Abstract P230: Markers of Hyperglycemia and Intracranial Atherosclerotic Stenosis by Magnetic Resonance Angiography
Introduction: Intracranial atherosclerotic stenosis (ICAS) is a common cause of stroke. Determinants of ICAS include conventional cardiovascular (CV) risk factors such as hypertension and dyslipidemia. The association of diabetes mellitus (DM) and/or hyperglycemia with ICAS, however, is less well documented.
Hypothesis: In a community-based population, biomarkers of hyperglycemia will be cross-sectionally associated with prevalent ICAS independent of CV risk factors.
Methods: Our analyses were conducted in a subsample of participants of the Atherosclerosis Risk in Communities (ARIC) Study who participated in the ARIC-Neurocognitive Study in 2011-13 with cerebrovascular magnetic resonance angiography and no history of stroke. For the present analyses, we grouped the participants into 3 categories based on the highest ICAS category among any of the intracranial arteries we assessed: “no stenosis”, “<50%”, or “≥50% (including occlusion)”. Diagnosed diabetes was defined as self-reported physician diagnosis or use of antidiabetic medication. Ordinal logistic regression provided odds ratios of prevalent ICAS according to quintile of glucose or glycated hemoglobin (HbA1c) adjusted for CV risk factors.
Results (Table): There were 1,658 individuals included in our study (age 67-90 years, women 58%, Black 29%), 31% (514/1658) had diagnosed diabetes, 10% (165/1658) had ≥50 % stenosis at any of the intracerebral arteries. In crude analyses, those with higher glucose and HbA1c were more likely to have ICAS among the non-diabetes and the diabetes. In logistic regression, highest quintile of glucose, relative to the lowest, had odds ratio of 2.26 (95% confidence interval 1.48, 3.45) for being in each successive ICAS category after adjustment for CV risk factors.
Conclusion: Higher glucose and HbA1c were associated with higher odds of ICAS independent of CV risk factors. The finding suggests that hyperglycemia plays a role in pathogenesis of ICAS.
Author Disclosures: A. Fujiyoshi: None. M.K. Suri: None. A. Alonso: None. E. Selvin: None. H. Chu: None. E. Guallar: None. Y. Qiao: None. Y. Zhang: None. B.A. Wasserman: None. A.R. Folsom: None.
- © 2016 by American Heart Association, Inc.