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Identification of high-risk plaque features in intracranial atherosclerosis: initial experience using a radiomic approach.

ABSTRACT: OBJECTIVES:To evaluate a quantitative radiomic approach based on high-resolution magnetic resonance imaging (HR-MRI) to differentiate acute/sub-acute symptomatic basilar artery plaque from asymptomatic plaque. METHODS:Ninety-six patients with basilar artery stenosis underwent HR-MRI between January 2014 and December 2016. Patients were scanned with T1- and T2-weighted imaging, as well as T1 imaging following gadolinium-contrast injection (CE-T1). The stenosis value, plaque area/burden, lumen area, minimal luminal area (MLA), intraplaque haemorrhage (IPH), contrast enhancement ratio and 94 quantitative radiomic features were extracted and compared between acute/sub-acute and asymptomatic patients. Multi-variate logistic analysis and a random forest model were used to evaluate the diagnostic performance. RESULTS:IPH, MLA and enhancement ratio were independently associated with acute/subacute symptoms. Radiomic features in T1 and CE-T1 images were associated with acute/subacute symptoms, but the features from T2 images were not. The combined IPH, MLA and enhancement ratio had an area under the curve (AUC) of 0.833 for identifying acute/sub-acute symptomatic plaques, and the combined T1 and CE-T1 radiomic approach had a significantly higher AUC of 0.936 (p = 0.01). Combining all features achieved an AUC of 0.974 and accuracy of 90.5%. CONCLUSIONS:Radiomic analysis of plaque texture on HR-MRI accurately distinguished between acutely symptomatic and asymptomatic basilar plaques. KEY POINTS:• High-resolution magnetic resonance imaging can assess basilar artery atherosclerotic plaque. • Radiomic features in T1 and CE-T1 images are associated with acute symptoms. • Radiomic analysis can accurately distinguish between acute symptomatic and asymptomatic plaque. • The highest accuracy may be achieved by combining radiomic and conventional features.

SUBMITTER: Shi Z

PROVIDER: S-EPMC6081255 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundIntracranial artery dissection (IAD) often causes headache and cerebral vascular ischemic events. The imaging characteristics of IAD remain unclear. This study aims to characterize the appearance of culprit and non-culprit IAD using high-resolution cardiovascular magnetic resonance imaging (hrCMR) and quantify the incremental value of hrCMR in identifying higher risk lesions.MethodsImaging data from patients who underwent intervention examination or treatment using digital subtraction angiography (DSA) and hrCMR using a 3 T CMR system within 30 days after the onset of neurological symptoms were collected. The CMR protocol included diffusion-weighted imaging (DWI), black blood T1-, T2- and contrast-enhanced T1-weighted sequences. Lesions were classified as culprit and non-culprit according to imaging findings and patient clinical presentations. Univariate and multivariate analyses were performed to assess the difference between culprit and non-culprit lesions and complementary value of hrCMR in identifying higher risk lesions.ResultsIn total, 75 patients were included in this study. According to the morphology, lesions could be classified into five types: Type I, classical dissection (n = 50); Type II, fusiform aneurysm (n = 1); Type III, long dissected aneurysm (n = 3); Type IV, dolichoectatic dissecting aneurysm (n = 9) and Type V, saccular aneurysm (n = 12). Regression analyses showed that age and hypertension were both associated with culprit lesions (age: OR, 0.83; 95% CI 0.75-0.92; p < 0.001 and hypertension: OR, 66.62; 95% CI 5.91-751.11; p = 0.001). Hematoma identified by hrCMR was significantly associated with culprit lesions (OR, 16.80; 95% CI 1.01-280.81; p = 0.037). Moreover, 17 cases (16 lesions were judged to be culprit) were diagnosed as IAD but not visible in DSA and 15 were Type I lesion.ConclusionhrCMR is helpful in visualizing and characterizing IAD. It provides a significant complementary value over DSA for the diagnosis of IAD.

Project description:BackgroundAtherosclerotic plaque instability is a common cause of stroke and ischemic infarction, and identification of monocyte-associated genes has become a prominent feature in cardiovascular research as a contributing/predictive marker.MethodsWhole genome sequencing data were downloaded from GSE159677, GSE41571, GSE120521, and GSE118481. Single-cell sequencing data analysis was conducted to cluster molecular subtypes of atherosclerotic plaques and identify specific genes. Differentially expressed genes (DEGs) between normal subjects and patients with unstable atheromatous plaques were screened. Weighted gene coexpression network analysis (WGCNA) was performed to find key module genes. In addition, GO and KEGG enrichment analyses explored potential biological signaling pathways to generate protein interaction (PPI) networks. GSEA and GSVA demonstrated activations in plaque instability subtypes.Results239 monocyte-associated genes were identified based on bulk and single-cell RNA-sequencing, followed by the recognition of 1221 atherosclerotic plaque-associated DEGs from the pooled matrix. GO and KEGG analyses suggested that DEGs might be related to inflammation response and the PI3K-Akt signaling pathway. Eight no-grey modules were obtained through WGCNA analysis, and the turquoise module has the highest correlation with unstable plaque (R 2 = 0.40), which contained 1323 module genes. After fetching the intersecting genes, CXCL3, FPR1, GK, and LST1 were obtained that were significantly associated with plaque instability, which had an intense specific interaction. Monocyte-associated genes associated with atherosclerotic plaque instability have certain diagnostic significance and are generally overexpressed in this patient population. In addition, 11 overlapping coexpressed genes (CEG) might also activated multiple pathways regulating inflammatory responses, platelet activation, and hypoxia-inducible factors. GSVA showed that the corresponding pathways were significantly activated in high expression samples.ConclusionsOverexpression of CXCL3, GK, FPR1, and LST1 was advanced recognition and intervention factors for unstable plaques, which might become targets for atherosclerosis rupture prevention. We also analyzed the potential mechanisms of CEG from inflammatory and oxidative stress pathways.

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Identification of high-risk plaque features in intracranial atherosclerosis: initial experience using a radiomic approach.

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