{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T10:55:43Z","timestamp":1790506543304,"version":"4.1.0"},"reference-count":71,"publisher":"MDPI AG","issue":"2","license":[{"start":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T00:00:00Z","timestamp":1768435200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"University of Medical Science of Pozna\u0144"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Pulmonary embolism (PE) is one of the most serious complications of antiphospholipid syndrome (APS), a systemic autoimmune disorder defined by thrombotic events and persistent antiphospholipid antibodies (aPLA). PE occurs in 11\u201320% of patients and may constitute the initial clinical manifestation. Young and middle-aged women are most frequently affected, and triple-positive aPLA profiles markedly increase the risk of recurrence and long-term morbidity, including chronic thromboembolic pulmonary hypertension (CTEPH). This review article summarizes current evidence on the epidemiology, pathophysiology, diagnostic approach, and management of PE in APS. Key mechanisms include anti-\u03b22-glycoprotein I-mediated endothelial and platelet activation, complement engagement, and neutrophil extracellular trap formation, resulting in immunothrombosis. Diagnostic pathways follow standard PE algorithms; however, chronically elevated D-dimer levels and lupus anticoagulant-related aPTT prolongation require careful interpretation and consideration. Long-term vitamin K antagonist therapy remains the standard of care, whereas direct oral anticoagulants are not recommended in high-risk APS. Future directions include improved risk stratification through detailed aPLA profiling and the use of emerging biomarkers, early screening for CTEPH, and the development of targeted therapies such as complement inhibition and anti-NETosis strategies.<\/jats:p>","DOI":"10.3390\/ijms27020895","type":"journal-article","created":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T16:21:13Z","timestamp":1768494073000},"page":"895","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Pulmonary Embolism in Antiphospholipid Syndrome (APS)\u2014Where Are We and Where Are We Going?"],"prefix":"10.3390","volume":"27","author":[{"given":"Mateusz","family":"Lucki","sequence":"first","affiliation":[{"name":"Department and Clinic of Cardiology, University of Medical Sciences, 60-545 Pozna\u0144, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3438-0764","authenticated-orcid":false,"given":"Bogna","family":"Grygiel-G\u00f3rniak","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, Rehabilitation and Internal Diseases, Poznan University of Medical Sciences, 61-701 Pozna\u0144, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8248-2247","authenticated-orcid":false,"given":"Ewa","family":"Lucka","sequence":"additional","affiliation":[{"name":"Clinical Rehabilitation Laboratory, Department of Rehabilitation and Physiotherapy, University of Medical Sciences, 60-545 Pozna\u0144, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maciej","family":"Lesiak","sequence":"additional","affiliation":[{"name":"Department and Clinic of Cardiology, University of Medical Sciences, 60-545 Pozna\u0144, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aleksander","family":"Araszkiewicz","sequence":"additional","affiliation":[{"name":"Department and Clinic of Cardiology, University of Medical Sciences, 60-545 Pozna\u0144, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2026,1,15]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1019","DOI":"10.1002\/art.10187","article-title":"Antiphospholipid syndrome: Clinical and immunologic mani-festations and patterns of disease expression in a cohort of 1000 patients","volume":"46","author":"Cervera","year":"2002","journal-title":"Arthritis Rheum."},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"1636171","DOI":"10.3389\/fimmu.2025.1636171","article-title":"Criteria and non-criteria anti-phospholipid antibodies in the different clinical forms of antiphospholipid syndrome","volume":"16","author":"Pleguezuelo","year":"2025","journal-title":"Front Immunol."},{"key":"ref_3","doi-asserted-by":"crossref","first-page":"324","DOI":"10.1007\/s11926-013-0324-4","article-title":"Inhibition of nitric oxide and antiphospholipid antibody-mediated thrombosis","volume":"15","author":"Mineo","year":"2013","journal-title":"Curr. 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