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• W2913783460 abstract "HomeStrokeVol. 42, No. 4Bridging Therapy in Acute Ischemic Stroke Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBBridging Therapy in Acute Ischemic StrokeAre We Ready for a New Standard of Care? Mikael Mazighi, MD, PhD and Julien Labreuche, Bst Mikael MazighiMikael Mazighi From INSERM U-698 (M.M., J.L.), Clinical Research in Atherothrombosis, Paris, France; and Denis Diderot University (M.M.), Paris VII, Neurology and Stroke Department, Hôpital Bichat, Paris, France. Search for more papers by this author and Julien LabreucheJulien Labreuche From INSERM U-698 (M.M., J.L.), Clinical Research in Atherothrombosis, Paris, France; and Denis Diderot University (M.M.), Paris VII, Neurology and Stroke Department, Hôpital Bichat, Paris, France. Search for more papers by this author Originally published3 Mar 2011https://doi.org/10.1161/STROKEAHA.110.609149Stroke. 2011;42:880–881Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2011: Previous Version 1 See related article, pages 993–997.Sixteen years after the results of The National Institute of Neurological Disorders and Stroke rtPA Stroke Study, intravenous alteplase (IV tissue plasminogen activator [tPA]) is still the unique recommended therapy for patients with acute ischemic stroke.1 Since 1995, no other acute stroke therapy has replaced this gold standard, but is IV tPA really a silver bullet? For sure, acute stroke therapy needs improvement in critical issues such as recanalization. Inability to achieve stable recanalization with IV tPA correlates with poor clinical outcome2; in this context, can we be satisfied with recanalization rates with IV tPA of 9% for internal carotid arteries or even 35% for middle cerebral arteries (MCA)?3–7 With the combination of IV and intra-arterial thrombolysis (ie, the “bridging therapy”), there is an opportunity to combine the advantages of 2 strategies: the rapidity of administration of the IV route and the arterial recanalization monitoring with additional thrombectomy of the endovascular approach.In this issue of Stroke, Rubiera et al report significantly higher recanalization rates with the “bridging therapy” compared with an IV tPA nonresponder control group (45.2% versus 18.1%, P=0.002). This increase in recanalization rates translated into more patients functionally independent at 3 months (OR, 3.75; 95% CI, 1.62 to 8.67). Previous studies have shown increased recanalization rates with the “bridging” approach but failed to show a significant clinical benefit at 3 months (OR, 1.23; 95% CI, 0.80 to 1.90 for Interventional Management of Stroke [IMS] and OR, 1.67; 95% CI, 0.86 to 3.23, for REcanalisation using Combined intravenous Alteplase and Neurointerventional ALgorithm for acute Ischemic StrokE [RECANALISE]).8,9 In IMS II and RECANALISE studies,8,9 the bridging therapy was not considered only for IV tPA nonresponder patients but for all patients with ischemic stroke 3 hours and documented arterial occlusion. With the Rubiera et al study, the benefit of the “bridging therapy” seems to increase when the target population is limited to IV tPA nonresponder patients. However, the reverse side of the medal is the safety. Albeit nonsignificant, a higher morbidity–mortality was associated with the “bridging therapy” in the Rubiera et al study (OR, 1.49; 95% CI, 0.70 to 3.16 for death and OR, 2.14; 95% CI, 0.58 to 7.83 for symptomatic intracranial hemorrhage). Is this observation due to the fact that IV tPA nonresponder patients are more severe or are we facing a narrow benefit–risk ratio? Like in carotid endarterectomy trials that showed clinical benefit at the expense of a maximum of 6% periprocedural risk at 30 days, trials will show that the clinical benefit of IV–intra-arterial procedures