BackgroundIt has been shown that intracranial atherosclerotic stenosis (ICAS) has heterogeneous features in terms of plaque instability and vascular remodeling. Therefore, quantitative information on the changes of intracranial atherosclerosis and lenticulostriate arteries (LSAs) may potentially improve understanding of the pathophysiological mechanisms underlying stroke and may guide the treatment and work-up strategies. Our present study aimed to use a novel whole-brain high-resolution cardiovascular magnetic resonance imaging (WB-HRCMR) to assess both ICAS plaques and LSAs in recent stroke patients.MethodsTwenty-nine symptomatic and 23 asymptomatic ICAS patients were enrolled in this study from Jan 2015 through Sep 2017 and all patients underwent WB-HRCMR. Intracranial atherosclerotic plaque burden, plaque enhancement volume, plaque enhancement index, as well as the number and length of LSAs were evaluated in two groups. Enhancement index was calculated as follows: ([Signal intensity (SI)plaque/SInormal wall on post-contrast imaging] − [SIplaque/SInormal wall on matched pre-contrast imaging])/(SIplaque / SInormal wall on matched pre-contrast imaging). Logistic regression analysis was used to investigate the independent high risk plaque and LSAs features associated with stroke.ResultsSymptomatic ICAS patients exhibited larger enhancement plaque volume (20.70 ± 3.07 mm3 vs. 6.71 ± 1.87 mm3
P = 0.001) and higher enhancement index (0.44 ± 0.08 vs. 0.09 ± 0.06 P = 0.001) compared with the asymptomatic ICAS. The average length of LSAs in symptomatic ICAS (20.95 ± 0.87 mm) was shorter than in asymptomatic ICAS (24.04 ± 0.95 mm) (P = 0.02). Regression analysis showed that the enhancement index (100.43, 95% CI − 4.02-2510.96; P = 0.005) and the average length of LSAs (0.80, 95% CI − 0.65-0.99; P = 0.036) were independent factors for predicting of stroke.ConclusionWB-HRCMR enabled the comprehensive quantitative evaluation of intracranial atherosclerotic lesions and perforating arteries. Symptomatic ICAS had distinct plaque characteristics and shorter LSA length compared with asymptomatic ICAS.
Statins have proven to exert protective effects in patients with symptomatic intracranial atherosclerotic stenosis (SICAS). It is unclear whether intensive lipid-lowering therapy (ILLT) can ameliorate atherosclerosis in asymptomatic ICAS (AICAS). A single-center, prospective cohort study was performed in 71 AICAS patients with lipid-lowering therapy. Vascular stenoses were evaluated with transcranial color-coded sonography (TCCS) before and after statin treatment. With target therapeutic level of low-density lipoprotein cholesterol (LDL-C) ≤ 1.8 mmol/L or ≥ 50% reduction from baseline after the two years of follow-up, patients were divided into intensive statin treatment (IST) group and standard statin treatment (SST) group. A total of 104 stenotic intracranial arteries were detected in 51 patients belonging to the IST group and 47 arteries in 20 patients of the SST group. In the first year, LDL-C levels were significantly decreased in the IST compared with SST groups (1.48 ± 0.26
vs.
2.20 ± 0.58, P=0.000). However, the ratio of regressed ICAS in IST was not significantly higher than that in SST (26.3%
vs.
5.9%, P=0.052). Forty-nine branches in 25 patients of the IST group and 16 branches in 7 patients of the SST group were followed up for two years. The LDL-C level was decreased in the IST compared with SST groups (1.55 ± 0.29
vs.
2.36 ± 0.77, P=0.048). The ratio of regressed ICAS in the IST group was significantly higher than that in SST group (34.7%
vs.
6.3%, P=0.017). We concluded that the degree of stenosis in AICAS can be ameliorated with intensive lipid-lowering therapy within two years; target LDL-C level can be reached by moderate-intensity statin treatment for Chinese AICAS patients.
Introduction:
Intracranial atherosclerotic disease (ICAD) is one of the most common causes of ischemic stroke worldwide. Despite aggressive medical management, the rate of recurrent stroke is 13% at 1 year. Intracranial vessel wall imaging (VWI) is a noninvasive,
“looking-beyond-the-lumen”
imaging method that can directly characterize the geometric and signal features of ICAD lesions. The present work sought to assess the feasibility of quantitatively monitoring regression or progression of ICAD plaques using VWI-based methods.
Methods:
Eight ischemic stroke patients (1F, 7M; age 27-66 ys) treated with intensive medical therapy underwent initial (4 days - 4 months of onset) and follow-up 3D VWI (6-13 months). Images were randomized and reviewed by two neuroradiologists to determine the culprit lesion in each subject. A custom-designed deep-learning-based intracranial vessel analysis method was used to segment vessel wall boundaries and quantify the following features of the culprit lesion, including peak normalized wall index (NWI), plaque volume, pre-contrast plaque-wall contrast ratio (CR), and post-contrast plaque enhancement ratio (ER).
Results:
No subjects except for subject #4 had a recurrent stroke during the follow-up period. The four plaque features exhibited different change patterns as shown in
Figure
. Subject #1 and #4 demonstrated an increase in plaque ER, volume, and peak NWI; subject #7 demonstrated an increase in plaque CR, volume and peak NWI. Other patients had a decrease or no change in these features.
Conclusions:
In this work, the interrogated plaque features demonstrated regression in most of patients after intensive medical therapy. Elevated values in some of these features appeared positively associated with stroke recurrence. Temporal changes in these features may have a strong indication on culprit lesions’ response to medical therapy. In conclusion, it is feasible to quantitatively monitor plaque-level treatment response.
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