Abstract WP169: Symptomatic Intracranial Atherosclerotic Stenosis: The Associations Between Cerebral Hemodynamics and the Stroke Mechanisms

Background: Intracranial atherosclerotic stenosis (ICAS) may cause ischemic stroke by various mechanisms; artery-to-artery (AA) embolism and hypoperfusion often co-exist and bear a high risk of recurrent stroke despite optimal medical treatment. Little is known regarding how ICAS lesions cause ischemic strokes via different mechanisms, while the hemodynamic features of ICAS lesions may play an important role. Methods: Patients with acute ischemic stroke attributed to 50-99% ICAS in the anterior circulation confirmed in CT angiography (CTA) were recruited from two teaching hospitals. We classified probable stroke mechanisms as parent artery atherosclerosis occluding penetrating artery (PAO), AA embolism, hypoperfusion, and mixed mechanisms, based on infarct topography and ICAS lesion features. Computational fluid dynamics (CFD) models were built based on CTA to simulate blood flow across culprit ICAS lesions. We calculated translesional pressure ratio (PR), the ratio of pressures distal and proximal to the lesion; and translesional wall shear stress ratio (WSSR), the ratio of WSS at the stenosis throat and at proximal normal vessel segment. We defined PR ≤ median as low PR, indicating larger pressure gradient across the lesion, hence restricted downstream perfusion; and WSSR ≥ 4 th quartile as high WSSR, indicating higher WSS upon the lesion. We associated PR and WSSR with probable stroke mechanisms. Results: Among 99 patients, 44 had AA embolism as a probable stroke mechanism, 13 with AA embolism alone and 31 with coexisting hypoperfusion; 18 and 37 respectively had isolated PAO and isolated hypoperfusion as the probable stroke mechanisms. High WSSR was independently associated with AA embolism (adjusted OR 4.86; p = 0.008). The significant, positive relationship between high WSSR and higher risk of AA embolism remained in those with a low PR (adjusted OR 4.01; p = 0.044), but not in those with a normal PR (p = 0.621). Conclusions: High WSS upon ICAS lesions may increase plaque vulnerability, but it may only cause distal arterial embolism when there is impaired cerebral perfusion. Therefore, in secondary prevention of ischemic stroke in ICAS via AA embolism, impaired cerebral perfusion may be an important therapeutic target.