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• W2800267908 abstract "HomeStrokeVol. 49, No. 5Advances in Stroke 2017 Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBAdvances in Stroke 2017 Julie Bernhardt, PhD, Richard D. Zorowitz, MD, Kyra J. Becker, MD, Emanuela Keller, MD, Gustavo Saposnik, MD, PhDc, Daniel Strbian, MD, PhD, MSc, Martin Dichgans, MD, Daniel Woo, MD, MS, Mathew Reeves, BVSc, PhD, Amanda Thrift, BSc, PhD, PGDipBiostat, Chelsea S. Kidwell, MD, Jean Marc Olivot, MD, PhD, Mayank Goyal, MD, FRCPC, Laurent Pierot, MD, PhD, Derrick A. Bennett, PhD, George Howard, DrPH, Gary A. Ford, FMedSci, Larry B. Goldstein, MD, Anna M. Planas, PhD, Midori A. Yenari, MD, Steven M. Greenberg, MD, PhD, Leonardo Pantoni, PhD, Sepideh Amin-Hanjani, MD and Michael Tymianski, MD Julie BernhardtJulie Bernhardt From the Florey Institute of Neuroscience and Mental Health, University of Melbourne, Australia (J.B.) Search for more papers by this author , Richard D. ZorowitzRichard D. Zorowitz MedStar National Rehabilitation Network and Department of Rehabilitation Medicine, Georgetown University School of Medicine, Washington, DC (R.D.Z.) Search for more papers by this author , Kyra J. BeckerKyra J. Becker Department of Neurology, University of Washington, Seattle (K.J.B.) Search for more papers by this author , Emanuela KellerEmanuela Keller Division of Internal Medicine, University Hospital of Zurich, Switzerland (E.K.) Search for more papers by this author , Gustavo SaposnikGustavo Saposnik Faculty of Medicine, University of Toronto, ON, Canada (G.S.) Search for more papers by this author , Daniel StrbianDaniel Strbian Department of Neurology, Helsinki University Central Hospital, Finland (D.S.) Search for more papers by this author , Martin DichgansMartin Dichgans Institute for Stroke and Dementia Research, Klinikum der Universität München, Ludwig-Maximilians-Universität LMU, Germany (M.D.) Munich Cluster for Systems Neurology (SyNergy), Germany (M.D.) Search for more papers by this author , Daniel WooDaniel Woo Department of Neurology, University of Cincinnati College of Medicine, OH (D.W.) Search for more papers by this author , Mathew ReevesMathew Reeves Department of Epidemiology and Biostatistics, Michigan State University, East Lansing (M.R.) Search for more papers by this author , Amanda ThriftAmanda Thrift Department of Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, Victoria, Australia (A.T.) Search for more papers by this author , Chelsea S. KidwellChelsea S. Kidwell Departments of Neurology and Medical Imaging, University of Arizona, Tucson (C.S.K.) Search for more papers by this author , Jean Marc OlivotJean Marc Olivot Acute Stroke Unit, Toulouse Neuroimaging Center and Clinical Investigation Center, Toulouse University Hospital, France (J.M.O.) Search for more papers by this author , Mayank GoyalMayank Goyal Department of Diagnostic and Interventional Neuroradiology, University of Calgary, AB, Canada (M.G.) Search for more papers by this author , Laurent PierotLaurent Pierot Department of Neuroradiology, Hôpital Maison Blanche, CHU Reims, Reims Champagne-Ardenne University, France (L.P.) Search for more papers by this author , Derrick A. BennettDerrick A. Bennett Clinical Trial Service Unit and Epidemiological Studies Unit (CTSU), Nuffield Department of Population Health, University of Oxford, United Kingdom (D.A.B.) Search for more papers by this author , George HowardGeorge Howard Department of Biostatistics, Ryals School of Public Health, University of Alabama at Birmingham (G.H.) Search for more papers by this author , Gary A. FordGary A. Ford Oxford Academic Health Science Network, United Kingdom (G.A.F.) Search for more papers by this author , Larry B. GoldsteinLarry B. Goldstein Department of Neurology, University of Kentucky, Lexington (L.B.G.) Search for more papers by this author , Anna M. PlanasAnna M. Planas Department of Brain Ischemia and Neurodegeneration, Institute for Biomedical Research of Barcelona (IIBB), Consejo Superior de Investigaciones CIentíficas (CSIC), Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain (A.M.P.) Search for more papers by this author , Midori A. YenariMidori A. Yenari Department of Neurology, University of California, San Francisco (M.A.Y.) San Francisco Veterans Affairs Medical Center, CA (M.A.Y.) Search for more papers by this author , Steven M. GreenbergSteven M. Greenberg Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston (S.M.G.) Search for more papers by this author , Leonardo PantoniLeonardo Pantoni ‘L. Sacco’ Department of Biomedical and Clinical Sciences, University of Milan, Italy (L.P.) Search for more papers by this author , Sepideh Amin-HanjaniSepideh Amin-Hanjani Department of Neurosurgery, University of Illinois at Chicago (S.A.