Fana Alemseged1, Felix C Ng2, Cameron Williams2, Volker Puetz2, Gregoire Boulouis2, Timothy John Kleinig2, Alessandro Rocco2, Teddy Y Wu2, Darshan Shah2, Francesco Arba2, Daniel Kaiser2, Francesca Di Giuliano2, Andrea Morotti2, Fabrizio Sallustio2, Helen M Dewey2, Peter Bailey2, Billy O'Brien2, Gagan Sharma2, Steven Bush2, Richard Dowling2, Marina Diomedi2, Leonid Churilov2, Bernard Yan2, Mark William Parsons2, Stephen M Davis2, Peter J Mitchell2, Nawaf Yassi2, Bruce C V Campbell2. 1. From the Department of Medicine and Neurology (F. Alemseged, G.S., L.C., B.Y., M.W.P., S.M.D., P.J.M., N.Y. B.C.V.C.), University of Melbourne, and Department of Radiology (C.W., S.B., R.D.), Royal Melbourne Hospital, Parkville, Australia; Stroke Unit (F. Alemseged, A.R., F.S., M.D.) and Department of Biomedicine and Prevention (F.D.), University Hospital of Tor Vergata, Rome, Italy; Department of Neurology (F.C.N.), Austin Health, Melbourne, Australia; Department of Neurology (V.P.), Institute of Neuroradiology (D.K.), and Dresden Neurovascular Center (V.P., D.K.), University of Technology Dresden, Germany; Department of Interventional Neuroradiology (G.B.), Sainte-Anne-Hospital, Paris, France; Department of Neurology (T.J.K.), Royal Adelaide Hospital, Australia; Department of Neurology (T.Y.W.), Christchurch Hospital, New Zealand; Division of Medicine (D.S.), Princess Alexandra Hospital, Brisbane, Australia; NEUROFARBA Department (F. Arba), Careggi University Hospital, Florence; ASST Valcamonica (A.M.), Department of Neurology, Esine, Italy; Department of Neurosciences (H.M.D.), Eastern Health, Melbourne; Department of Neurology (P.B.), Gold Coast University Hospital, Queensland; Department of Neurology (B.O.), Gosford Hospital, New South Wales; and Population Health and Immunity Division (N.Y.), The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia. fana.alemseged@mh.org.au. 2. From the Department of Medicine and Neurology (F. Alemseged, G.S., L.C., B.Y., M.W.P., S.M.D., P.J.M., N.Y. B.C.V.C.), University of Melbourne, and Department of Radiology (C.W., S.B., R.D.), Royal Melbourne Hospital, Parkville, Australia; Stroke Unit (F. Alemseged, A.R., F.S., M.D.) and Department of Biomedicine and Prevention (F.D.), University Hospital of Tor Vergata, Rome, Italy; Department of Neurology (F.C.N.), Austin Health, Melbourne, Australia; Department of Neurology (V.P.), Institute of Neuroradiology (D.K.), and Dresden Neurovascular Center (V.P., D.K.), University of Technology Dresden, Germany; Department of Interventional Neuroradiology (G.B.), Sainte-Anne-Hospital, Paris, France; Department of Neurology (T.J.K.), Royal Adelaide Hospital, Australia; Department of Neurology (T.Y.W.), Christchurch Hospital, New Zealand; Division of Medicine (D.S.), Princess Alexandra Hospital, Brisbane, Australia; NEUROFARBA Department (F. Arba), Careggi University Hospital, Florence; ASST Valcamonica (A.M.), Department of Neurology, Esine, Italy; Department of Neurosciences (H.M.D.), Eastern Health, Melbourne; Department of Neurology (P.B.), Gold Coast University Hospital, Queensland; Department of Neurology (B.O.), Gosford Hospital, New South Wales; and Population Health and Immunity Division (N.Y.), The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia.
