Association between type 2 diabetes mellitus, especially recently uncontrolled glycemia, and intracranial plaque characteristics: A high-resolution magnetic resonance imaging study.

AIMS/INTRODUCTION: Type 2 diabetes mellitus is a specific risk factor for intracranial atherosclerosis. The purpose of this study was to investigate the relationship between type 2 diabetes mellitus, especially uncontrolled glycemia, and intracranial plaque characteristics using high-resolution magnetic resonance imaging.

MATERIALS AND METHODS

A total of 263 patients (182 men; mean age 62.6 ± 11.5 years) with intracranial atherosclerotic plaques detected on high-resolution magnetic resonance imaging from December 2017 to March 2019 were included in this study. Patients were divided into different groups: (i) patients with and without type 2 diabetes mellitus; (ii) diabetes patients with uncontrolled glycemia (glycated hemoglobin level ≥7.0%) and controlled glycemia; and (iii), diabetes patients with diabetes duration of <5, 5-10 and >10 years. Comparisons of plaque features between groups were made, respectively.

RESULTS

Type 2 diabetes mellitus was diagnosed in 118 patients (44.9%). Diabetes patients had a significantly greater prevalence of enhanced plaque, greater maximum plaque length, maximum wall thickness and more severe luminal stenosis than non-diabetes patients. Compared with diabetes patients with controlled glycemia, those with uncontrolled glycemia had a significantly greater prevalence of enhanced plaque and greater maximum plaque length (all P < 0.05). There were no significant differences in plaque features among patients with different durations of type 2 diabetes mellitus. Uncontrolled glycemia was an independent factor for plaque enhancement after adjustment for potential confounding factors (odds ratio 5.690; 95% confidence interval 1.748-18.526; P = 0.004).

CONCLUSIONS

Type 2 diabetes mellitus is closely related to intracranial plaque enhancement and burden. Recently uncontrolled glycemia might play an important role in the development of enhanced plaque.