-H.) Search for more papers by this author and Michael TymianskiMichael Tymianski Departments of Surgery and Physiology, University of Toronto, ON, Canada (M.T.) Department of Surgery, University Health Network (Neurosurgery), Toronto, ON, Canada (M.T.) Krembil Research Institute, Toronto Western Hospital, ON, Canada (M.T.). Search for more papers by this author Originally published18 Apr 2018https://doi.org/10.1161/STROKEAHA.118.021380Stroke. 2018;49:e174–e199Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2018: Previous Version 1 Brain Recovery and RehabilitationFor stroke rehabilitation and recovery, 2017 was a year of reviews and research advances. Reviews included all aspects of poststroke rehabilitation and recovery. Cognitive rehabilitation for memory deficits was effective for memory improvements in the short term, but not in the long term.1 Circuit class therapy could improve mobility after stroke in a clinically meaningful way, even after 12 months poststroke.2 Electromechanical-assisted training for walking was most beneficial for subacute stroke survivors who were not ambulatory.3 Repetitive task training was effective regardless of the amount of task practice, type of intervention, or time since stroke.4 Physical activity training could positively affect poststroke cognition with small-to-moderate treatment effects that were apparent even in the chronic stroke phase.5 In all cases, more research was required to improve the quality of the findings, and a review of poststroke fatigue reported that the overall quality of the research was poor.6Discovery research provided more insight into basic aspects of stroke rehabilitation and recovery. Stradecki-Cohan et al7 studied Sprague–Dawley rats subjected to 5 to 6 days of no (0 m/min), mild (6 m/min), moderate (10 m/min), or heavy (15–18 m/min) treadmill exercise 3 to 4 days poststroke and demonstrated that moderate exercise enhanced cognitive function for 1 week after exercise completion, independent of changes in physical fitness. Chang et al8 demonstrated that the number of Met alleles in brain-derived neurotrophic factor genotypes and corticospinal tract (CST) functional integrity may be independent predictors of upper extremity motor outcome 3 months poststroke. Tu et al9 found that concentrations of FABP4 (fatty acid–binding protein 4), an intracellular lipid chaperone involved in coordination of lipid transportation and atherogenesis, were a novel independent prognostic marker for poor functional outcome and mortality 3 months poststroke.Imaging of the CST also played a role in poststroke functional prognosis. Schulz et al10 found that different degrees of CST disruption differed in their dependency on structural premotor–motor connections for residual motor output using diffusion-weighted imaging and probabilistic tractography. Liu et al11 reported that local diffusion homogeneity, a complementary marker for white matter alterations of the brain, in the ipsilesional CST paired with clinical assessment in acute stroke may accurately predict resolution of upper limb impairment within 12 weeks after subcortical infarction. Stinear et al12 demonstrated that stroke survivors with functional CSTs recovered proportionally to their initial upper limb motor impairments, but those without functional CSTs did not recover proportionally and were impacted by greater CST damage. Furthermore, lower limb motor impairment resolved by ≈70% within 3 months after stroke and did not follow the proportionality rule.13 Finally, Stinear et al14 applied the Predict Recovery Potential algorithm, consisting of an assessment of paretic shoulder abduction and wrist extension strength, transcranial magnetic stimulation to assess the functional integrity of the ipsilesional lateral CST 5 to 7 days poststroke, and diffusion-weighted magnetic resonance imaging (MRI) to a cohort of acute stroke patients and found that it predicted the primary clinical outcome for 80% of recruited subjects. They reported reduced length of stay by 6 days in subjects for whom therapy content was modified based on the algorithm, when compared with a historical control.14Clinical research continued to play a role in clarifying patterns of functional prognosis. Itaya et al15 reported that living situation, type of stroke, Functional Independence Measure motor and cognitive scores on admission, and paresis predicted discharge to home after acute stroke with a sensitivity of 88.0% and a specificity of 68.7%. Scrutinio et al16 developed a predictive models to assist clinicians in decision-making and planning rehabilitation care, including measures of time from stroke occurrence to rehabilitation admission, admission motor and cognitive Functional Independence Measure scores, and neglect; and age, male sex, time since stroke onset, and admission motor and cognitive Functional Independence Measure scores. MacIsaac et al17 developed a short-form Barthel Index that condensed function to bladder control, transfer, and mobility items. Wang et al18 developed a Functional Assessment of Stroke consisting of 29 