{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T04:59:38Z","timestamp":1761541178096,"version":"3.37.3"},"reference-count":17,"publisher":"Wiley","license":[{"start":{"date-parts":[[2014,1,1]],"date-time":"2014-01-01T00:00:00Z","timestamp":1388534400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"name":"Stein Erik Hagen Foundation"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2014]]},"abstract":"<jats:p><jats:italic>Background<\/jats:italic>. High levels of Pentraxin 3 (PTX3) are reported in acute myocardial infarction (AMI).<jats:italic>Aim<\/jats:italic>. To investigate circulating levels and gene expression of PTX3 in patients with AMI and stable angina pectoris (AP) undergoing PCI.<jats:italic>Methods<\/jats:italic>. Ten patients with AP and 20 patients with AMI were included. Blood samples were drawn before PCI in the AP group and after 3 and 12 hours and days 1, 3, 5, 7, and 14 in both groups.<jats:italic>Results<\/jats:italic>. Circulating PTX3 levels were higher in AMI compared to AP at 3 and 12 hours (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\"><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn>0.001<\/mml:mn><\/mml:math>and<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M2\"><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.003<\/mml:mn><\/mml:math>). Within the AMI group, reduction from 3 hours to all later time points was observed (all<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M3\"><mml:mi>P<\/mml:mi><mml:mo>\u2264<\/mml:mo><mml:mn>0.001<\/mml:mn><\/mml:math>). Within the AP group, increase from baseline to 3 hours (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M4\"><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.022<\/mml:mn><\/mml:math>), followed by reductions thereafter (all<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M5\"><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn>0.05<\/mml:mn><\/mml:math>), was observed. PTX3 mRNA increased in the AMI group from 3 hours to days 7 and 14 in a relative manner of 62% and 73%, while a relative reduction from baseline to 3 and 12 hours of 29% and 37% was seen in the AP group.<jats:italic>Conclusion<\/jats:italic>. High circulating PTX3 levels shortly after PCI in AMI indicate that AMI itself influences PTX3 levels. PTX3 mRNA might be in response to fluctuations in circulating levels.<\/jats:p>","DOI":"10.1155\/2014\/608414","type":"journal-article","created":{"date-parts":[[2014,3,11]],"date-time":"2014-03-11T17:02:11Z","timestamp":1394557331000},"page":"1-5","source":"Crossref","is-referenced-by-count":18,"title":["The Time Profile of Pentraxin 3 in Patients with Acute ST-Elevation Myocardial Infarction and Stable Angina Pectoris Undergoing Percutaneous Coronary Intervention"],"prefix":"10.1155","volume":"2014","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5012-9214","authenticated-orcid":true,"given":"Ragnhild","family":"Helseth","sequence":"first","affiliation":[{"name":"Department of Cardiology, Oslo University Hospital Ullev\u00e5l, P.O. Box 4956, Nydalen, 0424 Oslo, Norway"},{"name":"Faculty of Medicine, University of Oslo, P.O. Box 1078, Blindern, 0316 Oslo, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Svein","family":"Solheim","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Oslo University Hospital Ullev\u00e5l, P.O. Box 4956, Nydalen, 0424 Oslo, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Trine","family":"Opstad","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Oslo University Hospital Ullev\u00e5l, P.O. Box 4956, Nydalen, 0424 Oslo, Norway"},{"name":"Faculty of Medicine, University of Oslo, P.O. Box 1078, Blindern, 0316 Oslo, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1287-9174","authenticated-orcid":true,"given":"Pavel","family":"Hoffmann","sequence":"additional","affiliation":[{"name":"Section for Interventional Cardiology, Department of Cardiology, Division of Cardiovascular and Pulmonary Diseases, Oslo University Hospital Ullev\u00e5l, P.O. Box 4956, Nydalen, 0424 Oslo, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Harald","family":"Arnesen","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Oslo University Hospital Ullev\u00e5l, P.O. Box 4956, Nydalen, 0424 Oslo, Norway"},{"name":"Faculty of Medicine, University of Oslo, P.O. Box 1078, Blindern, 0316 Oslo, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ingebj\u00f8rg","family":"Seljeflot","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Oslo University Hospital Ullev\u00e5l, P.O. Box 4956, Nydalen, 0424 Oslo, Norway"},{"name":"Faculty of Medicine, University of Oslo, P.O. Box 1078, Blindern, 0316 Oslo, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","reference":[{"year":"2011","key":"1"},{"key":"2","doi-asserted-by":"publisher","DOI":"10.1161\/hc0902.104353"},{"key":"3","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/419804"},{"key":"4","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/920517"},{"key":"5","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000145167.30987.2E"},{"issue":"6","key":"6","doi-asserted-by":"crossref","first-page":"636","DOI":"10.1161\/01.CIR.102.6.636","volume":"102","year":"2000","journal-title":"Circulation"},{"key":"7","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.108.178947"},{"key":"8","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1100261"},{"issue":"6","key":"9","doi-asserted-by":"crossref","first-page":"686","DOI":"10.1111\/j.1365-2362.2012.02677.x","volume":"42","year":"2012","journal-title":"European Journal of Clinical Investigation"},{"key":"10","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.108.806547"},{"key":"11","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.107.749234"},{"key":"12","doi-asserted-by":"publisher","DOI":"10.1080\/00365510701884584"},{"key":"13","doi-asserted-by":"publisher","DOI":"10.1006\/meth.2001.1262"},{"key":"14","doi-asserted-by":"publisher","DOI":"10.1002\/art.33411"},{"key":"15","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20061301"},{"key":"16","doi-asserted-by":"publisher","DOI":"10.1016\/j.carpath.2010.02.005"},{"issue":"6, article e39484","key":"17","volume":"7","year":"2012","journal-title":"PLoS ONE"}],"container-title":["Mediators of Inflammation"],"original-title":[],"language":"en","link":[{"URL":"http:\/\/downloads.hindawi.com\/journals\/mi\/2014\/608414.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"http:\/\/downloads.hindawi.com\/journals\/mi\/2014\/608414.xml","content-type":"application\/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"http:\/\/downloads.hindawi.com\/journals\/mi\/2014\/608414.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2017,6,22]],"date-time":"2017-06-22T05:26:39Z","timestamp":1498109199000},"score":1,"resource":{"primary":{"URL":"http:\/\/www.hindawi.com\/journals\/mi\/2014\/608414\/"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2014]]},"references-count":17,"alternative-id":["608414","608414"],"URL":"https:\/\/doi.org\/10.1155\/2014\/608414","relation":{},"ISSN":["0962-9351","1466-1861"],"issn-type":[{"type":"print","value":"0962-9351"},{"type":"electronic","value":"1466-1861"}],"subject":[],"published":{"date-parts":[[2014]]}}}