{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T23:18:50Z","timestamp":1792019930784,"version":"4.4.0"},"reference-count":72,"publisher":"Oxford University Press (OUP)","issue":"38","license":[{"start":{"date-parts":[[2023,6,29]],"date-time":"2023-06-29T00:00:00Z","timestamp":1687996800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/501100017268","name":"Berlin Institute of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100017268","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010447","name":"German Centre for Cardiovascular Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100010447","id-type":"DOI","asserted-by":"publisher"}]},{"name":"FKZ","award":["81Z2100202"],"award-info":[{"award-number":["81Z2100202"]}]},{"DOI":"10.13039\/100011949","name":"Abbott Vascular","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100011949","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100010578","name":"German Cardiac Society","doi-asserted-by":"publisher","award":["#DGK12\/2020"],"award-info":[{"award-number":["#DGK12\/2020"]}],"id":[{"id":"10.13039\/501100010578","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Berlin Center for Translational Vascular Biomedicine"},{"DOI":"10.13039\/501100002839","name":"Charit\u00e9\u2014Universit\u00e4tsmedizin Berlin","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100002839","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Otto-Hess-Promotionsstipendium"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2023,10,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Rupture of the fibrous cap (RFC) and erosion of an intact fibrous cap (IFC) are the two predominant mechanisms causing acute coronary syndromes (ACS). It is uncertain whether clinical outcomes are different following RFC-ACS vs. IFC-ACS and whether this is affected by a specific inflammatory response. The prospective, translational OPTIcal-COherence Tomography in Acute Coronary Syndrome study programme investigates the impact of the culprit lesion phenotype on inflammatory profiles and prognosis in ACS patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>This analysis included 398 consecutive ACS patients, of which 62% had RFC-ACS and 25% had IFC-ACS. The primary endpoint was a composite of cardiac death, recurrent ACS, hospitalization for unstable angina, and target vessel revascularization at 2 years [major adverse cardiovascular events (MACE+)]. Inflammatory profiling was performed at baseline and after 90 days. Patients with IFC-ACS had lower rates of MACE+ than those with RFC-ACS (14.3% vs. 26.7%, P = 0.02). In 368-plex proteomic analyses, patients with IFC-ACS showed lower inflammatory proteome expression compared with those with RFC-ACS, including interleukin-6 and proteins associated with the response to interleukin-1\u03b2. Circulating plasma levels of interleukin-1\u03b2 decreased from baseline to 3 months following IFC-ACS (P &amp;lt; 0.001) but remained stable following RFC-ACS (P = 0.25). Interleukin-6 levels decreased in patients with RFC-ACS free of MACE+ (P = 0.01) but persisted high in those with MACE+.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This study demonstrates a distinct inflammatory response and a lower risk of MACE+ following IFC-ACS. These findings advance our understanding of inflammatory cascades associated with different mechanisms of plaque disruption and provide hypothesis generating data for personalized anti-inflammatory therapeutic allocation to ACS patients, a strategy that merits evaluation in future clinical trials.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/eurheartj\/ehad334","type":"journal-article","created":{"date-parts":[[2023,5,24]],"date-time":"2023-05-24T17:55:38Z","timestamp":1684950938000},"page":"3911-3925","source":"Crossref","is-referenced-by-count":57,"title":["Culprit plaque morphology determines inflammatory risk and clinical outcomes in acute coronary syndrome"],"prefix":"10.1093","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6144-5279","authenticated-orcid":false,"given":"Teresa","family":"Gerhardt","sequence":"first","affiliation":[{"name":"Department of Cardiology, Angiology and Intensive Care Medicine CBF, Deutsches Herzzentrum der Charit\u00e9, Germany and Berlin Institute of Health (BIH) , Hindenburgdamm 30, Berlin 12203 , Germany"},{"name":"DZHK (German Centre for Cardiovascular Research), Partner Site , Berlin , Germany"},{"name":"Cardiovascular Research Institute and the Department of Medicine, Cardiology, Icahn School of Medicine at Mount Sinai , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4892-6809","authenticated-orcid":false,"given":"Claudio","family":"Seppelt","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Angiology and Intensive Care Medicine CBF, Deutsches Herzzentrum der Charit\u00e9, Germany and Berlin Institute of Health (BIH) , Hindenburgdamm 30, Berlin 12203 , Germany"},{"name":"DZHK (German Centre for Cardiovascular Research), Partner Site , Berlin , Germany"},{"name":"Department of Medicine, Cardiology\/Angiology, Goethe University Hospital , Frankfurt , Germany"},{"name":"DZHK (German Centre for Cardiovascular Research), 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