Abstract P572: Cerebral Hemodynamics Underlying Artery-To-Artery Embolism in Symptomatic Intracranial Atherosclerotic Disease

Abstract

Background: Artery-to-artery embolism (AAE) is a common stroke mechanism in patients with symptomatic intracranial atherosclerotic disease (ICAD), which might be associated with a higher risk of recurrent stroke than other stroke mechanisms. We aimed to investigate cerebral hemodynamic features associated with AAE in symptomatic ICAD patients. Methods: Patients with acute, anterior-circulation ischemic stroke attributed to ICAD (50-99% stenosis) confirmed in CT angiography (CTA) were recruited from two teaching hospitals. We classified probable stroke mechanisms as isolated parent artery atherosclerosis occluding penetrating artery (PAO), AAE, hypoperfusion, and mixed mechanisms, based on infarct topography in MRI and ICAD lesion features. CTA-based computational fluid dynamics (CFD) models were built to simulate blood flow across culprit ICAD lesions. Translesional pressure ratio (PR=Pressure post-stenotic /Pressure pre-stenotic ) and translesional wall shear stress ratio (WSSR=WSS stenotic-throat /WSS pre-stenotic ) were calculated, to reflect the relative change of the two hemodynamic metrics across an ICAD lesion. PR ≤ median was defined as low PR, indicating a larger pressure gradient across the lesion; and WSSR ≥ 4 th quartile as high WSSR, indicating elevated WSS upon the lesion. We associated PR and WSSR with presence of AAE as a probable stroke mechanism. Results: Among 99 symptomatic ICAD patients, 44 had AAE as a probable stroke mechanism, 13 with AAE alone and 31 with coexisting hypoperfusion; the remaining patients respectively had isolated PAO (n=18) and isolated hypoperfusion (n=37) as the probable stroke mechanisms. High WSSR was independently associated with AAE (adjusted OR 4.21; 95% CI 1.33-13.26; p=0.014). The significant, positive relationship between high WSSR and higher risk of AAE remained in those with a low PR (adjusted OR 4.01; 95% CI 1.03-15.46; p=0.044), but not in those with a normal PR (p=0.621). Conclusions: High WSS upon ICAD lesions may increase plaque vulnerability and lead to distal embolism, while sustained antegrade flow across the ICAD lesion (normal PR) may help clear the emboli. In secondary prevention of symptomatic ICAD with AAE, impaired cerebral perfusion may be a therapeutic target.