Hypertension, intracranial arteriosclerosis, and structural brain changes in patients with TIA or ischemic stroke.

IF 4.5 3区 医学 Q1 CLINICAL NEUROLOGY
European Stroke Journal Pub Date : 2025-09-01 Epub Date: 2024-12-30 DOI:10.1177/23969873241307099
Xi Li, Bernhard P Berghout, Gijs van Rooijen, Mohammad Kamran Ikram, Bob Roozenbeek, Daniel Bos
{"title":"Hypertension, intracranial arteriosclerosis, and structural brain changes in patients with TIA or ischemic stroke.","authors":"Xi Li, Bernhard P Berghout, Gijs van Rooijen, Mohammad Kamran Ikram, Bob Roozenbeek, Daniel Bos","doi":"10.1177/23969873241307099","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Hypertension is a major risk factor of structural brain changes, including atrophy and cerebral small vessel disease. Intracranial arteriosclerosis could be an underlying mechanism between hypertension and structural brain changes. This study investigated whether intracranial carotid artery calcification (ICAC), as a proxy for intracranial arteriosclerosis, explains the association between hypertension and structural brain changes in patients with TIA or ischemic stroke.</p><p><strong>Patients and methods: </strong>About 968 patients (mean age 62.7 years) with TIA or ischemic stroke from a registry who underwent non-contrast CT (NCCT) and CT-angiography (CTA) were included in this study. Presence and volume (mm<sup>3</sup>) of ICAC were assessed on CTA. Subtypes of ICAC were assessed on NCCT, where ICAC was categorized into intimal and internal elastic lamina (IEL) type calcification. Structural brain changes, indicated by atrophy, periventricular and deep white matter lesions (WML), and lacunes were assessed on NCCT. Mediation analysis was performed using ICAC, ICAC volume, and ICAC subtypes as mediators.</p><p><strong>Results: </strong>ICAC was prevalent in 67.8% of patients, with 52.6% of them exhibiting intimal calcification, and 26.5% exhibiting IEL calcification. Atrophy, periventricular WML, deep WML, and lacunes were present in 48.1%, 56.4%, 43.0% and 17.1% of patients respectively. The presence of ICAC explained 7.1% of the association of hypertension with periventricular WML, 3.6% with deep WML, and 17.6% with lacunes. Hypertension was associated with increased atrophy through ICAC (OR: 1.02, 95% CI: 1.00-1.05). In subgroup analyses, IEL calcification partly explained the association between hypertension and periventricular WML (16.8%), and atrophy (OR: 1.12, 95% CI: 1.02-1.27). Intimal calcification did not explain any association.</p><p><strong>Conclusion: </strong>ICAC partially explained the association between hypertension and atrophy, periventricular and deep WML, and lacunes. Although intimal calcification was more prevalent in ischemic stroke patients, IEL calcification takes the leading role in explaining the association between hypertension and structural brain changes.</p>","PeriodicalId":46821,"journal":{"name":"European Stroke Journal","volume":"10 3","pages":"804-812"},"PeriodicalIF":4.5000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683788/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Stroke Journal","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/23969873241307099","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/12/30 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Introduction: Hypertension is a major risk factor of structural brain changes, including atrophy and cerebral small vessel disease. Intracranial arteriosclerosis could be an underlying mechanism between hypertension and structural brain changes. This study investigated whether intracranial carotid artery calcification (ICAC), as a proxy for intracranial arteriosclerosis, explains the association between hypertension and structural brain changes in patients with TIA or ischemic stroke.

Patients and methods: About 968 patients (mean age 62.7 years) with TIA or ischemic stroke from a registry who underwent non-contrast CT (NCCT) and CT-angiography (CTA) were included in this study. Presence and volume (mm3) of ICAC were assessed on CTA. Subtypes of ICAC were assessed on NCCT, where ICAC was categorized into intimal and internal elastic lamina (IEL) type calcification. Structural brain changes, indicated by atrophy, periventricular and deep white matter lesions (WML), and lacunes were assessed on NCCT. Mediation analysis was performed using ICAC, ICAC volume, and ICAC subtypes as mediators.

