Purpose

Type 2 Diabetes mellitus (T2DM) is a chronic disease that always starts in middle- and late-adulthood, it will cause major health complications, particularly in the blood vessels. T2DM patients frequently have significant multiple atherosclerotic plaques, such as intracranial atherosclerotic plaque. However the relationship between blood glycemic (BG) level in T2DM and intracranial atherosclerotic plaque properties were unknown. In this study, by imaging plaque with high-resolution Magnetic Resonance Imaging (MRI), we investigated the association between T2DM and characteristics of intracranial atherosclerotic plaque, then plaque burden and vulnerability were investigated.

Method

Three hundred and eleven patients who underwent high-resolution MRI examination for evaluating intracranial atherosclerosis were enrolled in this study. They were categorized into 3 groups according to health status and Hemoglobin A1C (HbA1c) level: patients without DM, n=172; DM patients with good BG control: HbA1c < 7%, n=55; DM patients with poor BG control: HbA1c ≥ 7%, n=84. All patients underwent MRI examinations on a MAGNETOM Prisma 3T MR scanner (Siemens Healthcare, Erlangen, Germany) with a 32-channel head coil. High-resolution (HR) intracranial artery wall images were acquired using a T1-weighted sampling perfection with application optimized contrasts (SPACE) sequence before and after contrast agent injection with following parameters: TR= 900 ms, TE= 15 ms, FOV= 170 × 170 mm2, voxel size= 0.53 × 0.53 × 0.53 mm3, and acquisition time = 8 min. Postcontrast T1WI was performed 5 min after the injection of single-dose (0.1mmol per kg of body weight) gadolinium-based contrast agent (Magnevist, Schering, Berlin, Germany). Characteristics of the intracranial plaques including plaque length, plaque thickness, lumen stenosis degree and strength of plaque enhancement were obtained after depicting the plaques region on HR intracranial artery vessel wall MR images. All these quantitative values were compared among 3 groups. The risk factors of the plaques for heavy burden and vulnerability were also analyzed. All continuous variables were expressed as means ± standard deviation and categorical variables were summarized as count. Characteristics of plaque between the 3 groups were compared using the analysis of variance for continuous variables and the chi-square test for categorical variables. Multivariate logistic regression was performed to determine independent indicators for heavy burden and strongly enhancement of plaque. All statistical analyses were performed by using SPSS 25.0. A P value < 0.05 indicated statistical significance.

Result

Results showed that plaque length were significant different between the non-DM group and the DM with poor BG control group (non-DM: 5.95 ± 3.67 mm, DM with poor BG: 8.39 ± 5.14 mm, P < 0.001), plaque thickness (non-DM: 1.66 ± 0.83 mm, DM with poor BG: 1.98 ± 0.89 mm, P = 0.039) and lumen stenosis degree (non-DM: 45.05 ± 32.00%, DM with poor BG: 62.51 ± 29.73%, P < 0.001) reached significant different as well. The proportion of strongly enhanced plaques was significant different between the 3 groups (non-DM: 63.4%, DM with good BG: 72.7%, DM with poor BG: 92.9%, all P < 0.001). The results of multivariate logistic regression analysis shows that the proportion of strongly enhancement plaque was significantly correlated with BG level (OR = 2.21, 95% CI: 1.53 - 3.19, 𝑃 < 0.001).

Discussion/Conclusion

In this study, we compared the BG level in patients and characteristics of intracranial atherosclerotic plaque using high-resolution MRI. The results indicated that patients with poor BGC had heavier intracranial plaque burden and more vulnerability than the patients without DM. When compared with non-DM, patients with good BGC showed no significant difference in plaque burden and plaque vulnerability. Our finding shows that the proportion of strongly enhancement plaque was significantly correlated with BG level, it suggests that BG level is an independent risk factor for the vulnerability of the intracranial atherosclerotic plaque.

Acknowledgements

No acknowledgement found.