Abstract 174: In-vivo Assessment of the Impact of Regional Intracranial Atherosclerotic Lesions on Brain Arterial 3D Hemodynamics
Purpose: To evaluate the feasibility of 4D flow MRI for the in-vivo assessment of the impact of regional stenotic lesions on intracranial arterial hemodynamics in patients with intracranial atherosclerotic disease (ICAD).
Method: 4D flow MRI data were acquired in 23 ICAD patients (13 male, 67±14 years) and 8 healthy volunteers (4 male, 60±11 years). The stenosed vessels were internal carotid artery (ICA, n=8), middle cerebral artery (MCA, n=11), and basilar artery (BA, n=7). 3D blood flow characteristics were visualized using time-integrated pathlines (Fig. 1a-c). Blood flow and peak velocity in the major intracranial arteries (ICA, MCA, PCA, and ACA) were quantified in manually positioned 2D planes (Fig. 1a). Asymmetry index (affected/non-affected for patients or left/right ratios for volunteers) of the blood flow (AI-F) and peak velocity (AI-V) were compared between patients and volunteers for the above 4 vessels.
Results: The following indices were significantly different between volunteers and patients with ICA and MCA stenosis (Fig. 1d, e). For patients with ICA stenosis compared to volunteers, the indices measured for ICA location were: AI-F (0.48±0.23 vs. 0.99±0.05, P<0.001) and AI-V (0.64±0.23 vs. 0.96±0.12, P=0.004) and for MCA location were: AI-F (0.66±0.28 vs. 0.94±0.09, P=0.016). For patients with MCA stenosis compared to volunteers, the indices for MCA location were: AI-F (0.42±0.22 vs. 0.94±0.09, P<0.001) and AI-V (0.71±0.21 vs. 1.00±0.18, P=0.008). PCA flow and ACA velocity indices were altered suggesting collateral flow ipsilateral to the ICA or MCA stenosis. No difference was observed between volunteers and patients with BA stenosis.
Conclusion: Our findings demonstrated the feasibility of 4D flow MRI to quantify the impact of a regional stenotic lesion on changes in other intracranial arterial hemodynamics. Quantitative hemodynamic markers may provide additional insight into the pathophysiology and risk stratification for ICAD patients.
Author Disclosures: C. Wu: None. T.J. Carroll: None. P. Vakil: None. A.R. Honarmand: None. S.A. Ansari: None. M. Markl: None. S. Prabhakaran: None.
- © 2015 by American Heart Association, Inc.