{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T01:49:52Z","timestamp":1778636992548,"version":"3.51.4"},"reference-count":46,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2019,10,7]],"date-time":"2019-10-07T00:00:00Z","timestamp":1570406400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100003793","name":"Hj\u00e4rt-Lungfonden","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003793","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Intern Med"],"published-print":{"date-parts":[[2020,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Despite extensive research in atherosclerosis, the mechanisms of coronary atherothrombosis in <jats:styled-content style=\"fixed-case\">ST<\/jats:styled-content>\u2010elevation myocardial infarction (<jats:styled-content style=\"fixed-case\">STEMI<\/jats:styled-content>) patients are undetermined.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objectives<\/jats:title><jats:p>Our aim was to find candidate genes involved in <jats:styled-content style=\"fixed-case\">STEMI<\/jats:styled-content> by analysing leucocyte gene expression in <jats:styled-content style=\"fixed-case\">STEMI<\/jats:styled-content> patients, without the influence of secondary inflammation from innate immunity, which was assumed to be a consequence rather than the cause of coronary atherothrombosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Fifty\u2010one patients were included at coronary angiography because of <jats:styled-content style=\"fixed-case\">STEMI<\/jats:styled-content>. Arterial blood was sampled in the acute phase (P1), at 24\u201348\u00a0h (P2) and at 3\u00a0months (P3). Leucocyte <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> was isolated and gene expression analysis was performed by Affymetrix Human Transcriptome Array 2.0. By omission of up\u2010 or downregulated genes at P2, secondary changes from innate immunity were excluded. Genes differentially expressed in P1 when compared to the convalescent sample in P3 were determined as genes involved in <jats:styled-content style=\"fixed-case\">STEMI<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Three genes were upregulated at P1 compared to P3; <jats:styled-content style=\"fixed-case\">ABCG<\/jats:styled-content>1 (<jats:italic>P<\/jats:italic>\u00a0=\u00a05.81\u00a0\u00d7\u00a010<jats:sup>\u22125<\/jats:sup>), <jats:styled-content style=\"fixed-case\">RAB<\/jats:styled-content>20 (<jats:italic>P<\/jats:italic>\u00a0=\u00a03.69\u00a0\u00d7\u00a010<jats:sup>\u22125<\/jats:sup>) and <jats:styled-content style=\"fixed-case\">TMEM<\/jats:styled-content>2 (<jats:italic>P<\/jats:italic>\u00a0=\u00a07.75\u00a0\u00d7\u00a010<jats:sup>\u22126<\/jats:sup>) whilst four were downregulated; <jats:styled-content style=\"fixed-case\">ACVR<\/jats:styled-content>1 (<jats:italic>P<\/jats:italic>\u00a0=\u00a09.01\u00a0\u00d7\u00a010<jats:sup>\u22125<\/jats:sup>), <jats:styled-content style=\"fixed-case\">NFATC<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">IP<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0=\u00a08.86\u00a0\u00d7\u00a010<jats:sup>\u22125<\/jats:sup>), <jats:styled-content style=\"fixed-case\">SUN<\/jats:styled-content>1 (<jats:italic>P<\/jats:italic>\u00a0=\u00a03.87\u00a0\u00d7\u00a010<jats:sup>\u22125<\/jats:sup>) and <jats:styled-content style=\"fixed-case\">TTC<\/jats:styled-content>9C (<jats:italic>P<\/jats:italic>\u00a0=\u00a07.18\u00a0\u00d7\u00a010<jats:sup>\u22126<\/jats:sup>). These genes were also highly expressed in carotid atherosclerotic plaques.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>We found seven genes involved in <jats:styled-content style=\"fixed-case\">STEMI<\/jats:styled-content>. The study is unique regarding the blood sampling in the acute phase and omission of secondary expressed genes from innate immunity. However, the results need to be replicated by future studies.<\/jats:p><\/jats:sec>","DOI":"10.1111\/joim.12976","type":"journal-article","created":{"date-parts":[[2019,10,7]],"date-time":"2019-10-07T12:15:47Z","timestamp":1570450547000},"page":"66-77","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["New candidate genes for <scp>ST<\/scp>\u2010elevation myocardial infarction"],"prefix":"10.1111","volume":"287","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4863-9682","authenticated-orcid":false,"given":"S.","family":"Cederstr\u00f6m","sequence":"first","affiliation":[{"name":"Division of Cardiovascular medicine Department of Clinical Sciences Karolinska Institutet Danderyd Hospital (KI DS) Stockholm Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P.","family":"Lundman","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular medicine Department of Clinical Sciences 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