Abstract P778: Hypertension and Vascular Cell Adhesion Molecule 1 Relate To % Change in National Institutes of Health Stroke Scale Score in Ischemic Stroke After Mechanical Thrombectomy

• Published in: Stroke (1970) Vol. 52; no. Suppl_1; p. AP778
• Main Authors: Maglinger, Benton, Sands, Madison, Frank, Jacqueline, Trout, Amanda L, Roberts, Jill, Grupke, Stephen, Turchan-Cholewo, Jadwiga, Stowe, Ann M, Fraser, Justin, Pennypacker, Keith
• Format: Journal Article
• Language: English
• Published: Lippincott Williams & Wilkins 01.03.2021
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/str.52.suppl_1.P778

IntroductionThe University of Kentucky Blood and Clot Thrombectomy Registry and Collaboration (BACTRAC) protocol utilizes thrombectomy to isolate intracranial (i.e. distal to thrombus) arterial blood and systemic (i.e. carotid) arterial blood from thrombectomy procedures to study stroke. Here, we investigate the relationship among Vascular Cell Adhesion Molecule 1 (VCAM1), hypertension (HTN), and stroke recovery in patients undergoing mechanical thrombectomy for emergent large vessel occlusion (ELVO) stroke. MethodsIntracranial and systemic plasma samples from 25 subjects underwent cardiometabolic proteomic analysis at Olink Proteomics. Demographic data including HTN status and both admission NIHSS and discharge NIHSS were included. Linear regression analysis was run on both intracranial and systemic VCAM1 expression levels against % change in NIHSS ((Admittance NIHSS - Discharge NIHSS)/Admittance NIHSS)) and two-tailed t-tests were run assessing VCAM1 expression with HTN vs. no HTN. ResultsIncreased expression of intracranial VCAM1 significantly correlated with a smaller % change in NIHSS (p=0.001). Similarly, increased systemic VCAM1 expression was also found to have a significant relationship with smaller % change in NIHSS (p=0.005). Subjects with hypertension had significantly higher intracranial (p=0.03) and systemic (p=0.001) VCAM1 levels compared to those without HTN. DiscussionVCAM1 mediates leukocyte-endothelial cell adhesion and has been shown to play a role in stroke. This study takes a novel approach of sampling both intracranial and systemic arterial blood during an ELVO stroke. We found increased intracranial and systemic VCAM1 independently correlate with a smaller % change in NIHSS, an indicator of poorer initial recovery. Although preliminary, these results suggest an informative role of VCAM1 levels at the time of infarct. Additionally, those with HTN had higher levels of intracranial and systemic VCAM1. These data are in line with previous studies suggesting VCAM1 is a marker of endothelial damage due to HTN leading to negative clinical outcomes. To better understand our findings, we plan to perform subset analyses investigating VCAM1 levels in relation to dyslipidemia, infarct time and infarct volume.