will be obtained at the expense of a procedure-related complication rate (eg, 10% symptomatic intracranial hemorrhagic risk) and limited to patients experiencing MCA or carotid occlusions. In IMS II and RECANALISE studies,8,9 mortality and intracranial bleeding were similar between “bridging therapy” and control groups with 10% symptomatic intracranial hemorrhage and 17% of deaths. Nonetheless, these findings illustrate that safety is the main limit of the “bridging approach.” This safety profile may not appear favorable compared with the European Cooperative Acute Stroke Study (ECASS) III trial and Safe Implementation of Thrombolysis in Stroke–International Stroke Thrombolysis Registry (SITS-ISTR) with rates of intracranial hemorrhage of approximately 2.5%.10,11 Should we remember that these trials did not include patients based on documented large artery occlusions and that studies that focused on IV tPA-treated patients with proximal MCA and persistent occlusion reported mortality rates as high as 42%?12 These elements underline the need to evaluate therapeutic approaches in the subset of different ischemic stroke populations (eg, limited to patients with large vessel occlusions of the anterior circulation). In this perspective, a remake of the Prolyse in Acute Cerebral Thromboembolism (PROACT) II study13 limited to patients with MCA occlusions and a control group including the gold standard (ie, IV tPA) is relevant. This is supported by a meta-analysis on mechanical endovascular therapy showing that patients with a favorable outcome are those with an isolated MCA occlusion and treated in association with thrombolysis.14 Pending the results of ongoing randomized trials such as IMS III, there is evidence to support “bridging therapy” as a therapeutic alternative in patients with acute ischemic stroke and documented intracranial artery occlusion such as the MCA. Last but not least, it is not clear to what extend the “bridging therapy” is a model of provision of care applicable to every stroke unit with accessible endovascular therapists and facilities 24 hours/day. We definitely need more than one string to our bow …DisclosuresNone.FootnotesThe opinions in this editorial are not necessarily those of the editors or of the American Heart Association.Correspondence to Mikael Mazighi, MD, PhD, Department of Neurology and Stroke Centre, Bichat University Hospital, 46, rue Henri Huchard, 75018 Paris, France. E-mail mikael.[email protected]aphp.frReferences1. Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rtPA Stroke Study Group. N Engl J Med. 1995; 333:1581–1587.CrossrefMedlineGoogle Scholar2. Saqqur M, Molina CA, Salam A, Siddiqui M, Ribo M, Uchino K, Calleja S, Garami Z, Khan K, Akhtar N, O'Rourke F, Shuaib A, Demchuk AM, Alexandrov AV. Clinical deterioration after intravenous recombinant tissue plasminogen activator treatment: a multicenter transcranial Doppler study. Stroke. 2007; 38:69–74.LinkGoogle Scholar3. del Zoppo GJ, Poeck K, Pessin MS, Wolpert SM, Furlan AJ, Ferbert A, Alberts MJ, Zivin JA, Wechsler L, Busse O, Greenlee R, Brass L, Mohr JP, Feldmann E, Hacke W, Kase CS, Biller J, Gress D, Otis SM. Recombinant tissue plasminogen activator in acute thrombotic and embolic stroke. Ann Neurol. 1992; 32:78–86.CrossrefMedlineGoogle Scholar4. Felberg RA, Okon NJ, El-Mitwalli A, Burgin WS, Grotta JC, Alexandrov AV. Early dramatic recovery during intravenous tissue plasminogen activator infusion: clinical pattern and outcome in acute middle cerebral artery stroke. Stroke. 2002; 33:1301–1307.LinkGoogle Scholar5. Christou I, Alexandrov AV, Burgin WS, Wojner AW, Felberg RA, Malkoff M, Grotta JC. Timing of recanalization after tissue plasminogen activator therapy determined by transcranial Doppler correlates with clinical recovery from ischemic stroke. Stroke. 