MRI Using Ferumoxytol Improves the Visualization of Central Nervous System Vascular Malformations
Background and Purpose—Central nervous system vascular malformations (VMs) result from abnormal vasculo- and/or angiogenesis. Cavernomas and arteriovenous malformations are also sites of active inflammation. The aim of this study was to determine whether MRI detection of VMs can be improved by administration of ferumoxytol iron oxide nanoparticle, which acts as a blood pool agent at early time points and an inflammatory marker when taken up by tissue macrophages.
Methods—Nineteen patients (11 men, 8 women; mean age, 47.5 years) with central nervous system VMs underwent 3-T MRI both with gadoteridol and ferumoxytol. The ferumoxytol-induced signal changes on the T1-, T2-, and susceptibility-weighted images were analyzed at 25 minutes (range, 21 to 30 minutes) and 24 hours (range, 22 to 27 hours).
Results—Thirty-five lesions (capillary telangiectasia, n=6; cavernoma, n=21; developmental venous anomaly, n=7; arteriovenous malformation, n=1) were seen on the pre- and postgadoteridol images. The postferumoxytol susceptibility-weighted sequences revealed 5 additional VMs (3 capillary telangiectasias, 2 cavernomas) and demonstrated further tributary veins in all patients with developmental venous anomalies. The 24-hour T1 and T2 ferumoxytol-related signal abnormalities were inconsistent among patients and within VM types. No additional area of T1 or T2 enhancement was noted with ferumoxytol compared with gadoteridol in any lesion.
Conclusions—Our findings indicate that the blood pool agent ferumoxytol provides important information about the number and true extent of VMs on the susceptibility-weighted MRI. The use of ferumoxytol as a macrophage imaging agent in the visualization of inflammatory cells within and around the lesions warrants further investigation.
- central nervous system
- magnetic resonance imaging
- ultrasmall superparamagnetic iron oxide nanoparticles
- vascular malformations
- Received November 4, 2010.
- Revision received December 7, 2010.
- Accepted December 9, 2010.
- © 2011 American Heart Association, Inc.