Impact of Previous Glycemic Control on High-Resolution MRI Plaque Characteristics and Stroke Mechanisms in Patients with Middle Cerebral Artery Atherosclerosis

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BACKGROUND AND PURPOSE: Although diabetes mellitus (DM) is a consistently documented risk factor for the plaque vulnerability, the effect of diabetes mellitus and glycemic control on the characteristics of intracranial plaques and stroke mechanism has yet to be explored. This study aimed to explore whether prestroke glycemic control is linked to plaque instability and could result in varying types and mechanisms of stroke. MATERIALS AND METHODS: We retrospectively included 107 patients with infarction attributed to atherosclerotic stenosis of the M1 segment of the MCA within 4 weeks of symptom onset, all of whom underwent high-resolution MR imaging. Patients were categorized into 4 groups based on their history of diabetes mellitus (DM) and their prestroke glycemic control: non-diabetes mellitus, glycosylated hemoglobin (HbA1c) <7.0%, HbA1c 7.0–8.9%, and HbA1c ≥ 9.0%. The morphology and composition of intracranial atherosclerotic plaques were evaluated by HR-MRI. The degree of plaque enhancement was measured by the plaque-to-pituitary stalk contrast ratio based on signal intensity values on postcontrast T1 images. The infarct pattern and stroke mechanisms were analyzed through diffusion-weighted imaging. RESULTS: Among the enrolled 107 patients with stroke, 49 (45.79%) had DM. The remodeling index, wall index, and the degree of stenosis did not differ between the 4 groups. Poor glycemic control was associated with a higher prevalence of large cortical/cortical–deep patterns (25.9% in non-DM, 35.7% in HbA1c <7.0%, 39.1% in HbA1c 7.0–8.9%, and 41.7% in HbA1c ≥ 9.0% group). Compared with non-DM group, the proportion of artery-to-artery embolism and mixed mechanisms tends to increase along with increased HbA1c levels. The higher prevalence of intraplaque hemorrhage (40.8% versus 19.0%, P = .01), discontinuity of plaque surface (34.7% versus 12.7%, P = .01), and complicated plaque (defined as plaques with surface defects or hemorrhage) (55.1% versus 22.4%, P < .001) was significantly observed in diabetic patients more so than non-DM patients. HbA1c ≥ 9.0% was independently associated with an increased degree of plaque enhancement (coefficient: 0.35, P < .001). CONCLUSIONS: Poor glycemic control is independently linked to heightened plaque enhancement and a higher prevalence of complicated plaque. More large cortical/cortical–deep patterns were found, which may be associated with a small increase in artery-to-artery embolism and mixed mechanisms in such patients.

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