Results: ICAC was prevalent in 67.8% of patients, with 52.6% of them exhibiting intimal calcification, and 26.5% exhibiting IEL calcification. Atrophy, periventricular WML, deep WML, and lacunes were present in 48.1%, 56.4%, 43.0% and 17.1% of patients respectively. The presence of ICAC explained 7.1% of the association of hypertension with periventricular WML, 3.6% with deep WML, and 17.6% with lacunes. Hypertension was associated with increased atrophy through ICAC (OR: 1.02, 95% CI: 1.00-1.05). In subgroup analyses, IEL calcification partly explained the association between hypertension and periventricular WML (16.8%), and atrophy (OR: 1.12, 95% CI: 1.02-1.27). Intimal calcification did not explain any association.

Conclusion: ICAC partially explained the association between hypertension and atrophy, periventricular and deep WML, and lacunes. Although intimal calcification was more prevalent in ischemic stroke patients, IEL calcification takes the leading role in explaining the association between hypertension and structural brain changes.

Abstract Image

Abstract Image

Abstract Image

TIA或缺血性脑卒中患者的高血压、颅内动脉硬化和脑结构改变。
简介:高血压是脑结构改变的主要危险因素,包括脑萎缩和脑血管疾病。颅内动脉硬化可能是高血压与脑结构改变之间的潜在机制。本研究探讨了颅内颈动脉钙化(ICAC)作为颅内动脉硬化的代表,是否解释了TIA或缺血性卒中患者高血压与脑结构改变之间的关系。患者和方法:约968例TIA或缺血性卒中患者(平均年龄62.7岁)接受了非对比CT (NCCT)和CT血管造影(CTA),纳入本研究。在CTA上评估廉政公署的存在和体积(mm3)。在NCCT上评估了ICAC的亚型,其中将ICAC分为内膜和内弹性层(IEL)型钙化。在NCCT上评估脑结构变化,表现为萎缩,脑室周围和深部白质病变(WML),以及凹窝。采用ICAC、ICAC volume和ICAC亚型作为中介进行中介分析。结果:67.8%的患者出现了ICAC,其中52.6%表现为内膜钙化,26.5%表现为IEL钙化。萎缩、脑室周围WML、深部WML和腔隙分别占48.1%、56.4%、43.0%和17.1%。ICAC的存在解释了7.1%的高血压与室周WML相关,3.6%与深部WML相关,17.6%与腔隙相关。通过ICAC,高血压与萎缩增加相关(OR: 1.02, 95% CI: 1.00-1.05)。在亚组分析中,IEL钙化部分解释了高血压与心室周围WML(16.8%)和萎缩之间的关联(OR: 1.12, 95% CI: 1.02-1.27)。内膜钙化不能解释任何关联。结论:ICAC部分解释了高血压与脑萎缩、脑室周围、深部WML和脑陷窝的关系。虽然在缺血性卒中患者中内膜钙化更为普遍,但IEL钙化在解释高血压与脑结构改变之间的关系中起主要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
7.50
自引率
6.60%
发文量
102
期刊介绍: Launched in 2016 the European Stroke Journal (ESJ) is the official journal of the European Stroke Organisation (ESO), a professional non-profit organization with over 1,400 individual members, and affiliations to numerous related national and international societies. ESJ covers clinical stroke research from all fields, including clinical trials, epidemiology, primary and secondary prevention, diagnosis, acute and post-acute management, guidelines, translation of experimental findings into clinical practice, rehabilitation, organisation of stroke care, and societal impact. It is open to authors from all relevant medical and health professions. Article types include review articles, original research, protocols, guidelines, editorials and letters to the Editor. Through ESJ, authors and researchers have gained a new platform for the rapid and professional publication of peer reviewed scientific material of the highest standards; publication in ESJ is highly competitive. The journal and its editorial team has developed excellent cooperation with sister organisations such as the World Stroke Organisation and the International Journal of Stroke, and the American Heart Organization/American Stroke Association and the journal Stroke. ESJ is fully peer-reviewed and is a member of the Committee on Publication Ethics (COPE). Issues are published 4 times a year (March, June, September and December) and articles are published OnlineFirst prior to issue publication.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信