{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T04:02:14Z","timestamp":1791259334693,"version":"4.1.0"},"reference-count":34,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2025,5,1]],"date-time":"2025-05-01T00:00:00Z","timestamp":1746057600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100006108","name":"National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["KL2\u2010TR2385"],"award-info":[{"award-number":["KL2\u2010TR2385"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 AG080011"],"award-info":[{"award-number":["R01 AG080011"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 AG068398"],"award-info":[{"award-number":["R01 AG068398"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>There are limited population\u2010based data regarding the prevalence of cerebral amyloid angiopathy (CAA) and associated risks of mortality and incident cerebrovascular events.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We performed a retrospective cohort study using inpatient and outpatient claims from 2008 to 2022 from a 5% national sample of Medicare beneficiaries. CAA and ischemic and hemorrhagic stroke were identified using validated International Classification of Diseases 10th Revision (ICD\u201010) codes. We ascertained CAA from October 1, 2015 through 2022, and used data from 2008 through September 30, 2015 to ascertain comorbidities including prevalent stroke. We used Cox regression to examine the association of CAA with subsequent death and incident stroke subtypes after adjustment for demographics, vascular risk factors, and Charlson comorbidities.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Among 1,920,312 Medicare beneficiaries in our sample, 2,161 (11.3 per 10,000) had a diagnosis of CAA. In adjusted Cox regression analysis, there was an association between CAA and subsequent mortality (HR 4.9; 95% CI 4.6\u20135.2). Among 1,872,474 patients without prevalent stroke, including 900 of the CAA patients, there was a significant association between CAA and an increased risk of any stroke (HR 8.0; 95% CI 6.7\u20139.6), ischemic stroke (HR 4.6; 95% CI 3.6\u20136.0), intracerebral hemorrhage (HR 26.9; 95% CI 20.3\u201335.6), and subarachnoid hemorrhage (HR 21.6; 95% CI 12.2\u201338.1). After a diagnosis of CAA, absolute risks of ischemic stroke and intracerebral hemorrhage were broadly similar.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>In a large, nationwide cohort of Medicare beneficiaries, the prevalence of clinically diagnosed CAA was approximately 11 per 10,000. CAA was associated with an increased risk of mortality and incident stroke, both hemorrhagic and ischemic. ANN NEUROL 2025;98:249\u2013257<\/jats:p><\/jats:sec>","DOI":"10.1002\/ana.27253","type":"journal-article","created":{"date-parts":[[2025,5,1]],"date-time":"2025-05-01T07:40:57Z","timestamp":1746085257000},"page":"249-257","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Prevalence of Cerebral Amyloid Angiopathy and Associated Risk of Subsequent Ischemic and Hemorrhagic Stroke and Mortality in a Nationwide Cohort"],"prefix":"10.1002","volume":"98","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4502-1572","authenticated-orcid":false,"given":"Samuel S.","family":"Bruce","sequence":"first","affiliation":[{"name":"Clinical and Translational Neuroscience Unit, Department of Neurology and Feil Family Brain and Mind Research Institute, Weill Cornell Medicine  New York New York 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USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8424-6128","authenticated-orcid":false,"given":"Babak B.","family":"Navi","sequence":"additional","affiliation":[{"name":"Clinical and Translational Neuroscience Unit, Department of Neurology and Feil Family Brain and Mind Research Institute, Weill Cornell Medicine  New York New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gloria C.","family":"Chiang","sequence":"additional","affiliation":[{"name":"Brain Health Imaging Institute and Department of Radiology, Weill Cornell Medicine  New York New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Costantino","family":"Iadecola","sequence":"additional","affiliation":[{"name":"Clinical and Translational Neuroscience Unit, Department of Neurology and Feil Family Brain and Mind Research Institute, Weill Cornell Medicine  New York New York 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