items from 4 short-form tests of the Fugl-Meyer Assessment upper extremity, Fugl-Meyer Assessment lower extremity, Postural Assessment Scale for Stroke patients, and Barthel Index. Kapoor et al19 reported that the modified Rankin Scale (mRS; modified Barthel index) was inadequate to measure overall stroke outcomes as more than half of stroke survivors with excellent functional recovery measured this way continued to have cognitive impairment and participation restrictions, and one third of patients continue to have depression 2 to 3 years poststroke.Drug trials continued to have mixed results. A phase IIb double-blind, randomized, placebo-controlled trial of intravenous infusions of the monoclonal antibody GSK249320 within 72 hours of stroke demonstrated no improvement on gait velocity compared with placebo.20 However, stroke survivors with persistent fatigue reported reduced fatigue and improved quality of life after taking modafinil 200 mg by mouth daily.21Technology played a role in stroke rehabilitation. A preliminary study of the Fitbit One positioned on the nonparetic ankle accurately measured walking steps during inpatient rehabilitation physical therapy sessions.22 A powered exoskeleton driven by a brain–computer interface, using neural activity from the unaffected cortical hemisphere, produced significant average increases in the Action Research Arm Test score, as well as improvements in grasp strength, Motricity Index, and the Canadian Occupational Performance Measure.23Finally, 2 groups are attempting to facilitate or advocate for quality stroke rehabilitation and recovery research. First, the National Institutes of Health (NIH) instituted NIH StrokeNet, a network of centers that forms a foundation for stroke recovery and rehabilitation research. Several issues that the Working Group are addressing to improve the ability to complete meaningful clinical trials successfully include variable patterns of postacute stroke care delivery; challenges in recruiting and retaining subjects after discharge from the acute care setting; challenges in dealing with social and pragmatic factors in stroke rehabilitation research; the importance of concomitant activity and therapy during research participation; the competition among stroke rehabilitation and recovery research, other stroke trials, and healthcare business practices; the need to implement biomarkers; and standardization of outcomes measures.24 The other group is an international roundtable of stroke rehabilitation and recovery research experts who are developing a conceptually rigorous framework for stroke rehabilitation and recovery research. They have defined the concepts of rehabilitation and recovery and made recommendations in the areas of basic science, biomarkers of stroke recovery, measurement in clinical trials, and intervention development and reporting.25 Subsequently, they have defined the concept of sensorimotor recovery and measures consistent with this definition.26Critical Care/Emergency MedicineNovel Oral Anticoagulants and Intracranial HemorrhageWith the increasing use of novel oral anticoagulants (NOACs) or direct oral anticoagulants, vascular neurologists and neurocritical care providers are more commonly encountering situations in which decisions need to be made about either starting or reversing these medications. The most common clinical indication for the NOACs is atrial fibrillation, and the most dreaded complication of NOACs is intracranial hemorrhage (ICH). This brief review will summarize the data on the safety and efficacy of the NOACs, with an emphasis on ICH, as well as the strategies to reverse the anticoagulation effects of the NOACs in those suffering bleeding complications.NOACs and the Risk of ICHThe NOACs, including dabigatran (a direct thrombin inhibitor), apixaban and rivaroxaban (factor Xa inhibitors), and edoxaban (Xa and prothrombinase inhibitor), have at least equal efficacy, and to some extent a better safety profile, compared with vitamin K antagonists (VKAs), in patients with atrial fibrillation.27–31 A meta-analysis of the randomized trials comparing 42 411 patients treated with NOACs and 29 272 treated with warfarin showed that NOACs significantly reduced stroke and systemic embolic events compared with warfarin (relative risk reduction [RR], 0.81; 95% confidence interval [CI], 0.73–0.91; P<0.0001), a result that was mainly driven by a reduction in ICH (RR, 0.49; 95% CI, 0.38–0.64; P<0.0001).32 The relative reduction in ICH, including intracerebral hemorrhage, subarachnoid hemorrhage, subdural hemorrhage, and epidural hemorrhage, observed with NOACs compared with warfarin was over 50% (RR, 0.48; 95% CI, 0.39–0.59; P<0.0001). All-cause mortality was also less in individuals taking NOACs (RR, 0.90; 95% CI, 0.85–0.95; P=0.0003), but there was an associated increase in gastrointestinal bleeding (RR, 1.25; 95% CI, 1.01–1.55; P=0.04).More recent evidence from 28 high-quality