Abstract 105: Collateral Blood Flow and Inflammatory Markers in Intracranial Atherosclerosis: Angiography and Biomarker Correlates in the BIOSIS and SAMMPRIS Trials
Background: Collateral blood flow, modulated by inflammation and arteriogenesis, alters ischemic injury in intracranial atherosclerosis. We investigated the potential link between several inflammatory and arteriogenic biomarkers with angiographic findings at enrollment in BIOSIS/SAMMPRIS.
Methods: Baseline angiography and blood biomarkers of BIOSIS/SAMMPRIS, which included subjects with stroke or TIA due to 70-99% intracranial stenosis were analyzed. Collateral blood flow status at angiography was categorized by the combination of antegrade flow (TICI) and corresponding extent of collaterals (ASITN/SIR). Collateral status was analyzed with respect to blood progenitor cell markers (CD34) at baseline and inflammatory biomarkers (Plasminogen Activator Inhibitor-1 (PAI-1), E-selectin, high sensitivity C-reactive protein (hsCRP) and Lipoprotein-associated phospholipase A2 (Lp-PLA2) activity and concentrations) at baseline, 30 days and 4 months.
Results: 376 subjects (mean age 60.44 years SD 11; 149/376 (39.6%) women) enrolled in BIOSIS/SAMMPRIS had angiography of collaterals and biomarker data. Collateral perfusion was impaired in 71 (19%) and intermediate in 188 (50%), with robust collaterals in 117 (30%) subjects. Better collateral status was associated with younger age (p=0.001), male sex (p=0.029) and greater baseline physical activity (p=0.007). Baseline blood progenitor cell (CD34+) counts were unrelated to angiographic features at enrollment, whereas inflammatory Lp-PLA2activity was linked (p=0.059) with blood flow categories, and lower hsCRP (p=0.025) with better collaterals. Lp-PLA2activity was lowest in those with robust collaterals at 30 days (p=0.070) and 4 months (p=0.120). Those with robust collaterals had the greatest decrease in Lp-PLA2activity (p=0.021) and concentration (p=0.027) by 30 days, with a continued decline of Lp-PLA2activity (p=0.037) to 4 months. Disparate trends in inflammatory markers were seen in the medical and stenting arms.
Conclusions: Inflammatory biomarkers are linked with collateral blood flow status in intracranial atherosclerosis. The impact of physical activity, medications and other therapeutic investigations may disclose important mechanisms to avert ischemia.
Author Disclosures: D.S. Liebeskind: Consultant/Advisory Board; Modest; Medtronic, Stryker. Research Grant; Significant; NIH-NINDS. S.M. Noreen: None. Q. Long: Research Grant; Significant; NIH, PCORI, VA and AHA grants. Consultant/Advisory Board; Modest; Eisai. Y. Zhao: None. A. Quyyumi: None. N. Le: None. E.K. Waller: None. G.A. Cotsonis: Research Grant; Significant; NIH. M.J. Lynn: Research Grant; Significant; NIH. B. Lane: None. F. Nahab: 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. H.J. Cloft: None. D.J. Fiorella: None. 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). T.N. Turan: Research Grant; Significant; NIIH. J.F. Arenillas: Research Grant; Significant; Spanish Ministry of Science. Consultant/Advisory Board; Modest; BMS/Pfizer, Bayer, St Jude. M.I. Chimowitz: Research Grant; Significant; NIH. M. Frankel: Research Grant; Significant; NIH.
- © 2016 by American Heart Association, Inc.