{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T16:40:25Z","timestamp":1790700025023,"version":"4.1.0"},"reference-count":37,"publisher":"Wiley","license":[{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2016]]},"abstract":"<jats:p>\n                    <jats:italic>Background and Aims<\/jats:italic>\n                    . Neutrophil extracellular traps (NETs) have been identified in acute myocardial infarction. We assessed the time profile and association with infarct size for NETs markers in ST-elevation myocardial infarction (STEMI) and stable angina pectoris (AP).\n                    <jats:italic>Methods.<\/jats:italic>\n                    In 20 patients with STEMI and 10 with AP undergoing percutaneous coronary intervention (PCI), blood samples were collected before PCI (only AP group) and after 3 and 12 hours, days 1, 3, 5, 7, and 14 for measurement of NETs markers.\n                    <jats:italic>Results<\/jats:italic>\n                    . Double-stranded deoxyribonucleic acid (dsDNA) and nucleosome levels were higher in STEMI than AP until day 3 and 12 hours (\n                    <mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\">\n                      <mml:mi>p<\/mml:mi>\n                      <mml:mo>&lt;<\/mml:mo>\n                      <mml:mn fontstyle=\"italic\">0.03<\/mml:mn>\n                    <\/mml:math>\n                    , all). DsDNA declined after day 5 in both groups (\n                    <mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M2\">\n                      <mml:mi>p<\/mml:mi>\n                      <mml:mo>&lt;<\/mml:mo>\n                      <mml:mn fontstyle=\"italic\">0.04<\/mml:mn>\n                    <\/mml:math>\n                    , all), while nucleosomes declined until day 3 only in the AP group\n                    <mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M3\">\n                      <mml:mo stretchy=\"false\">(<\/mml:mo>\n                      <mml:mi>p<\/mml:mi>\n                      <mml:mo>&lt;<\/mml:mo>\n                      <mml:mn fontstyle=\"italic\">0.05<\/mml:mn>\n                    <\/mml:math>\n                    , all). DsDNA correlated with peak troponin T and creatine kinase MB (CKMB) at day 5 (\n                    <mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M4\">\n                      <mml:mi>r<\/mml:mi>\n                      <mml:mo>=<\/mml:mo>\n                      <mml:mn fontstyle=\"italic\">0.48<\/mml:mn>\n                    <\/mml:math>\n                    ,\n                    <mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M5\">\n                      <mml:mi>p<\/mml:mi>\n                      <mml:mo>=<\/mml:mo>\n                      <mml:mn fontstyle=\"italic\">0.03<\/mml:mn>\n                    <\/mml:math>\n                    , both) and with MRI-measured infarct size at days 5 and 7\n                    <mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M6\">\n                      <mml:mo stretchy=\"false\">(<\/mml:mo>\n                      <mml:mi>r<\/mml:mi>\n                      <mml:mo>=<\/mml:mo>\n                      <mml:mn fontstyle=\"italic\">0.61<\/mml:mn>\n                    <\/mml:math>\n                    ,\n                    <mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M7\">\n                      <mml:mi>p<\/mml:mi>\n                      <mml:mo>=<\/mml:mo>\n                      <mml:mn fontstyle=\"italic\">0.01<\/mml:mn>\n                    <\/mml:math>\n                    and\n                    <mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M8\">\n                      <mml:mi>r<\/mml:mi>\n                      <mml:mo>=<\/mml:mo>\n                      <mml:mn fontstyle=\"italic\">0.52<\/mml:mn>\n                    <\/mml:math>\n                    ,\n                    <mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M9\">\n                      <mml:mi>p<\/mml:mi>\n                      <mml:mo>=<\/mml:mo>\n                      <mml:mn fontstyle=\"italic\">0.04<\/mml:mn>\n                    <\/mml:math>\n                    , resp.), while nucleosomes correlated with infarct size at day 5 (\n                    <mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M10\">\n                      <mml:mi>r<\/mml:mi>\n                      <mml:mo>=<\/mml:mo>\n                      <mml:mn fontstyle=\"italic\">0.58<\/mml:mn>\n                    <\/mml:math>\n                    ,\n                    <mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M11\">\n                      <mml:mi>p<\/mml:mi>\n                      <mml:mo>=<\/mml:mo>\n                      <mml:mn fontstyle=\"italic\">0.02<\/mml:mn>\n                    <\/mml:math>\n                    ).\n                    <jats:italic>Conclusions<\/jats:italic>\n                    . High levels of NETs markers were observed in STEMI shortly after revascularisation and were partly associated with infarct size. The decline thereafter in both groups indicates a role for NETs in both acute and chronic atherothrombosis.\n                  <\/jats:p>","DOI":"10.1155\/2016\/2182358","type":"journal-article","created":{"date-parts":[[2016,12,16]],"date-time":"2016-12-16T06:53:32Z","timestamp":1481871212000},"page":"1-8","source":"Crossref","is-referenced-by-count":41,"title":["The Time Course of Markers of Neutrophil Extracellular Traps in Patients Undergoing Revascularisation for Acute Myocardial Infarction or Stable Angina Pectoris"],"prefix":"10.1155","volume":"2016","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5012-9214","authenticated-orcid":true,"given":"Ragnhild","family":"Helseth","sequence":"first","affiliation":[{"name":"Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital Ullev\u00e5l, Oslo, Norway"},{"name":"Faculty of Medicine, University of Oslo, Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3321-6572","authenticated-orcid":true,"given":"Svein","family":"Solheim","sequence":"additional","affiliation":[{"name":"Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital Ullev\u00e5l, Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harald","family":"Arnesen","sequence":"additional","affiliation":[{"name":"Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital Ullev\u00e5l, Oslo, Norway"},{"name":"Faculty of Medicine, University of Oslo, Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4071-3358","authenticated-orcid":true,"given":"Ingebj\u00f8rg","family":"Seljeflot","sequence":"additional","affiliation":[{"name":"Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital Ullev\u00e5l, Oslo, Norway"},{"name":"Faculty of Medicine, University of Oslo, Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Trine Baur","family":"Opstad","sequence":"additional","affiliation":[{"name":"Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital Ullev\u00e5l, Oslo, Norway"},{"name":"Faculty of Medicine, University of Oslo, Oslo, 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