2000; 31:1812–1816.LinkGoogle Scholar6. Alexandrov AV, Demchuk AM, Felberg RA, Christou I, Barber PA, Burgin WS, Malkoff M, Wojner AW, Grotta JC. High rate of complete recanalization and dramatic clinical recovery during tPA infusion when continuously monitored with 2-MHz transcranial Doppler monitoring. Stroke. 2000; 31:610–614.LinkGoogle Scholar7. Demchuk AM, Tanne D, Hill MD, Kasner SE, Hanson S, Grond M, Levine SR. Predictors of good outcome after intravenous tPA for acute ischemic stroke. Neurology. 2001; 57:474–480.CrossrefMedlineGoogle Scholar8. Mazighi M, Serfaty JM, Labreuche J, Laissy JP, Meseguer E, Lavallee PC, Cabrejo L, Slaoui T, Guidoux C, Lapergue B, Klein IF, Olivot JM, Raphaeli G, Gohin C, Claeys ES, Amarenco P. Comparison of intravenous alteplase with a combined intravenous–endovascular approach in patients with stroke and confirmed arterial occlusion (RECANALISE study): a prospective cohort study. Lancet Neurol. 2009; 8:802–809.CrossrefMedlineGoogle Scholar9. The Interventional Management of Stroke (IMS) II study. Stroke. 2007; 38:2127–2135.LinkGoogle Scholar10. Hacke W, Lichy C. Thrombolysis for acute stroke under antiplatelet therapy: safe enough to be beneficial?Nat Clin Pract Neurol. 2008; 4:474–475.CrossrefMedlineGoogle Scholar11. Wahlgren N, Ahmed N, Davalos A, Hacke W, Millan M, Muir K, Roine RO, Toni D, Lees KR. Thrombolysis with alteplase 3–4.5 h after acute ischaemic stroke (SITS-ISTR): an observational study. Lancet. 2008; 372:1303–1309.CrossrefMedlineGoogle Scholar12. Alexandrov AV, Grotta JC. Arterial reocclusion in stroke patients treated with intravenous tissue plasminogen activator. Neurology. 2002; 59:862–867.CrossrefMedlineGoogle Scholar13. Furlan A, Higashida R, Wechsler L, Gent M, Rowley H, Kase C, Pessin M, Ahuja A, Callahan F, Clark WM, Silver F, Rivera F. Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in Acute Cerebral Thromboembolism. JAMA. 1999; 282:2003–2011.CrossrefMedlineGoogle Scholar14. Rouchaud A, Mazighi M, Labreuche J, Laissy JP, Meseguer E, Lavallee PC, Cabrejo L, Slaoui T, Guidoux C, Lapergue B, Klein IF, Olivot JM, Claeys ES, Amarenco P. Outcomes of mechanical endovascular therapy for acute ischemic stroke: a clinical registry study and systematic review. Stroke. 2011; 42;In press.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Byrne J (2017) Re-establishing Blood Flow After Intravascular Thrombosis Tutorials in Endovascular Neurosurgery and Interventional Neuroradiology, 10.1007/978-3-319-54835-7_17, (337-352), . Schönenberger S and Bösel J (2015) Periinterventionelles Management der akuten endovaskulären SchlaganfallbehandlungPeri-interventional management of acute endovascular stroke treatment, Der Nervenarzt, 10.1007/s00115-015-4269-x, 86:10, (1217-1225), Online publication date: 1-Oct-2015. Mazighi M, Meseguer E, Labreuche J and Amarenco P (2012) Bridging Therapy in Acute Ischemic Stroke, Stroke, 43:5, (1302-1308), Online publication date: 1-May-2012. Byrne J (2012) Re-establishing Blood Flow After Intravascular Thrombosis Tutorials in Endovascular Neurosurgery and Interventional Neuroradiology, 10.1007/978-3-642-19154-1_17, (285-298), . Blacker D and Phatouros C (2011) Beyond IV thrombolysis for acute ischaemic stroke, Internal Medicine Journal, 10.1111/j.1445-5994.2011.02518.x, 41:8, (645-645), Online publication date: 1-Aug-2011. April 2011Vol 42, Issue 4 Advertisement Article InformationMetrics © 2011 American Heart Association, Inc.https://doi.org/10.1161/STROKEAHA.110.609149PMID: 21372303 Manuscript receivedDecember 30, 2010Manuscript acceptedJanuary 4, 2011Originally publishedMarch 3, 2011 Keywordsendovascularacute strokeIV tPAalteplasethrombolysisPDF download Advertisement SubjectsIschemic StrokeTreatment" @default.
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