Abstract Details

Title Does Diabetes Mellitus Influence the Association Between Stress Hyperglycemia and Leptomeningeal Collateral Circulation in Acute Ischemic Stroke Patients?

Topic Cerebrovascular Disease and Interventional Neurology

Presentation(s) P8 - Poster Session 8 (8:00 AM-9:00 AM)

Poster/Presentation
Number 13-008

Objective To determine if stress hyperglycemia (SHG) has a differential impact on leptomeningeal collateral (LMC) circulation in acute ischemic stroke (AIS) based on the presence or absence of diabetes mellitus (DM)

Background SHG is associated with poor LMC in AIS and subsequently, reperfusion therapy outcomes. It is unclear if the impact of SHG on LMCs varies based on the DM status.

Design/Methods In this retrospective single-center study, we reviewed patients admitted with AIS, who either had internal carotid artery or middle cerebral artery occlusion, with fasting glucose and CTA obtained within 24 hours of admission. SHG calculated using the formula: admission blood glucose/[(28.7 × HbA1c%) – 46.7]. CTA collaterals were classified using the Regenhardt et al. system. We further reclassified into “Good” (included symmetric and intermediate) and “Poor”(Malignant). Wilcoxon Rank Sum Test was used to compare SHR in individuals with good and poor collaterals

Results

A total of 266 patients were included, 54.5% (n=145) were males, 45.5% (n=121) were females. Among them, 20% (n=53) had a history of DM. CTA collateral score was deemed malignant in 24.5% (n=65), and symmetric in 35% (n=93). Overall, SHR showed lower values in individuals with good collateral, compared to poor collateral status (P=0.02). When analyzing DM and non-DM patients separately, we found that non-DM patients with good collaterals had a significantly lower SHR (0.9±0.2 vs 1.2±0.2, p < 0.01). In contrast, among DM patients, SHR scores were similar between those with good and poor collaterals (1±0.4 vs 1.1±0.2, p = 0.07)

Conclusions SHG at admission is a useful predictor of poor collaterals. SHG is more strongly associated with poor collaterals in non-DM patients compared to those with DM in our study which contrasts with some prior studies. Additional larger population-based studies are necessary to validate this association.

Authors/Disclosures
Emanuele Camerucci, MD (Kansas University Medical Center) PRESENTER	Dr. Camerucci has nothing to disclose.
Tuqa Asedi, MD	Dr. Asedi has nothing to disclose.
Chelsey M. Schartz	Ms. Schartz has nothing to disclose.
Dina M. Al-Nuaimi, MD	Miss Al-Nuaimi has nothing to disclose.
Hussein Alsadi (University of Kansas Medical Center)	Hussein Alsadi has nothing to disclose.
Mohammed Qussay Ali Al-Sabbagh, MD (University of Kansas Medical Center)	Dr. Al-Sabbagh has nothing to disclose.
Prasanna Venkatesan Eswaradass, MD (University of Kansas Health System)	Dr. Eswaradass has nothing to disclose.

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