Ogawa Ito Ai, Shindo Akihiro, Ii Yuichiro, Matsuura Keita, Tabei Ken-Ichi, Maeda Masayuki, Umino Maki, Suzuki Yume, Shiba Masato, Toma Naoki, Suzuki Hidenori, Tomimoto Hidekazu
Department of Neurology, Mie University Graduate School of Medicine, Tsu, Japan.
Department of Neurology, Mie University Graduate School of Medicine, Tsu, Japan,
Cerebrovasc Dis Extra. 2019;9(2):57-65. doi: 10.1159/000500112. Epub 2019 Jun 14.
Since the advent of magnetic resonance imaging technology, cerebral microbleeds can be diagnosed in vivo. However, the underlying mechanism of cerebral microbleed formation is not fully understood.
This study aimed to identify the factors associated with cerebral microbleeds after carotid artery stenting (CAS).
We retrospectively examined 125 patients who underwent CAS for carotid stenosis. Cerebral microbleeds were investigated using T2*-weighted gradient-echo (GRE) imaging before and after CAS. We analyzed the possible association of new microbleeds with the following risk factors: the number of baseline microbleeds and ischemic cerebral lesions, the occurrence of cerebral hyperperfusion syndrome, and new ischemic cerebral lesions after CAS.
Baseline cerebral microbleeds were detected in 53 patients (42.4%). New cerebral microbleeds after CAS were observed in 13 of 125 patients (10.4%) and were exclusively associated with new ischemic lesions but not with other risk factors. No patient showed a merged image of a new cerebral microbleed on GRE imaging or a new ischemic lesion on diffusion-weighted imaging. Lobar and deep microbleeds were noted in 12/13 (92.3%) and 1 patient (7.7%), respectively. Of 12 patients with new microbleeds, 10 (76.9%) and 2 (15.4%) had a new microbleed in the ipsilateral and contralateral hemispheres, respectively.
We found that new cerebral microbleeds developed after CAS and that these might be associated with new ischemic lesions, mostly in the territory of the treated carotid artery. We speculate that these microbleeds result from the deoxygenation of hemoglobin in the embolus or, alternatively, small hemorrhagic transformation of ischemic lesions.
自磁共振成像技术问世以来,脑微出血可在体内被诊断出来。然而,脑微出血形成的潜在机制尚未完全明确。
本研究旨在确定颈动脉支架置入术(CAS)后脑微出血的相关因素。
我们回顾性研究了125例因颈动脉狭窄接受CAS的患者。在CAS前后使用T2*加权梯度回波(GRE)成像对脑微出血进行检查。我们分析了新出现的微出血与以下危险因素的可能关联:基线微出血和缺血性脑病变的数量、脑过度灌注综合征的发生情况以及CAS后新出现的缺血性脑病变。
53例患者(42.4%)检测到基线脑微出血。125例患者中有13例(10.4%)在CAS后出现新的脑微出血,且仅与新的缺血性病变相关,与其他危险因素无关。没有患者在GRE成像上显示新的脑微出血与扩散加权成像上的新缺血性病变合并的图像。叶性和深部微出血分别见于12/13例(92.3%)和1例(7.7%)。在12例有新微出血的患者中,10例(76.9%)和2例(15.4%)分别在同侧和对侧半球出现新的微出血。
我们发现CAS后会出现新的脑微出血,且这些微出血可能与新的缺血性病变相关,主要发生在接受治疗的颈动脉供血区域。我们推测这些微出血是由栓子中血红蛋白的脱氧作用引起的,或者是缺血性病变的小出血性转化所致。