TY - JOUR AU - Cohen G. AU - Lindley R. AU - Peeters A. AU - Sandercock P. AU - Wardlaw J. AU - Mair G. AU - von Kummer R. AU - Adami A. AU - Farrall A. AU - Morris Z. AU - von Heijne A. AU - Bradey N. AU - Cala L. AU - Potter G. AB -

OBJECTIVE: To investigate whether the location and extent of the CT hyperdense artery sign (HAS) at presentation affects response to IV alteplase in the randomized controlled Third International Stroke Trial (IST-3). METHODS: All prerandomization and follow-up (24-48 hours) CT brain scans in IST-3 were assessed for HAS presence, location, and extent by masked raters. We assessed whether HAS grew, persisted, shrank, or disappeared at follow-up, the association with 6-month functional outcome, and effect of alteplase. IST-3 is registered (ISRCTN25765518). RESULTS: HAS presence (vs absence) independently predicted poor 6-month outcome (increased Oxford Handicap Scale [OHS]) on adjusted ordinal regression analysis (odds ratio [OR] 0.66, p < 0.001). Outcome was worse in patients with more (vs less) extensive HAS (OR 0.61, p = 0.027) but not in proximal (vs distal) HAS (p = 0.420). Increasing age was associated with more HAS growth at follow-up (OR 1.01, p = 0.013). Treatment with alteplase increased HAS shrinkage/disappearance at follow-up (OR 0.77, p = 0.006). There was no significant difference in HAS shrinkage with alteplase in proximal (vs distal) or more (vs less) extensive HAS (p = 0.516 and p = 0.580, respectively). There was no interaction between presence vs absence of HAS and benefit of alteplase on 6-month OHS (p = 0.167). CONCLUSIONS: IV alteplase promotes measurable reduction in HAS regardless of HAS location or extent. Alteplase increased independence at 6 months in patients with and without HAS. CLASSIFICATION OF EVIDENCE: This study provides Class I evidence that for patients within 6 hours of ischemic stroke with a CT hyperdense artery sign, IV alteplase reduced intra-arterial hyperdense thrombus.

AD - From the Division of Neuroimaging Sciences (G.M., Z.M., A.J.F., G.C., J.M.W.) and the Division of Clinical Neurosciences (P.A.G.S.), University of Edinburgh, UK; the Department of Neuroradiology (R.v.K.), Dresden University Stroke Centre, Germany; Danderyd Hospital (A.v.H.), Stockholm, Sweden; Neuroradiology (N.B.), James Cook University Hospital, Middlesborough, UK; School of Pathology and Laboratory Medicine (L.C.), University of Western Australia, Perth; Cliniques Universitaires St Luc (A.P.), Neurologie, Belgium; Stroke Center (A.A.), Sacro Cuore-Don Calabria Hospital, Negrar, Italy; the Department of Neuroradiology (G.P.), Salford Royal NHS Foundation Trust, Manchester, UK; and the Westmead Hospital Clinical School and The George Institute for Global Health (R.I.L.), University of Sydney, Australia.
From the Division of Neuroimaging Sciences (G.M., Z.M., A.J.F., G.C., J.M.W.) and the Division of Clinical Neurosciences (P.A.G.S.), University of Edinburgh, UK; the Department of Neuroradiology (R.v.K.), Dresden University Stroke Centre, Germany; Danderyd Hospital (A.v.H.), Stockholm, Sweden; Neuroradiology (N.B.), James Cook University Hospital, Middlesborough, UK; School of Pathology and Laboratory Medicine (L.C.), University of Western Australia, Perth; Cliniques Universitaires St Luc (A.P.), Neurologie, Belgium; Stroke Center (A.A.), Sacro Cuore-Don Calabria Hospital, Negrar, Italy; the Department of Neuroradiology (G.P.), Salford Royal NHS Foundation Trust, Manchester, UK; and the Westmead Hospital Clinical School and The George Institute for Global Health (R.I.L.), University of Sydney, Australia. joanna.wardlaw@ed.ac.uk. AN - 26658907 BT - Neurology C2 - PMC4731690 DA - 93625559517 DP - NLM ET - 2015/12/15 LA - eng LB - AUS
PROF
PDO
FY16 M1 - 2 N1 - Mair, Grant
von Kummer, Rudiger
Morris, Zoe
von Heijne, Anders
Bradey, Nick
Cala, Lesley
Peeters, Andre
Farrall, Andrew J
Adami, Alessandro
Potter, Gillian
Cohen, Geoff
Sandercock, Peter A G
Lindley, Richard I
Wardlaw, Joanna M
IST-3 Collaborative Group
G0902303/Medical Research Council/United Kingdom
United States
Neurology. 2016 Jan 12;86(2):118-25. doi: 10.1212/WNL.0000000000002236. Epub 2015 Dec 9. N2 -

OBJECTIVE: To investigate whether the location and extent of the CT hyperdense artery sign (HAS) at presentation affects response to IV alteplase in the randomized controlled Third International Stroke Trial (IST-3). METHODS: All prerandomization and follow-up (24-48 hours) CT brain scans in IST-3 were assessed for HAS presence, location, and extent by masked raters. We assessed whether HAS grew, persisted, shrank, or disappeared at follow-up, the association with 6-month functional outcome, and effect of alteplase. IST-3 is registered (ISRCTN25765518). RESULTS: HAS presence (vs absence) independently predicted poor 6-month outcome (increased Oxford Handicap Scale [OHS]) on adjusted ordinal regression analysis (odds ratio [OR] 0.66, p < 0.001). Outcome was worse in patients with more (vs less) extensive HAS (OR 0.61, p = 0.027) but not in proximal (vs distal) HAS (p = 0.420). Increasing age was associated with more HAS growth at follow-up (OR 1.01, p = 0.013). Treatment with alteplase increased HAS shrinkage/disappearance at follow-up (OR 0.77, p = 0.006). There was no significant difference in HAS shrinkage with alteplase in proximal (vs distal) or more (vs less) extensive HAS (p = 0.516 and p = 0.580, respectively). There was no interaction between presence vs absence of HAS and benefit of alteplase on 6-month OHS (p = 0.167). CONCLUSIONS: IV alteplase promotes measurable reduction in HAS regardless of HAS location or extent. Alteplase increased independence at 6 months in patients with and without HAS. CLASSIFICATION OF EVIDENCE: This study provides Class I evidence that for patients within 6 hours of ischemic stroke with a CT hyperdense artery sign, IV alteplase reduced intra-arterial hyperdense thrombus.

PY - 2016 SN - 1526-632X (Electronic)
0028-3878 (Linking) SP - 118 EP - 25 T2 - Neurology TI - Effect of alteplase on the CT hyperdense artery sign and outcome after ischemic stroke VL - 86 Y2 - FY16 ER -