Abstract 096: Hypoperfusion Intensity Ratio Suggests Collateral Status, Stroke Mechanism, and Clinical Stability in Large Vessel Occlusion

Abstract

Introduction Hypoperfusion Intensity Ratio (HIR), defined by the ratio of Tmax >10s/Tmax >6s on perfusion imaging, has been directly correlated with collateral status, stroke mechanism, and clinical outcomes in patients with acute large vessel occlusions [1,2]. We report a case of a patient with mild neurological symptoms despite an acute MCA M1 occlusion in which a very favorable HIR may have predicted clinical stability, extensive atherosclerotic burden, and compensatory leptomeningeal collaterals. Our aim was to provide support of the utility of HIR in quantifying collateral status and possibly predicting the underlying stroke mechanism and stroke progression of patients with acute large vessel occlusions. Methods Case report. Results A 61‐year‐old woman with a history of hypertension and hyperlipidemia, who is an active smoker with a known right extracranial carotid stenosis presented with acute left facial droop (NIHSS 1) upon awakening. CT head did not demonstrate early ischemic changes. CT angiogram demonstrated a right MCA M1 occlusion, marked narrowing of the right common carotid artery, and severe narrowing of the proximal innominate artery (Figure 1, Image A). CT perfusion demonstrated a Tmax >6s delay of 41mL and HIR of 0, suggestive of robust collaterals (Figure 1, Image B). The patient was out of the window for tenecteplase administration. Thrombectomy was deferred due to a low NIHSS. MRI showed a right putamen and corona radiata infarct. DSA demonstrated crossed collateralization across the anterior communicating artery and robust right ACA‐MCA and PCA‐MCA leptomeningeal collaterals and retrograde filling of the brachiocephalic and right common carotid artery via the right vertebral artery. These findings were supported by quantitative MRA, which showed decreased blood flow in the right ICA, increased blood flow in right A2, increased blood flow in left A1, and retrograde right vertebral flow indicative of a brachiocephalic steal phenomenon. Her neurological exam remained stable upon discharge. She will be evaluated for brachiocephalic revascularization as an outpatient. Conclusion We present a patient with very mild symptoms due to an acute large vessel occlusion who remained clinically stable despite an acute MCA M1 occlusion, which was likely caused by ischemic conditioning related to chronic hypoperfusion secondary to severe brachiocephalic and right common carotid artery stenosis. Favorable HIR on perfusion imaging was predictive of robust collaterals, the underlying stroke mechanism, and the stable clinical course. Since clinical equipoise exists regarding the treatment of patients with low NIHSS in the setting of an acute large vessel occlusion, individualized selection remains paramount. HIR may serve as a quantitative radiographic marker to rapidly quantify collateral status and assist in decision‐making. Future studies exploring the role of HIR in predicting stroke progression are warranted.