Abstract 16: Temporal Changes in Hemodynamics in Patients With Vertebrobasilar Disease: Results From the Prospective Multicenter VERiTAS Study
Introduction: The role of regional hypoperfusion as an important contributor to stroke risk in atherosclerotic vertebrobasilar (VB) disease has recently been confirmed by the observational Vertebrobasilar Flow Evaluation and Risk of Transient Ischemic Attack and Stroke (VERiTAS) Study. We examined the stability of hemodynamic status over time and relationship to stroke risk in patients followed in this prospective cohort.
Methods: VERiTAS enrolled patients with recent VB TIA or stroke and ≥50% atherosclerotic stenosis or occlusion of vertebral and/or basilar arteries. Large vessel flow in the vertebrobasilar territory was assessed using quantitative MRA, and patients were designated as low flow or normal flow based on distal territory regional flow, incorporating collateral capacity. Patients underwent standard medical management and follow-up for primary outcome event of VB territory stroke. QMRA imaging was repeated at 6, 12 and 24 months. Flow status over time was examined relative to baseline, and relative to subsequent stroke risk using survival analysis.
Results: Of 72 enrolled subjects, 50, 45 and 28 had follow-up QMRA at 6, 12 and 24 months respectively. 18 (25%) were characterized as low flow at baseline, 10% at 6 m, 20 % at 12m and 11% at 24m. Over 18±7months of follow-up, 7 of the 12 low flow patients (58%) with follow-up imaging had improved their flow status (low to normal) while only 3 of 44 normal flow patients (7%) had worsened. Baseline flow status has previously been demonstrated to be an independent stroke risk predictor; flow status at latest follow-up and prior to event remained a strong predictor of subsequent stroke (HR 4.9, CI 1.4 to16.9, p=0.01).
Conclusions: There is potential both for improvement and worsening of hemodynamics in patients with atherosclerotic VB disease; improvement, likely attributable to development of collateral supply, was evident more frequently than worsening, presumably due to progression of disease. Flow status, both at baseline and over time, remains a robust risk factor for subsequent stroke, thus serving as an important prognostic marker.
Author Disclosures: S. Amin-Hanjani: Research Grant; Modest; NIH/NINDS. Other Research Support; Modest; VasSol, Inc, GE Helathcare. C.P. Derdeyn: Ownership Interest; Modest; Pulse Therapeutics. Consultant/Advisory Board; Modest; Penumbra (DSMB, 3D SEPARATOR Trial), Microvention (Core Lab, LVIS Trial), Pulsar Vascular (Core Lab, ANSWERS Trial). X. Du: None. L. Rose-Finnell: None. D.K. Pandey: None. D. Richardson: None. M.S.V. Elkind: Expert Witness; Modest; BMS-Sanofi. Consultant/Advisory Board; Modest; BMS-Pfizer, Boehringer-Ingelheim, Sanofi-Regeneron, BioTelemetry/Cardionet. Research Grant; Significant; BMS-Sanofi, diaDexus. Consultant/Advisory Board; Significant; Hi-Tech. G.J. Zipfel: Research Grant; Modest; Barnes Jewish Hospital Foundation, McDonnell Center for Cellular and Molecular Neurobiology. Research Grant; Significant; NIH/NINDS. D.S. Liebeskind: Consultant/Advisory Board; Modest; Medtronic, Stryker. Research Grant; Significant; NIH-NINDS. F.L. Silver: Speakers' Bureau; Significant; Boehringer Ingelheim Canada. Consultant/Advisory Board; Significant; Boehringer Ingelheim Canada. S.E. Kasner: None. P.B. Gorelick: Other Research Support; Significant; Lundbeck, Inc. F.T. Charbel for the VERiTAS Study Group: Ownership Interest; Significant; VasSol, Inc..
- © 2016 by American Heart Association, Inc.