Abstract 175: Vessel Wall Imaging at 3-Tesla in Patients with Symptomatic Intracranial Stenosis and Age-Matched Healthy Controls
Purpose: To translate a recently-proposed ultra-high field (7 Tesla) MRI protocol for assessing intracranial (IC) vessel wall morphology to the clinically available field strength of 3T to enable vessel wall imaging (VWI) routinely without contrast agent administration.
Methods: Following protocol development, IC stenosis patients (n=16) and healthy volunteers (n=16) provided informed, written consent and underwent FLAIR, angiography, and a custom VWI protocol (3D turbo spin echo, TR=1500 ms; spatial resolution=0.5 mm isotropic, and anti-driven +90 equilibrium pulse). A board-certified neuroradiologist, blinded to clinical history, reviewed all images.
Results: Vessel wall abnormalities were detected in all (12/16) participants with significant (>50%) flow-limiting stenosis on angiography. Fig. 1 demonstrates changes for two individuals with VWI lesions. Two participants had advanced moyamoya disease and extensive collateralization on DSA, both of whom had corresponding findings on VWI.
Fig. 1: IC stenosis visualized by VWI and DSA. A) 57 yr/M with flow-limiting basilar artery stenosis. VWI (left) in the coronal plane shows hyperintense signal of a vessel wall lesion in the basilar artery (red arrow). AP projection from the left vertebral injection during DSA (right) shows stenosis in the same region (red arrow). B) 53 yr/M following L MCA territory stroke. VWI (left) demonstrates wall thickening (red arrow) of left distal ICA continuous in the left proximal MCA which corresponds to stenosis on DSA (right, AP view from L ICA injection).
Discussion: We show that it is possible to perform VWI without contrast at 3T and still retain an acceptable image quality for discerning IC vessel abnormalities. Cerebrovascular reactivity (CVR) data were also acquired in all patients as part of an ongoing IC stenosis clinical trial; parallel work is focused on characterizing relationships between vessel wall disease and parenchymal reactivity.
Author Disclosures: D.F. Arteaga: None. M.J. Donahue: None. C.C. Faraco: None. L.C. Jordan: None. J.C.W. Siero: None. J. Hendrikse: None. M.K. Strother: None.
This research has received full or partial funding support from the American Heart Association, Greater Southeast Affiliate – Alabama, Florida, Georgia, Louisiana, Mississippi, Puerto Rico, Tennessee, U.S. Virgin Islands.
- © 2015 by American Heart Association, Inc.