University of Miami, 1120 NW 14th Street, Suite 1357, Miami, FL 33136, USA.
The University of Chicago, Chicago, IL, USA.
J Stroke Cerebrovasc Dis. 2021 Feb;30(2):105504. doi: 10.1016/j.jstrokecerebrovasdis.2020.105504. Epub 2020 Dec 1.
Intracranial atherosclerotic disease (ICAD) is a common cause of ischemic stroke with a high risk of clinical stroke recurrence. Multiple mechanisms may underlie cerebral ischemia in this condition. The study's objective is to discern the mechanisms of recurrent ischemia in ICAD through imaging biomarkers of impaired antegrade flow, poor distal perfusion, abnormal vasoreactivity, and artery-to-artery embolism.
This prospective multicenter observational study enrolled patients with recent (≤21 days) ischemic stroke or transient ischemic attack (TIA) caused by ICAD with 50-99% stenosis treated medically. We obtained baseline quantitative MRA (QMRA), perfusion MRI (PWI), transcranial Doppler vasoreactivity (VMR), and emboli detection studies (EDS). The primary outcome was ischemic stroke in the territory of the stenotic artery within 1 year of follow-up; secondary outcomes were TIA at 1 year and new infarcts in the territory on MRI at 6-8 weeks.
Amongst 102 of 105 participants with clinical follow-up (mean 253±131 days), the primary outcome occurred in 8.8% (12.7/100 patient-years), while 5.9% (8.5/100 patient-years) had a TIA. A new infarct in the territory of the symptomatic artery was noted in 24.7% at 6-8 weeks. A low flow state on QMRA was noted in 25.5%, poor distal perfusion on PWI in 43.5%, impaired vasoreactivity on VMR in 67.5%, and microemboli on EDS in 39.0%. No significant association was identified between these imaging biomarkers and primary or secondary outcomes.
Despite intensive medical management in ICAD, there is a high risk of clinical cerebrovascular events at 1 year and an even higher risk of new imaging-evident infarcts in the subacute period after index stroke. Hemodynamic and plaque instability biomarkers did not identify a higher risk group. Further work is needed to identify mechanisms of ischemic stroke and infarct recurrence and their consequence on long-term physical and cognitive outcomes.
ClinicalTrials.gov: NCT02121028.
颅内动脉粥样硬化性疾病(ICAD)是缺血性卒中的常见病因,其临床卒中复发风险较高。在这种情况下,可能存在多种导致脑缺血的机制。本研究旨在通过对前向血流受损、远端灌注不良、血管反应性异常和动脉到动脉栓塞等影像生物标志物进行识别,以了解 ICAD 中复发性缺血的机制。
本前瞻性多中心观察性研究纳入了近期(≤21 天)由狭窄 50%-99%的 ICAD 导致的缺血性卒中和短暂性脑缺血发作(TIA)的患者,这些患者接受了药物治疗。我们获得了基线定量磁共振血管造影(QMRA)、灌注磁共振成像(PWI)、经颅多普勒血管反应性(VMR)和栓子检测研究(EDS)。主要结局是在随访 1 年内,狭窄动脉供血区发生缺血性卒中;次要结局是在 1 年内发生 TIA,以及在 6-8 周时 MRI 上显示新的梗死灶。
在 105 名接受临床随访的患者中有 102 名(平均随访 253±131 天),主要结局发生在 8.8%(100 患者-年中有 12.7 例),而 5.9%(100 患者-年中有 8.5 例)发生了 TIA。在症状性动脉供血区,6-8 周时发现新的梗死灶的比例为 24.7%。QMRA 显示低血流状态的比例为 25.5%,PWI 显示远端灌注不良的比例为 43.5%,VMR 显示血管反应性受损的比例为 67.5%,EDS 显示微栓子的比例为 39.0%。这些影像学标志物与主要或次要结局之间未发现显著关联。
尽管对 ICAD 进行了强化药物治疗,但在 1 年内仍有发生临床脑血管事件的高风险,在指数性卒中后亚急性期甚至有更高的新影像学证实的梗死灶风险。血流动力学和斑块不稳定性生物标志物未能识别出更高危的患者群体。需要进一步研究以确定缺血性卒中和梗死复发的机制及其对长期身体和认知结局的影响。
ClinicalTrials.gov:NCT02121028。