real-world observational studies confirms the findings of the randomized controlled trials (RCTs) on the efficacy and safety of NOACs (dabigatran, rivaroxaban, and apixaban) in comparison to warfarin in patients with atrial fibrillation.33 In particular, all 3 of these drugs were associated with a lower risk of ICH (apixaban hazard ratio [HR], 0.45; 95% CI, 0.31–0.63; dabigatran HR, 042; 95% CI, 0.37–0.49; rivaroxaban HR, 0.64; 95% CI, 0.47–0.86). Although the risk of ischemic stroke (IS) and systemic embolism was similar for all drugs, apixaban and dabigatran were both associated with lower mortality and apixaban was associated with fewer major and gastrointestinal hemorrhages.On the basis of MarketScan data in the specific subgroup of patients with nonvalvular atrial fibrillation who have had a previous IS or transient ischemic attack, neither apixaban nor dabigatran reduced the combined primary end point of IS or ICH (HR, 0.70; 95% CI, 0.33–1.48 and HR, 0.53; 95% CI, 0.26–1.07), whereas rivaroxaban reduced the same combined end point (HR, 0.45; 95% CI, 0.29–0.72).34 In these analyses, the rate of ICH was similar for the NOACs and warfarin. In a sample of Medicare beneficiaries, however, apixaban use was associated with the highest treatment persistence and lowest risk of any bleeding, compared with warfarin, rivaroxaban, and dabigatran.35In summary, compared with VKAs, the NOACs, dabigatran, rivaroxaban, apixaban, and edoxaban, are at least as effective as VKAs to prevent IS and IS/systemic embolism in patients with atrial fibrillation. Importantly, ICH is reduced by roughly half.32 Further, when compared with warfarin, NOACs have a more rapid onset of action, a shorter half-life, more predictable pharmacokinetics, less potential drug–drug interactions, and do not require routine monitoring.36Current guidelines for antithrombotic therapy in nonvalvular atrial fibrillation, including the European Society of Cardiology and the American Heart Association/American College of Cardiology/Heart Rhythm Society, generally recommend NOACs in preference to or as an alternative to warfarin for stroke prevention,37,38 and for patients who need to be anticoagulated despite a high risk for bleeding complications (as estimated by the HAS-BLED score [hypertension, abnormal renal or hepatic function, stroke history, bleeding history or predisposition, labile international normalized ratio, elderly (age >65 years), drug or alcohol abuse]), NOACs are felt to be a safer option than warfarin,39 especially in light of the fact that the risk of major bleeding with apixaban in the AVERROES trial (Apixaban Versus Acetylsalicylic Acid to Prevent Stroke in Atrial Fibrillation Patients Who Have Failed or Are Unsuitable for Vitamin K Antagonist Treatment) was as low as that seen with aspirin.28Unfortunately, there are no direct comparisons of the 4 NOACs, and indirect comparisons between the RCTs are problematic as patients had different risk profiles (ie, different CHADS2 or CHA2DS2-VASc scores [congestive heart failure, hypertension, age (≥75 years), diabetes, prior stroke or transient ischemic attack, vascular disease, age (65–74 years), sex category]). Individual assessment of the optimal drug choice and dose adjustments is required for each patient. The elderly with renal dysfunction and with prior strokes are at increased risk of both ischemic events and bleeding events; such individuals require a more nuanced approach to anticoagulant treatment.When and whether to resume anticoagulation after ICH is a common clinical dilemma.40 The risk of thromboembolic events, based on a stratification scheme such as the CHA2DS2-VASc score, has to be balanced against the risk of ICH recurrence. Factors associated with the risk of ICH reoccurrence include increasing age, poor blood pressure (BP) control, lobar ICH location, the presence of microbleeds on susceptibility-weighted imaging, concurrent aspirin use, and the presence of apolipoprotein E ε2 or ε4 alleles and must be taken into account.32,40NOAC ReversalThe most commonly encountered reason for reversing the anticoagulant effects of NOACs in the neurological intensive care unit is ICH. Hemorrhage enlargement after initial presentation with intracerebral hemorrhage is common and portends a poor outcome.41 Further, patients who suffer an intracerebral hemorrhage while anticoagulated do worse than patients who are not anticoagulated.42 Fortunately, the risk of ICH with NOACs is generally less than that with warfarin.43 Nonetheless, individuals will still present with ICH while anticoagulated with an NOAC. It is thus prudent to understand the most expedient methods for reversing the biological effects of these drugs in the hopes of preventing intracerebral hemorrhage growth, especially in light of data that show rapid reversal of anticoagulation by VKAs is associated with a decrease in hemorrhage enlargement.44,45Observational data suggest that