Abstract
OBJECTIVE: To investigate the efficacy of tenecteplase (TNK), a genetically modified variant of alteplase with greater fibrin specificity and longer half-life than alteplase, prior to endovascular thrombectomy (EVT) in patients with basilar artery occlusion (BAO). METHODS: To determine whether TNK is associated with better reperfusion rates than alteplase prior to EVT in BAO, clinical and procedural data of consecutive patients with BAO from the Basilar Artery Treatment and Management (BATMAN) registry and the Tenecteplase vs Alteplase before Endovascular Therapy for Ischemic Stroke (EXTEND-IA TNK) trial were retrospectively analyzed. Reperfusion >50% or absence of retrievable thrombus at the time of the initial angiogram was evaluated. RESULTS: We included 110 patients with BAO treated with IV thrombolysis prior to EVT (mean age 69 [SD 14] years; median NIH Stroke Scale score 16 [interquartile range (IQR) 7-32]). Nineteen patients were thrombolysed with TNK (0.25 mg/kg or 0.40 mg/kg) and 91 with alteplase (0.9 mg/kg). Reperfusion >50% occurred in 26% (n = 5/19) of patients thrombolysed with TNK vs 7% (n = 6/91) thrombolysed with alteplase (risk ratio 4.0, 95% confidence interval 1.3-12; p = 0.02), despite shorter thrombolysis to arterial puncture time in the TNK-treated patients (48 [IQR 40-71] minutes) vs alteplase-treated patients (110 [IQR 51-185] minutes; p = 0.004). No difference in symptomatic intracranial hemorrhage was observed (0/19 [0%] TNK, 1/91 [1%] alteplase; p = 0.9). CONCLUSIONS: TNK may be associated with an increased rate of reperfusion in comparison with alteplase before EVT in BAO. Randomized controlled trials to compare TNK with alteplase in patients with BAO are warranted. CLINICALTRIALSGOV IDENTIFIERS: NCT02388061 and NCT03340493. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that TNK leads to higher reperfusion rates in comparison with alteplase prior to EVT in patients with BAO.
OBJECTIVE: To investigate the efficacy of tenecteplase (TNK), a genetically modified variant of alteplase with greater fibrin specificity and longer half-life than alteplase, prior to endovascular thrombectomy (EVT) in patients with basilar artery occlusion (BAO). METHODS: To determine whether TNK is associated with better reperfusion rates than alteplase prior to EVT in BAO, clinical and procedural data of consecutive patients with BAO from the Basilar Artery Treatment and Management (BATMAN) registry and the Tenecteplase vs Alteplase before Endovascular Therapy for Ischemic Stroke (EXTEND-IA TNK) trial were retrospectively analyzed. Reperfusion >50% or absence of retrievable thrombus at the time of the initial angiogram was evaluated. RESULTS: We included 110 patients with BAO treated with IV thrombolysis prior to EVT (mean age 69 [SD 14] years; median NIH Stroke Scale score 16 [interquartile range (IQR) 7-32]). Nineteen patients were thrombolysed with TNK (0.25 mg/kg or 0.40 mg/kg) and 91 with alteplase (0.9 mg/kg). Reperfusion >50% occurred in 26% (n = 5/19) of patients thrombolysed with TNK vs 7% (n = 6/91) thrombolysed with alteplase (risk ratio 4.0, 95% confidence interval 1.3-12; p = 0.02), despite shorter thrombolysis to arterial puncture time in the TNK-treated patients (48 [IQR 40-71] minutes) vs alteplase-treated patients (110 [IQR 51-185] minutes; p = 0.004). No difference in symptomatic intracranial hemorrhage was observed (0/19 [0%] TNK, 1/91 [1%] alteplase; p = 0.9). CONCLUSIONS: TNK may be associated with an increased rate of reperfusion in comparison with alteplase before EVT in BAO. Randomized controlled trials to compare TNK with alteplase in patients with BAO are warranted. CLINICALTRIALSGOV IDENTIFIERS: NCT02388061 and NCT03340493. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that TNK leads to higher reperfusion rates in comparison with alteplase prior to EVT in patients with BAO.
Authors: Aristeidis H Katsanos; Klearchos Psychogios; Guillaume Turc; Simona Sacco; Diana Aguiar de Sousa; Gian Marco De Marchis; Lina Palaiodimou; Dimitrios K Filippou; Niaz Ahmed; Amrou Sarraj; Bijoy K Menon; Georgios Tsivgoulis Journal: JAMA Netw Open Date: 2022-03-01
Authors: Katharina Gruber; Björn Misselwitz; Helmuth Steinmetz; Waltraud Pfeilschifter; Ferdinand O Bohmann Journal: Front Neurol Date: 2021-06-11 Impact factor: 4.003