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计算机断层扫描灌注中高缺血性缺损是大动脉炎脑血管缺血事件的危险因素:一项前瞻性观察研究。

High ischemic deficit in computed tomography perfusion is a risk factor for cerebral vascular ischemic events in Takayasu arteritis: a prospective observational study.

作者信息

Chen Rongyi, Sun Ying, Liu Ying, Ding Jing, Jiang Lindi

机构信息

Department of Rheumatology, Zhongshan Hospital Fudan University, No.180, Fenglin Road, Xuhui District, Shanghai, 200032, China.

Center of Evidence-based Medicine, Fudan University, Shanghai, 200032, China.

出版信息

BMC Rheumatol. 2025 Aug 13;9(1):100. doi: 10.1186/s41927-025-00551-6.

DOI:10.1186/s41927-025-00551-6
PMID:40804749
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12344923/
Abstract

BACKGROUND

Patients suffering from Takayasu arteritis (TA) with stenosis or occlusion of supra-aortic trunks carry a high risk of cerebral vascular ischemic events (CVIEs). We explored the relationship between cerebral blood perfusion and CVIEs in TA.

METHODS

Patients with involvement of supra-aortic trunks undergoing computed tomographic perfusion (CTP) were enrolled. The primary endpoint was CVIEs. The secondary endpoint was a poor outcome (modified Rankin scale, mRS > 3). The relationship between CTP parameters, ischemic deficit (time to maximum, T >6 s) and ischemic core (cerebral blood flow, CBF < 30%), CVIEs, and a poor outcome during follow-up was analyzed with Spearman correlation, Cox regression, cluster analysis, and Kaplan–Meier curves.

RESULTS

Eighty-one patients were enrolled. The median volume of the ischemic deficit was 2.5 (IQR 0–34.1) mL. The ischemic deficit was related to a previous ischemic stroke, abnormal vision, and vertebral-artery stenosis (all  < 0.05). During a median follow-up of 16.0 (IQR 3.0–29.0) months, 16 cases suffered CVIEs, including ischemic stroke (11 cases, 68.8%), ablepsia (six, 37.5%), death (three, 18.8%), other worsening cerebral ischemic symptoms (three, 18.8%). The CVIEs were independently associated with the ischemic deficit (hazard ratio, HR = 15.66[4.09–59.96],  < 0.001), hemoglobin (HR = 0.96[0.93–0.99],  = 0.003), and tocilizumab use (HR = 5.71[1.63–20.00],  < 0.001). The AUC of the ischemic deficit to predict CVIEs was 0.79 (95%CI = 62.07–95.62) at 1 year and 0.81 (95%CI = 0.65–0.96) at 3 years, respectively. Furthermore, patients could be clustered into three groups. Cluster 1 (inflammation type) and cluster 2 (non-inflammation type) shared a similar risk for CVIEs. Cluster 3 (inflammation with low-perfusion type) carried the highest risk for a CVIE (HR 35.21[4.63–267.58],  < 0.001) compared with cluster 1. Kaplan–Meier curves revealed that patients with high ischemic deficit or belonging to cluster 3 carried a higher risk of CVIEs or a poor outcome.

CONCLUSIONS

The high ischemic deficit is a risk factor for CVIEs in TA with involvement of supra-aortic trunks. Patients with inflammation and high ischemic deficit carry a high risk of suffering CVIEs and a poor outcome during follow-up.

RETROSPECTIVELY REGISTERED. TRIAL REGISTRATION: ClinicalTrials.gov NCT03893136

REGISTRATION DATE

2019-03-25.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1186/s41927-025-00551-6.

摘要

背景

患有Takayasu动脉炎(TA)且主动脉弓上分支存在狭窄或闭塞的患者发生脑血管缺血事件(CVIEs)的风险很高。我们探讨了TA患者脑血流灌注与CVIEs之间的关系。

方法

纳入接受计算机断层扫描灌注(CTP)检查且主动脉弓上分支受累的患者。主要终点是CVIEs。次要终点是不良结局(改良Rankin量表,mRS>3)。采用Spearman相关性分析、Cox回归分析、聚类分析和Kaplan–Meier曲线分析CTP参数、缺血性缺损(达峰时间,T>6秒)和缺血核心(脑血流量,CBF<30%)与随访期间CVIEs及不良结局之间的关系。

结果

共纳入81例患者。缺血性缺损的中位数体积为2.5(IQR 0–34.1)mL。缺血性缺损与既往缺血性卒中、视力异常和椎动脉狭窄相关(均P<0.05)。在中位随访期16.0(IQR 3.0–29.0)个月期间,16例发生CVIEs,包括缺血性卒中(11例,68.8%)、失明(6例,37.5%)、死亡(3例,18.8%)、其他脑缺血症状恶化(3例,18.8%)。CVIEs与缺血性缺损(风险比,HR = 15.66[4.09–59.96],P<0.001)、血红蛋白(HR = 0.96[0.93–0.99],P = 0.003)和使用托珠单抗(HR = 5.71[1.63–20.00],P<0.001)独立相关。缺血性缺损预测CVIEs的1年AUC为0.79(95%CI = 62.07–95.62),3年AUC为0.81(95%CI = 0.65–0.96)。此外,患者可分为三组。第1组(炎症型)和第2组(非炎症型)发生CVIEs的风险相似。与第1组相比,第3组(炎症伴低灌注型)发生CVIEs的风险最高(HR 35.2[4.63–267.58],P<0.001)。Kaplan–Meier曲线显示,缺血性缺损高或属于第3组的患者发生CVIEs或不良结局的风险更高。

结论

高缺血性缺损是主动脉弓上分支受累的TA患者发生CVIEs的危险因素。炎症且缺血性缺损高的患者在随访期间发生CVIEs和不良结局的风险很高。

回顾性注册。试验注册:ClinicalTrials.gov NCT03893136

注册日期

2019年3月25日。

补充信息

在线版本包含可在10.1186/s41927-025-00551-6获取的补充材料。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd5c/12344923/176c1c5f7a01/41927_2025_551_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd5c/12344923/27e92b27eb8e/41927_2025_551_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd5c/12344923/57786738679e/41927_2025_551_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd5c/12344923/176c1c5f7a01/41927_2025_551_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd5c/12344923/27e92b27eb8e/41927_2025_551_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd5c/12344923/57786738679e/41927_2025_551_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd5c/12344923/176c1c5f7a01/41927_2025_551_Fig3_HTML.jpg

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