the outcomes of intracerebral hemorrhage associated with the NOACs are similar to that in patient on VKAs—baseline intracerebral hemorrhage volume, the rates of hematoma expansion, 90-day mortality and functional outcome are similar.46–48 The half-lives of the NOACs are much shorter than that of warfarin, but the risk of hemorrhage expansion occurs early after presentation and it is incumbent on the practitioner to reverse the anticoagulant effects of the NOAC as quickly as possible.Dabigatran is a direct thrombin inhibitor and currently the only NOAC with a Food and Drug Administration–approved reversal agent, idarucizumab. Treatment with idarucizumab decreases dabigatran levels and normalizes laboratory measures of anticoagulation (including the diluted thrombin time and ecarin clotting time) almost immediately.49 In a study of the safety and efficacy of idarucizumab for dabigatran reversal, 98 of 301 (32.6%) patients who presented with uncontrolled bleeding had an ICH. Data show that essentially all patients in this study had full reversal at 4 hours after administration of idarucizumab.50 Thrombotic events occurred within 30 days after treatment in 14 of 301 (4.6%) patients who presented with bleeding complications and were treated with idarucizumab. As this was a single-arm trial, there are no data to prove that reversal of dabigatran with idarucizumab improves outcome from ICH, but with the approval/availability of idarucizumab, such a study could not be ethically done. Laboratory data suggest that prothrombin complex concentrate (PCC) does not adequately reverse the anticoagulation effects of dabigatran, and PCC should not be given to patients who present with an ICH while on dabigatran.51At present, there are no approved specific reversal agents for the oral factor Xa inhibitors (apixaban, rivaroxaban, and edoxaban). PCCs are often used to reverse Xa inhibitors, and laboratory studies confirm rapid normalization of selected clotting parameters with 4 factor PCC.52 Data to support the clinical efficacy of PCCs in patients who experience ICH while taking Xa inhibitors, however, are limited. In a multicenter observational study, the use of PCCs did not seem to prevent intracerebral hemorrhage growth or improve outcome.53Andexanet alfa is a specific reversal agent designed to neutralize the anticoagulant effects of factor Xa inhibitors. In a trial of healthy older volunteers, andexanet reversed the anticoagulant effects of apixaban and rivaroxaban within minutes.54 In a trial of 67 patients with acute major bleeding events within 18 hours after receiving a factor Xa inhibitor, andexanet reduced antifactor Xa activity and achieved effective hemostasis in 79% of patients by 12 hours after infusion.55 ICH was the presenting bleeding complication in 28 of 67 (42%) patients, and thrombotic events occurred in 12 of 67 (18%) within 30 days of andexanet administration. As with the trial of idarucizumab for neutralization of the effects of dabigatran, this single-arm trial cannot address whether andexanet improves outcome from ICH in patients on apixaban or rivaroxaban. Additional clinical studies are ongoing.Aripazine (also known as ciraparantag or PER977) is small molecule that binds to unfractionated and low–molecular weight heparins, fondaparinux, dabigatran, and Xa inhibitors. Aripazine has been shown to reverse the effects of edoxaban in healthy volunteers within 10 minutes.56 Advanced phase clinical studies of aripazine are underway.In summary, for patients who suffer an ICH while taking dabigatran, treatment with idarucizumab is indicated. For patients who suffer an ICH on apixaban, rivaroxaban, or edoxaban, the current recommendation is to administer PCCs. In the near future, however, it is possible that specific reversal agents will be available.Emerging TherapiesOver the past 2 years, the results of large clinical trials provided data that have the potential to change clinical practice of stroke care. Some of the results can be seen as hypothesis generating and need to be confirmed by subsequent trials. Herein, we discuss the highlights of several relevant articles during the past 2 years that have influenced the field of emerging therapies for stroke.Acute Stroke Recanalization TreatmentThe ENCHANTED (Enhanced Control of Hypertension and Thrombolysis Stroke Study)57 was a noninferiority trial assigning randomly 3310 thrombolysis-eligible patients to low-dose intravenous alteplase (0.6 mg/kg body weight) or to standard dose (0.9 mg/kg of body weight). The trial also included 935 patients who were randomly assigned to intensive or guideline-recommended BP management, the results of this BP substudy are yet to be published. The idea behind the trial was based on the data from Asian cohorts, and the low dose was considered to be noninferior compared with the standard dose on the efficacy and to have lower frequency of intracerebral hemorrhagic complications. Affordability