Get access

Elevated glucose level adversely affects infarct volume growth and neurological deterioration in non-diabetic stroke patients, but not diabetic stroke patients

Authors


Abstract

Background and purpose

Hyperglycemia is recognized as a common occurrence associated with a high risk of poor outcome in ischaemic stroke patients. However, little is known about the association between elevated glucose level, growth of infarct volume and neurological deterioration in ischaemic stroke patients without diabetes. The present study aimed to clarify this issue in acute ischaemic stroke patients with arterial occlusion.

Methods

We studied 375 acute ischaemic stroke patients with arterial occlusion within 24 h of onset. Diabetes was diagnosed in patients with a known history of diabetes or HbA1c value ≥ 6.5%. Infarct volume was measured on admission and at follow-up within 48 h using diffusion-weighted imaging. Neurological deterioration was defined as an increase of ≥ 4 points in National Institutes of Health Stroke Scale score within 7 days of stroke onset. We examined the relationship between glucose level on admission, infarct volume growth and neurological deterioration in three categories (all patients, non-diabetes and diabetes) using multivariate modeling.

Results

Diabetes was present in 104 patients (27.7%). Multivariate regression analysis showed that elevated glucose level was independently associated with infarct volume growth in all patients (P = 0.034) and non-diabetes (P = 0.002), but not in diabetes (P = 0.871). Moreover, elevated glucose level was independently associated with neurological deterioration in all patients [odds ratio (OR), 1.010; 95% confidence interval (CI), 1.004–1.017; P = 0.002] and non-diabetes (OR, 1.014; 95% CI, 1.002–1.026; P = 0.022), but not diabetes (OR, 1.006; 95% CI, 0.998–1.014; P = 0.151).

Conclusions

Glucose level appears to influence infarct volume growth and neurological deterioration, particularly in non-diabetic patients with ischaemic stroke.

Get access to the full text of this article

Ancillary