Abstract WP194: Quantified Effects of Intra-Arterial Vasodilatory Therapy for Cerebral Vasospasm

Abstract

Introduction: Cerebral vasospasm is a major cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage (aSAH). Though used routinely in clinical practice, objective metrics to evaluate effectiveness of intra-arterial vasodilatory treatment (IAT) have not been identified. To quantify effects of IAT on flow dynamics in cerebral vasospasm, we retrospectively compared Lindegaard ratios (LR) of aSAH patients pre-and post-IAT. Methods: Subjects included 24 aSAH patients undergoing IAT in the bilateral middle cerebral arteries (MCA) for cerebral vasospasm, diagnosed by standard clinical and radiographic criteria. Subjects were excluded if balloon angioplasty was performed prior to/within 2 days of the index procedure. All subjects received 10 mg IA milrinone, a non-catecholamine phosphodiesterase inhibitor drug, per MCA. Transcranial doppler (TCD) ultrasound was measured pre-IAT (D0) and at D+1 and D+2 post-IAT. LR was calculated as the ratio of mean flow velocities in the middle cerebral artery (MCA) to the ipsilateral extracranial internal carotid artery. Standard threshold for vasospasm is defined as LR>3. Results: Right and left LR were aggregated, total N=48. Average pre-IAT LR was 2.96 (R 2.67/L 3.25±1.29). Post-IA LR were 2.72±1.12 and 3.15±1.55 at D+1 and D+2, respectively. Subjects with pre-IA LR>3 showed an average LR decrease of 21% post-IAT D+1 (p=0.01) and an 8% decrease at D+2 (p=0.16) [Fig.1A]. Subjects with pre-IAT<3 experienced an average LR increase of 28% by D+2 (p=0.02) [Fig 1B]. Conclusion: Subjects with TCD confirmed vasospasm (LR>3) at D0 showed a significant improvement in cerebral blood flow one day after therapy. Subjects who did not meet TCD threshold for vasospasm (LR<3) showed little change one day post-IAT but worsening cerebral blood flow by day two post-IAT. Further study is needed to determine whether LR can be used to predict benefit or objectively assess effectiveness of IAT in aSAH patients with cerebral vasospasm.