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We aimed to evaluate associations of circulating LPS with prothrombotic markers in AF patients. A total of 157 (women, 57.3%) ambulatory anticoagulant-na\u00efve AF patients aged from 42 to 86 years were recruited. Clinical data together with serum LPS, inflammation, endothelial injury, coagulation and fibrinolysis markers, including fibrin clot permeability (K<jats:sub>s<\/jats:sub>) and clot lysis time (CLT), were analyzed. A median LPS concentration was 73.0 (58.0-100.0) pg\/mL and it showed association with CLT (<jats:italic>r<\/jats:italic>\u2009=\u20090.31,<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001) and plasminogen activator inhibitor-1 (PAI-1,<jats:italic>r<\/jats:italic>\u2009=\u20090.57,<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001), but not other fibrinolysis proteins, thrombin generation, inflammatory markers, or K<jats:sub>s<\/jats:sub>. There were weak associations of LPS with von Willebrand factor (vWF,<jats:italic>r<\/jats:italic>\u2009=\u20090.2,<jats:italic>p<\/jats:italic>\u2009=\u20090.013), cardiac troponin I (<jats:italic>r<\/jats:italic>\u2009=\u20090.16,<jats:italic>p<\/jats:italic>\u2009=\u20090.045), and growth differentiation factor-15 (<jats:italic>r<\/jats:italic>\u2009=\u20090.27,<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001). No associations of LPS and CHA<jats:sub>2<\/jats:sub>DS<jats:sub>2<\/jats:sub>-VASc or other clinical variables were observed. Multivariable regression adjusted for potential confounders showed that serum LPS \u2265 100 pg\/mL was an independent predictor of prolonged CLT. This study is the first to demonstrate antifibrinolytic effects of elevated LPS in AF patients largely driven by enhanced PAI-1 release.<\/jats:p>","DOI":"10.1007\/s11239-024-02980-5","type":"journal-article","created":{"date-parts":[[2024,4,21]],"date-time":"2024-04-21T14:01:21Z","timestamp":1713708081000},"page":"842-851","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Impaired fibrinolysis in patients with atrial fibrillation and elevated circulating lipopolysaccharide"],"prefix":"10.1007","volume":"57","author":[{"given":"Marcin","family":"Sadowski","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Micha\u0142","family":"Z\u0105bczyk","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0667-8109","authenticated-orcid":false,"given":"Anetta","family":"Undas","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2024,4,21]]},"reference":[{"key":"2980_CR1","doi-asserted-by":"publisher","first-page":"657","DOI":"10.1093\/cvr\/cvab346","volume":"118","author":"N Li","year":"2022","unstructured":"Li N, Durgan DJ, Wehrens XHT (2022) Gut microbiota: a key regulator of ageing-associated atrial fibrillation? 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All patients included gave their informed consent.This work was supported by the Jagiellonian University Medical College (grant no. N41\/DBS\/000516, to MZ).The authors have no relevant financial or non-financial interests to disclose.All authors contributed to the study conception and design. Material preparation, data collection and analysis were performed by MS, MZ, and AU. The first draft of the manuscript was written by MS and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Statements and declarations"}}]}}