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Injury upon acute myocardial infarction (AMI) induces an early excessive inflammatory response. The value of IL-8 and neutrophil-related biomarkers for AMI patient outcomes is incompletely understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>AMI patients sampled\u2009\u2264\u200924\u00a0h after symptom onset were included from SPUM-ACS cohort. One hundred twelve cases with all-cause mortality or recurrent AMI within 1\u00a0year were matched 1:1 to event-free controls by age, sex, AMI subtype, symptom onset time, and recruiting sites.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Cases showed higher IL-8 (median: 66.82 vs. 41.24\u00a0pg\/mL;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.001), cfDNA (393.9 vs. 223.8\u00a0ng\/mL;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001), MPO (683.4 vs. 602.2\u00a0ng\/mL;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.030), and neutrophil-to-lymphocyte ratio (NLR) than controls (6.22 vs. 4.76;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.013). IL-8 and cfDNA were higher in the death subgroup than recurrent AMI (IL-8: 71.16 vs. 51.52\u00a0pg\/mL;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.026; cfDNA: 420.5 vs. 239.7\u00a0ng\/mL;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.030). Notably, IL-8 peaked in the hyper-acute phase (&lt;\u20096\u00a0h), earlier than high-sensitivity troponin T (hsTnT). This aligned with its associations with death or recurrent AMI (OR\u2009=\u20091.62;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.021), death (OR\u2009=\u20092.14;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.019), and early presenters (&lt;\u20096\u00a0h, OR\u2009=\u20092.65;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.008) after adjusting for confounders (estimated glomerular filtration rate [eGFR], high-sensitivity C-reactive protein [hsCRP], N-terminal pro-B-type natriuretic peptide [NT-proBNP], and hsTnT). IL-8, along with cfDNA, NLR, and hsCRP clustered in patients with increased Killip Class and worse outcomes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>IL-8 and neutrophil-related biomarkers were associated with 1-year mortality in AMI patients, especially in the hyper-acute phase.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Clinical trial registration<\/jats:title>\n                    <jats:p>NCT01000701.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Graphical Abstract<\/jats:title>\n                    <jats:p>\n                      IL-8 level is associated with 1-year mortality in patients with AMI. IL-8 and neutrophil-related biomarkers were measured in 112 AMI case\u2013control pairs within 24\u00a0h of symptom onset from the SPUM-ACS cohort. After adjusting for key confounders (eGFR, hsTnT, NT-proBNP, and hsCRP), elevated IL-8 levels were independently associated with 1-year composite outcome (all-cause mortality or recurrent AMI: OR 1.62;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.021), all-cause mortality alone (OR 2.14;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.019), and showed the strongest association in early presenters within the hyper-acute phase (&lt;\u20096\u00a0h, OR 2.65;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.008). Difference of IL-8 levels within case\u2013control pair peaked during hyper-acute phase, elevating earlier than hsTnT, which rose progressively across later symptom onset time windows. The temporal panel shows the mean within-pair difference in standardized, log-transformed IL-8 and hsTnT by symptom onset window, as in Fig.\u00a03B. AMI, acute myocardial infarction; eGFR, estimated glomerular filtration rate; hsCRP, high-sensitivity C-reactive protein; hsTnT, high-sensitivity troponin T; IL, interleukin; NT-proBNP, N-terminal pro-B-type natriuretic peptide; OR, odds ratio.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s00392-026-03026-x","type":"journal-article","created":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T09:13:03Z","timestamp":1790068383000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Interleukin-8 and other neutrophil-related biomarkers are associated with 1-year mortality in patients with acute myocardial infarction"],"prefix":"10.1007","author":[{"given":"Yu-Jen","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael A.","family":"Matter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valentina A.","family":"Rossi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dik","family":"Heg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah","family":"Costantino","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francesco","family":"Paneni","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Camilla","family":"Gallino","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Barbara E.","family":"St\u00e4hli","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lorenz","family":"R\u00e4ber","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephan","family":"Windecker","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fran\u00e7ois","family":"Mach","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Baris","family":"Gencer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roland","family":"Klingenberg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicolas","family":"Rodondi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Nanchen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mitchell P.","family":"Levesque","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olga V.","family":"Demler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank","family":"Ruschitzka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian M.","family":"Matter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,9,22]]},"reference":[{"key":"3026_CR1","doi-asserted-by":"publisher","first-page":"593","DOI":"10.1586\/1744666X.2014.894886","volume":"10","author":"RC Russo","year":"2014","unstructured":"Russo RC, Garcia CC, Teixeira MM, Amaral FA (2014) The CXCL8\/IL-8 chemokine family and its receptors in inflammatory diseases. 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DH is affiliated with the Department of Clinical Research (DCR) of the University of Bern, which follows a staff policy of not accepting honoraria or consultancy fees. However, the DCR is involved in the design, conduct, or analysis of clinical studies funded by not-for-profit and for-profit organizations. In particular, pharmaceutical and medical device companies provide direct funding to some of these studies. For an up-to-date list of the DCR\u2019s funding sources, see\n                      \n                      . ML has received unrelated research funding from Novartis, Roche, Leica, Bacoba, Scailyte, Oncobit, Tcypher, and Molecular Partners. ML is also a founder and board member of the cancer monitoring company Oncobit. FR has not received personal payments by pharmaceutical companies or device manufacturers in the last 3\u00a0years (remuneration for the time spent in activities, such as participation as steering committee member of clinical trials and member of the Pfizer Research Award selection committee in Switzerland, was made directly to the University of Zurich). The Department of Cardiology (University Hospital of Zurich\/University of Zurich) reports research-, educational-, and\/or travel grants from Abbott, Abiomed, Alnylam, Amarin, Amgen, AstraZeneca, At the Limits Ltd., Bayer, Biotronik, BMS, Boehringer Ingelheim, Boston Scientific, Bracco, CM Microport, Concept Medical, CTI, Daiichi Sankyo, Edwards Lifesciences, FomF GmbH, Hamilton Health Sciences, IHF, Innosuisse, LumiraDx, Kantar, LabPoint, MedAlliance, Medcon International, Medical Education Global Solutions, Medtronic, MicroPort, Monocle, Novartis, Novo Nordisk, OM Pharma, Pfizer, Quintiles Switzerland Sarl, RecorMedical, Roche Diagnostics, Roche Pharma, Sahajanand IN, Sanofi, Sarstedt AG, Servier, Terumo Deutschland, Trama Solutions, V-Wave, Vifor, and ZOLL. These grants do not impact his personal remuneration. CMM has received research grants to the institution from Eli\u00a0Lilly, AstraZeneca, Roche, Amgen, Novartis, Novo Nordisk, and MSD including speaker or consultant fees. OVD was partially supported in the past by Kowa Research Institute for a project unrelated to the current manuscript.","order":3,"name":"Ethics","label":"Competing interests","group":{"name":"EthicsHeading","label":"Declarations"}}]}}