{"title":"White Matter Hyperintensity Multispot Pattern Lesions and Cerebrovascular Amyloid Burden in Cerebral Amyloid Angiopathy.","authors":"Andreas Charidimou, Jean-Claude Baron","doi":"10.1161/STROKEAHA.125.051482","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>We investigated the relationship between white matter hyperintensity (WMH) multispot pattern lesions, a supporting magnetic resonance imaging marker of cerebral amyloid angiopathy (CAA), and positron emission tomography-based amyloid-β burden across a range of cerebrovascular amyloid deposition.</p><p><strong>Methods: </strong>Twenty-one nondemented subjects (11 patients with probable CAA; median age, 71 [63-77] years; 82% males; and 10 healthy subjects; median age, 63.5 [61-68] years; 50% males) underwent brain magnetic resonance imaging and 11C-Pittsburgh compound B-positron emission tomography imaging. WMH multispot lesions were evaluated on FLAIR sequences. The association between whole cortex 11C-Pittsburgh compound B binding and WMH multispot lesions count was assessed using Kendall tau, adjusting for key markers of CAA through a hierarchical residualization approach.</p><p><strong>Results: </strong>The unadjusted analysis showed a positive correlation between WMH multispot lesions count and whole cortex 11C-Pittsburgh compound B binding (tau-b=0.495; <i>P</i>=0.0017). Sequential adjustments for the presence of severe magnetic resonance imaging-visible perivascular spaces in the centrum semiovale, lobar cerebral microbleeds, age, and total WMH burden led to a progressive decline in correlation. The largest reduction occurred after adjusting for age (tau-b=0.307; <i>P</i>=0.0484) indicating its role as a potential confounder. In the fully adjusted model, the association remained significant (tau-b=0.316; <i>P</i>=0.0423), suggesting a partially independent relationship between WMH multispot lesions count and whole cortex amyloid burden. The results were consistent in a subanalysis within the probable CAA.</p><p><strong>Conclusions: </strong>This pilot study suggests a positive association between cerebrovascular amyloid deposition and WMH multispot lesions in CAA, with potential pathophysiological and clinical implications. These exploratory observations require confirmation in larger studies.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":""},"PeriodicalIF":7.8000,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Stroke","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1161/STROKEAHA.125.051482","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: We investigated the relationship between white matter hyperintensity (WMH) multispot pattern lesions, a supporting magnetic resonance imaging marker of cerebral amyloid angiopathy (CAA), and positron emission tomography-based amyloid-β burden across a range of cerebrovascular amyloid deposition.
Methods: Twenty-one nondemented subjects (11 patients with probable CAA; median age, 71 [63-77] years; 82% males; and 10 healthy subjects; median age, 63.5 [61-68] years; 50% males) underwent brain magnetic resonance imaging and 11C-Pittsburgh compound B-positron emission tomography imaging. WMH multispot lesions were evaluated on FLAIR sequences. The association between whole cortex 11C-Pittsburgh compound B binding and WMH multispot lesions count was assessed using Kendall tau, adjusting for key markers of CAA through a hierarchical residualization approach.
Results: The unadjusted analysis showed a positive correlation between WMH multispot lesions count and whole cortex 11C-Pittsburgh compound B binding (tau-b=0.495; P=0.0017). Sequential adjustments for the presence of severe magnetic resonance imaging-visible perivascular spaces in the centrum semiovale, lobar cerebral microbleeds, age, and total WMH burden led to a progressive decline in correlation. The largest reduction occurred after adjusting for age (tau-b=0.307; P=0.0484) indicating its role as a potential confounder. In the fully adjusted model, the association remained significant (tau-b=0.316; P=0.0423), suggesting a partially independent relationship between WMH multispot lesions count and whole cortex amyloid burden. The results were consistent in a subanalysis within the probable CAA.
Conclusions: This pilot study suggests a positive association between cerebrovascular amyloid deposition and WMH multispot lesions in CAA, with potential pathophysiological and clinical implications. These exploratory observations require confirmation in larger studies.
期刊介绍:
Stroke is a monthly publication that collates reports of clinical and basic investigation of any aspect of the cerebral circulation and its diseases. The publication covers a wide range of disciplines including anesthesiology, critical care medicine, epidemiology, internal medicine, neurology, neuro-ophthalmology, neuropathology, neuropsychology, neurosurgery, nuclear medicine, nursing, radiology, rehabilitation, speech pathology, vascular physiology, and vascular surgery.
The audience of Stroke includes neurologists, basic scientists, cardiologists, vascular surgeons, internists, interventionalists, neurosurgeons, nurses, and physiatrists.
Stroke is indexed in Biological Abstracts, BIOSIS, CAB Abstracts, Chemical Abstracts, CINAHL, Current Contents, Embase, MEDLINE, and Science Citation Index Expanded.