Introduction

Despite significant improvements in prevention, diagnosis, and treatment in recent decades, atherosclerotic cardiovascular disease (ASCVD), mainly stroke and heart attack, remains the leading cause of death and disability worldwide^1-2. Currently, angiography-defined luminal stenosis is the only validated criterion for risk assessment, including digital subtraction angiography (DSA), magnetic resonance angiography (MRA), and computed tomography angiography (CTA)³. However, serious limitations exist⁴. Increasing evidence has shown that detailed lesion morphological and compositional features are more relevant to patient clinical presentations and subsequent events^5-7. Advanced high-resolution multi-contrast MRI (hrMRI) has enabled characterization of detailed architectures in atherosclerosis noninvasively. This study was designed to explore the coexistence and differences of lesion architecture in the atherosclerosis in the intracranial and coronary territories in patients with and without ASCVD using hrMRI and CTA.

Method

Forty-four patients (age 66 ± 9 years, 28 men) underwent both hrMRI and CCTA were included. The ASCVD group was defined as patients who had a cardiac or/and cerebral ischemic event. The non-event group included patients with atherosclerotic plaques in the head and neck arteries and coronary arteries, but without any ischemic cardiovascular event. In hrMRI, if there was only one lesion on the ipsilateral side of ischemia, it was considered as the culprit, and if multiple plaques were present on the ipsilateral side, the most stenotic one was considered as the culprit⁸. In CCTA, culprit lesions associated with cardiac ischemic events were identified based on findings on electrocardiography, wall motion abnormalities on echocardiography, or angiographic appearance during invasive coronary angiography^9-10. Other lesions, if present, were treated as non-culprits. All MR images were obtained in a 3T scanner (MAGNETOM Prisma, Siemens Healthcare, Erlangen, Germany) with a 64-channel head-and-neck coil. The brain imaging protocol included diffusion-weighted imaging (DWI), T1-weighted and T2-weighted imaging, and T2 fluid-attenuated inversion recovery (FLAIR). The hrMRI protocol included 3D time-of-flight magnetic resonance angiography (MRA) (TR 900 ms, TE 16 ms, FOV 238 mm × 169 mm, Matrix 317 × 384, slice thickness 5 mm, slice interval 1.5 mm, layer number 336, turbo factor 52, acquisition factor 2, scanning time 8 min 42 s), 3D black blood T1-weighted Sampling Perfection with Application optimized Contrast using different flip angle Evolution (SPACE) sequence (3D T1) (TR 900 ms, TE 16 ms, FOV 238 mm × 169 mm, Matrix 318 × 448, slice thickness 0.53 mm, layer number 240, turbo factor 52, acquisition factor 2, scanning time 8 min 06 s), 3D black blood T2-weighted SPACE sequence (3D T2) (TR 1200 ms, TE 122 ms, FOV 180 mm × 180 mm, Matrix 248 × 256, slice thickness 0.7 mm, layer number 72, turbo factor 56, acquisition factor 2, scanning time 5 min 07 s) and postcontrast 3D black blood T1-weighted SPACE sequence (3D CE-T1) (parameters were same as 3D T1). CCTA was performed using a third-generation dual-source CT (SOMATOM Force, Siemens Healthcare, Erlangen, Germany). All hrMRI images were independently analyzed by two neuroradiologists using MR-VascularView to quantify plaque morphological and compositional features (Fig. 1). CCTA images were analyzed independently by another two independent radiologists using coronary-specific analysis software (CoronaryDoc) (Fig. 1). Student's t-test or Wilcoxon rank-sum test was used where appropriate to compare continuous parameters between two groups and χ2 test for categorical data.

Results

In intracranial plaques, compared to the non-event group, the ASCVD group had more severe stenosis grades and statistically significant differences in lipid plaque volume (LPV), lipid plaque volume ratio (LPR), and calcified plaque volume (CPV). Similarly, in coronary plaques, the ASCVD group had plaques with greater stenosis, more severe stenosis grades, larger volumes, longer length, larger fibro-lipid plaque volume (FLPV), larger fibrotic plaque volume (FPV), and higher fibrotic plaque volume ratio (FPR) compared to the non-event group. Furthermore, there were statistically significant differences in stenosis, stenosis grades, plaque length, and plaque volume between non-event plaque, non-culprit plaque, and culprit plaque. Finally, in image analysis of hrMRI, there were differences between intraplaque hemorrhage volume ratio (IPHR), LPR, FPV, and CPV among the three groups of plaques, and FLPV and FPV were significantly different among the three different plaque types from coronary artery.

Discussion & Conclusions

This study conducted an initial exploration into the similarity of characteristics of intracranial and coronary plaques obtained through different imaging within the same patient. Our results indicate that, for the same patient, there is a consistent pattern of change in plaque characteristics between intracranial and coronary arteries.

Acknowledgements

Thanks to technician Shengmei Lin, Jiawei Su and nurse Fang Huang who helped in the MR examination; thanks to Fayang Lian who works in the scientific research department of the hospital to provide scientific consultation. Thanks very much to Professor Zhongzhao Teng and his team members for their technical support.

References

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