Detection of Intracranial In-Stent Restenosis Using Quantitative Magnetic Resonance Angiography
journal contributionposted on 2011-05-27, 00:00 authored by Sepideh Amin-Hanjani, Ali Alaraj, Mateo Calderon-Arnulphi, Victor A. Aletich, Keith R. Thulborn, Fady T. Charbel
BACKGROUND AND PURPOSE: In-stent restenosis (ISR) after angioplasty/stenting for intracranial stenosis has been reported in up to 25% to 30% of patients. Detection and monitoring of ISR relies primarily on serial catheter angiography, because noninvasive imaging methods are typically hampered by stent-related artifact. We examined the value of serial vessel flow measurements using quantitative magnetic resonance angiography (QMRA) in detection of ISR. Material and METHODS: Records of patients undergoing stenting for intracranial symptomatic stenosis >50% between 2005 and 2009 were retrospectively reviewed. Angiographic images were graded by a blinded neurointerventionalist for stenosis pretreatment, immediately after treatment, and during follow-up. Flow in the affected vessel measured by QMRA was recorded; > 25% reduction in flow was considered indicative of an adverse change. Clinical data regarding neurological outcome were also collected. RESULTS: Twenty-eight patients underwent stenting during the time interval studied. Of these, 12 patients (mean age, 55.5 years; 8 female) had contemporaneous angiography and QMRA and were analyzed. Median follow-up was 9 months. Six patients (50%) demonstrated angiographic restenosis 2 to 12 months after treatment; all had an analogous decrease in flow in the vessel of interest. Of 3 patients with more severe flow decrement (> 50%), 2 experienced stroke. None of the patients without angiographic ISR demonstrated a flow decrease on QMRA. CONCLUSIONS: In this preliminary series, flow decrease on QMRA is highly predictive of angiographic ISR. Additionally, the degree of flow decrement correlates with symptomatic ISR. QMRA may provide a useful noninvasive tool for serial monitoring after intracranial stenting.
Funding support for this project was provided by the Dr Ralph and Marian Falk Research Trust Foundation. F.T.C. has financial interest in VasSol. S.A.H. receives grant support from NIH/NINDS and other research support (no direct funding) from G.E. Healthcare and VasSol, Inc.
Publisher StatementThe original version of this publication is available through the American Heart Association (www.ahajournals.org) at DOI: 10.1161/STROKEAHA.110.594739.
PublisherAmerican Heart Association