Monash Cardiovascular Research Centre, Victorian Heart Institute, Monash University and MonashHeart, Monash Health, Clayton, VIC, Australia.
Department of Medicine, Monash University, Clayton, VIC, Australia.
Int J Stroke. 2023 Aug;18(7):829-838. doi: 10.1177/17474930231158538. Epub 2023 Mar 2.
Spontaneous cervical artery dissection (sCAD) is a leading cause of ischemic stroke in young patients. Studies using high-resolution magnetic resonance imaging and positron emission tomography have suggested vessel wall inflammation to be a pathogenic factor in sCAD. Computed tomography (CT) attenuation of perivascular adipose tissue (PVAT) is an established non-invasive imaging biomarker of inflammation in coronary arteries, with higher attenuation values reflecting a greater degree of vascular inflammation.
We evaluate the CT attenuation of PVAT surrounding the internal carotid artery (PVAT) with and without spontaneous dissection.
Single-center prospective observational study of 56 consecutive patients with CT-verified spontaneous dissection of the internal carotid artery (ICA). Of these patients, six underwent follow-up computed tomography angiography (CTA). Twenty-two patients who underwent CTA for acute neurological symptoms but did not have dissection formed the control group. Using semi-automated research software, PVAT was measured as the mean Hounsfield unit (HU) attenuation of adipose tissue within a defined volume of interest surrounding the ICA.
PVAT was significantly higher around dissected ICA compared with non-dissected contralateral ICA in the same patients (-58.7 ± 10.2 vs -68.9 ± 8.1 HU, < 0.0001) and ICA of patients without dissection (-58.7 ± 10.2 vs -69.3 ± 9.3 HU, < 0.0001). After a median follow-up of 89 days, there was a significant reduction in PVAT around dissected ICA (-57.5 ± 13.4 to -74.3 ± 10.5 HU, < 0.05), while no change was observed around non-dissected contralateral ICA (-71.0 ± 4.4 to -74.1 ± 4.1 HU, = 0.19). ICA dissection was an independent predictor of PVAT following multivariable adjustment for age and the presence of ICA occlusion.
PVAT is elevated in the presence of sCAD and may decrease following the acute event.
自发性颈内动脉夹层(sCAD)是年轻患者缺血性脑卒中的主要原因。使用高分辨率磁共振成像和正电子发射断层扫描的研究表明,血管壁炎症是 sCAD 的致病因素。计算机断层扫描(CT)测量血管周围脂肪组织(PVAT)衰减是冠状动脉炎症的一种既定的非侵入性成像生物标志物,较高的衰减值反映了更大程度的血管炎症。
我们评估了颈内动脉(ICA)周围的 PVAT(PVAT)的 CT 衰减与自发性动脉夹层的存在与否。
对 56 例经 CT 证实的颈内动脉自发性夹层患者进行单中心前瞻性观察性研究。其中 6 例患者进行了随访 CT 血管造影(CTA)。22 例因急性神经症状而行 CTA 但无夹层的患者作为对照组。使用半自动研究软件,通过定义在颈内动脉周围的感兴趣容积内的脂肪组织的平均亨斯菲尔德单位(HU)衰减值来测量 PVAT。
与同一患者的未夹层对侧颈内动脉相比,夹层颈内动脉周围的 PVAT 明显更高(-58.7±10.2 对-68.9±8.1 HU,<0.0001),也高于无夹层患者的颈内动脉(-58.7±10.2 对-69.3±9.3 HU,<0.0001)。在中位数为 89 天的随访后,夹层颈内动脉周围的 PVAT 明显减少(-57.5±13.4 对-74.3±10.5 HU,<0.05),而未夹层对侧颈内动脉周围的 PVAT 没有变化(-71.0±4.4 对-74.1±4.1 HU,=0.19)。在多变量调整年龄和颈内动脉闭塞后,颈内动脉夹层是 PVAT 的独立预测因子。
sCAD 存在时 PVAT 升高,急性事件后可能会降低。