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.