019,4,24]],"date-time":"2019-04-24T00:00:00Z","timestamp":1556064000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["European Heart Journal: Acute Cardiovascular Care"],"published-print":{"date-parts":[[2020,6]]},"abstract":"<jats:sec><jats:title>Aims:<\/jats:title><jats:p>We investigated the dynamics, associations with patient characteristics, other biomarkers, and clinical outcomes of pentraxin 3 in acute coronary syndrome.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and results:<\/jats:title><jats:p>In multivariate analyses, pentraxin 3 measured in 5154 patients randomised in the Platelet Inhibition and Patients Outcomes (PLATO) trial (NCT00391872) was compared with leukocytes, high-sensitivity C-reactive protein, interleukin-6, cystatin C, N-terminal prohormone brain natriuretic peptide, high-sensitivity troponin T and growth differentiation factor 15 concerning prediction of clinical outcome. Pentraxin 3 peaked earlier than high-sensitivity C-reactive protein and was more strongly correlated with N-terminal prohormone brain natriuretic peptide and high-sensitivity troponin T than with high-sensitivity C-reactive protein. The frequency of cardiovascular death, spontaneous myocardial infarction or stroke by quartiles of pentraxin 3 at admission was 6.1%, 7.3%, 9.7% and 10.7%, respectively ( p&lt;0.0001). The hazard ratio per 50% increase of pentraxin 3 was 1.13 (95% confidence interval: 1.07\u20131.19), p&lt;0.0001. This association remained significant after stepwise adjustments for leukocytes\/high-sensitivity C-reactive protein (1.09 (1.02\u20131.15)), p=0.009, interleukin-6 (1.07 (1.01\u20131.14)), p=0.026, and cystatin C (1.07 (1.00\u20131.13)), p=0.044, but not after adjustment for N-terminal prohormone brain natriuretic peptide, high-sensitivity troponin T and growth differentiation factor 15. Admission pentraxin 3 was also associated with several of the individual endpoint components (cardiovascular death\/spontaneous myocardial infarction; p=0.008, cardiovascular death; p=0.026, and spontaneous myocardial infarction; p=0.017), but not with stroke. Pentraxin 3 measured in the chronic phase (i.e. at one month) was still predictive of the composite endpoint in univariate analysis (1.12 (1.04\u20131.20) per 50% increase) p=0.0024, but not after adjustment for the other biomarkers.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion:<\/jats:title><jats:p>Admission level of pentraxin 3 is a modestly stronger predictor than high-sensitivity C-reactive protein and interleukin-6, but not than N-terminal prohormone brain natriuretic peptide or high-sensitivity troponin T, concerning cardiovascular outcome in acute coronary syndrome. Pentraxin 3 is more strongly correlated with N-terminal prohormone brain natriuretic peptide and high-sensitivity troponin T than with high-sensitivity C-reactive protein.<\/jats:p><\/jats:sec>","DOI":"10.1177\/2048872619846334","type":"journal-article","created":{"date-parts":[[2019,4,24]],"date-time":"2019-04-24T14:06:20Z","timestamp":1556114780000},"page":"313-322","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":8,"title":["Pentraxin-3 vs C-reactive protein and other prognostic biomarkers in acute coronary syndrome: A substudy of the Platelet Inhibition and Patients Outcomes (PLATO) trial"],"prefix":"10.1093","volume":"9","author":[{"given":"Frederic","family":"Kontny","sequence":"first","affiliation":[{"name":"Department of Cardiology, Stavanger University Hospital, Norway"},{"name":"Drammen Heart Center, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"Andersen","sequence":"additional","affiliation":[{"name":"Department of Anaesthesiology, Stavanger University Hospital, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thor","family":"Ueland","sequence":"additional","affiliation":[{"name":"Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Norway"},{"name":"K.G. Jebsen Thrombosis Research and Expertise Center (TREC), University of Troms\u00f8, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Axel","family":"\u00c5kerblom","sequence":"additional","affiliation":[{"name":"Department of Medical Sciences, Cardiology Uppsala University, Sweden"},{"name":"Uppsala Clinical Research Center, Uppsala University, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tatevik G","family":"Lakic","sequence":"additional","affiliation":[{"name":"Uppsala Clinical Research Center, Uppsala University, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Annika E","family":"Michelsen","sequence":"additional","affiliation":[{"name":"Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Norway"},{"name":"K.G. Jebsen Thrombosis Research and Expertise Center (TREC), University of Troms\u00f8, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P\u00e5l","family":"Aukrust","sequence":"additional","affiliation":[{"name":"Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Norway"},{"name":"K.G. Jebsen Thrombosis Research and Expertise Center (TREC), University of Troms\u00f8, Norway"},{"name":"Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital Rikshospitalet, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maria","family":"Bertilsson","sequence":"additional","affiliation":[{"name":"Uppsala Clinical Research Center, Uppsala University, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard C","family":"Becker","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Health and Disease, Academic Health Center, Cincinnati, OH, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anders","family":"Himmelmann","sequence":"additional","affiliation":[{"name":"AstraZeneca Research and Development, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefan K","family":"James","sequence":"additional","affiliation":[{"name":"Department of Medical Sciences, Cardiology Uppsala University, Sweden"},{"name":"Uppsala Clinical Research Center, Uppsala University, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Agneta","family":"Siegbahn","sequence":"additional","affiliation":[{"name":"Department of Medical Sciences, Cardiology Uppsala University, Sweden"},{"name":"Department of Medical Sciences, Clinical Chemistry, Uppsala University, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert F","family":"Storey","sequence":"additional","affiliation":[{"name":"Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lars","family":"Wallentin","sequence":"additional","affiliation":[{"name":"Department of Medical Sciences, Cardiology Uppsala University, Sweden"},{"name":"Uppsala Clinical Research Center, Uppsala University, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"name":"for the 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