{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T17:19:56Z","timestamp":1782407996323,"version":"3.54.5"},"reference-count":53,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"12","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[2025,12]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Biomarkers may increase the understanding of the pathophysiology of brain lesions in newly evaluated atrial fibrillation. BTG (\u03b2-thromboglobulin) is released from platelet alpha granules upon activation, reflecting platelet activation or destruction, or both. We assessed the association of plasma BTG with cerebral microbleeds (CMBs) and ischemic brain lesions using brain magnetic resonance imaging (bMRI) in patients with atrial fibrillation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>BTG was analyzed using the Luminex assay. CMBs and ischemic brain lesions were detected by standardized bMRI of 1724 patients from the Swiss-Atrial Fibrillation cohort, a prospective, national, multicenter cohort study that enrolled patients between 2014 and 2017. For this cross-sectional analysis, associations of BTG with bMRI lesions were evaluated by logistic and linear regression analyses using 2 models. The first model was adjusted for age and sex, and the second model was additionally multivariable-adjusted for a large number of clinical characteristics, including coronary artery disease, hypertension, diabetes, chronic kidney disease, history of heart failure, major bleeding, as well as concomitant platelet inhibitor, and anticoagulation therapy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>Mean age at baseline was 72.5 years (SD, 8.4), and 27.3% were female. On bMRI, CMBs were found in 369 patients (21.4%) and cerebral infarcts in 635 (36.8%). After multivariable adjustment, a 1-unit increase of log-transformed plasma BTG was associated with 25% lower odds of having CMBs (odds ratio, 0.75 [95% CI, 0.59\u20130.96]). However, BTG was not associated with the presence of large noncortical or cortical infarcts (odds ratio, 0.85 [95% CI, 0.66\u20131.09]) or small noncortical infarcts (odds ratio, 1.06 [95% CI, 0.83\u20131.35]).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>In patients with atrial fibrillation, the platelet-specific biomarker BTG was inversely and independently associated with CMBs on bMRI. Low-grade platelet activation may improve vascular integrity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>REGISTRATION:<\/jats:title>\n                    <jats:p>\n                      URL:\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/www.clinicaltrials.gov\">https:\/\/www.clinicaltrials.gov<\/jats:ext-link>\n                      ; Unique identifier: NCT02105844.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/strokeaha.124.049972","type":"journal-article","created":{"date-parts":[[2025,9,17]],"date-time":"2025-09-17T09:01:40Z","timestamp":1758099700000},"page":"3414-3423","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":2,"title":["Plasma \u03b2-Thromboglobulin Is Inversely Associated With Cerebral Microbleeds in Atrial Fibrillation"],"prefix":"10.1161","volume":"56","clinical-trial-number":[{"clinical-trial-number":"nct02105844","registry":"10.18810\/clinical-trials-gov"}],"author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-1960-0041","authenticated-orcid":true,"given":"Benedict C.","family":"Kupper","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Cantonal Hospital of Baden, Switzerland (B.C.K., J.H.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9887-2469","authenticated-orcid":true,"given":"Martin F.","family":"Reiner","sequence":"additional","affiliation":[{"name":"Department of Cardiology, University Heart Center, University Hospital Zurich, Switzerland (M.F.R.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5042-8353","authenticated-orcid":true,"given":"Laura","family":"Werlen","sequence":"additional","affiliation":[{"name":"Department of Clinical Research (L.W.), 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