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短暂性脑缺血发作(TIA)或缺血性卒中患者的高血压、颅内动脉硬化和脑结构改变。

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

作者信息

Li Xi, Berghout Bernhard P, van Rooijen Gijs, Ikram Mohammad Kamran, Roozenbeek Bob, Bos Daniel

机构信息

Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands.

Department of Public Health, Erasmus University Medical Center, Rotterdam, The Netherlands.

出版信息

Eur Stroke J. 2025 Sep;10(3):804-812. doi: 10.1177/23969873241307099. Epub 2024 Dec 30.

DOI:10.1177/23969873241307099
PMID:40936340
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11683788/
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 (mm) 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.

摘要

引言

高血压是脑部结构改变的主要危险因素,包括萎缩和脑小血管疾病。颅内动脉硬化可能是高血压与脑部结构改变之间的潜在机制。本研究调查了作为颅内动脉硬化替代指标的颅内颈动脉钙化(ICAC)是否能解释短暂性脑缺血发作(TIA)或缺血性中风患者中高血压与脑部结构改变之间的关联。

患者与方法

本研究纳入了约968例来自登记处的TIA或缺血性中风患者(平均年龄62.7岁),这些患者接受了非增强CT(NCCT)和CT血管造影(CTA)检查。在CTA上评估ICAC的存在情况和体积(mm)。在NCCT上评估ICAC的亚型,其中ICAC被分为内膜和内弹性膜(IEL)型钙化。在NCCT上评估由萎缩、脑室周围和深部白质病变(WML)以及腔隙所指示的脑部结构改变。使用ICAC、ICAC体积和ICAC亚型作为中介进行中介分析。

结果

67.8%的患者存在ICAC,其中52.6%表现为内膜钙化,26.5%表现为IEL钙化。分别有48.1%、56.4%、43.0%和17.1%的患者存在萎缩、脑室周围WML、深部WML和腔隙。ICAC的存在解释了高血压与脑室周围WML关联的7.1%、与深部WML关联的3.6%以及与腔隙关联的17.6%。高血压通过ICAC与萎缩增加相关(比值比:1.02,95%置信区间:1.00 - 1.05)。在亚组分析中,IEL钙化部分解释了高血压与脑室周围WML(16.8%)以及萎缩(比值比:1.12,95%置信区间:1.02 - 1.27)之间的关联。内膜钙化未解释任何关联。

结论

ICAC部分解释了高血压与萎缩、脑室周围和深部WML以及腔隙之间的关联。尽管内膜钙化在缺血性中风患者中更为常见,但IEL钙化在解释高血压与脑部结构改变之间的关联中起主导作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afcb/12420999/0dcdb77f92e4/10.1177_23969873241307099-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afcb/12420999/6816a69ff816/10.1177_23969873241307099-img2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afcb/12420999/c4d96b9605e0/10.1177_23969873241307099-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afcb/12420999/0dcdb77f92e4/10.1177_23969873241307099-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afcb/12420999/6816a69ff816/10.1177_23969873241307099-img2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afcb/12420999/c4d96b9605e0/10.1177_23969873241307099-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afcb/12420999/0dcdb77f92e4/10.1177_23969873241307099-fig2.jpg

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