of the low-dose treatment was another aspect driving the need for this trial. The noninferior design of the trial was recently addressed.58 Treatment with the low-dose alteplase did not reach the prespecified noninferiority boundaries on the primary objective (3-month disability or death, mRS score of 2–6) despite the fact that two thirds of the patients were from Asia, where low-dose alteplase is frequently the treatment of choice because of a presumed high risk of ICH associated with the standard-dose treatment. The percentage of a good functional outcome (mRS score of 0–1) was 48.9% and 46.8% in the standard-dose and low-dose groups, respectively. This was true despite lower rate of major symptomatic ICHs in the low-dose group (1.0% versus 2.1%). Most probably, major hemorrhage occurred in patients with large infarctions and had no impact on the patients’ outcome anyway. It would be of interest to have the data of low-dose alteplase in patients with white matter lesions. The trial may be seen as a hypothesis generating for a possible future trial testing low dose versus standard dose in patients on antiplatelet medication. Nonetheless, the trial provided no evidence that treatment of low-dose alteplase should replace the standard dose in acute stroke patients with different ethnical backgrounds and pre-medication.The DAWN (DWI or CTP Assessment With Clinical Mismatch in the Triage of Wake Up and Late Presenting Strokes Undergoing Neurointervention With Trevo).59 The trial has clearly showed us that endovascular therapy compared with best medical treatment is associated with an improvement in clinical outcomes (>70% relative reduction in disability) and higher likelihood of functional independence in patients with a large vascular occlusion treated within 24 hours from last known well. It is important to note that the last time seen well does not equal to the first time seen unwell. The majority of patients qualified as wake-up strokes (more commonly in the intervention group) with an average time since last seen well of 13 hours and 5 hours from the time of first observation of stroke symptoms, which is similar to previous endovascular trials. On the other hand, it seems that recanalization treatment may be effective beyond generally accepted time delays from symptom onset as long as the infarct core is relatively small and there is substantial amount of the tissue to be saved. In fact, a clinical-core mismatch as defined by the DAWN trials seems a relevant selection criterion independent of the time of presentation. We still have limited understanding of the therapeutic benefits among patients with larger core infarcts (involving more than one third of the middle cerebral artery) or how to select patients when DAWN prespecified imaging criteria (RAPID automatic patient selection tool) is not available.Advances in the Management of Hypertension in Acute StrokeThe ATACH-II (Antihypertensive Treatment of Acute Cerebral Hemorrhage II)60 trial tested 2 different strategies of acute BP management in patients with intracerebral hemorrhage. One thousand patients were randomized to a systolic BP (SBP) target of 110 to 139 or 140 to 179 mm Hg; the trial was stopped because of futility data. There was a clear and early difference in BP values between groups; however, this did not translate into the 3-month functional outcome and mortality. There was no intergroup difference on early neurological deterioration. However, patients in the aggressive BP management had higher frequency of renal adverse events, which could have been caused by renal hypoperfusion. There was only a trend for a smaller frequency of hematoma expansion in patients randomized to aggressive BP reduction. However, we need to point out that hematoma expansion was much less frequent than expected even in the conservatively treated patients. Of note, hematomas had a small baseline volume (median 10 mL). It appears from these results that hematoma expansion occurs despite early and aggressive BP management. The same held true for the INTERACT-II trial (Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial), however, in that trial majority of the patients have not reached the target BP value within prespecified time window, which clearly differs from ATACH-II. It might be of interest to perform a trial similar to ATACH-II but with the BP management already in a prehospital setting. Such trial should analyze not only possible benefits of such an approach but also potential harms of aggressive BP lowering (at least cerebral and renal perfusion).The SPRINT (Systolic Blood Pressure Intervention Trial)61 involved 9361 hypertensive patients (mean age, 68 years) randomized to 2 SBP management groups (target <120 versus <140 mm Hg). Th" @default.
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• W2800267908 title "Advances in Stroke 2017" @default.
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