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9/8/2009
1
National Stroke Association presents
Acute Stroke Treatment:Acute Stroke Treatment:Evidence and Opportunities
September 10, 2009
This program is supported by educationalgrants from Genentech, Inc. and Penumbra,Inc.
AccreditationThis activity has been planned andimplemented in accordance with theEssential Areas and policies of theAccreditation Council of Continuing MedicalEducation through the joint sponsorship ofg j p pMedical Education Resources and NationalStroke Association.Medical Education Resources is accreditedby the ACCME to provide continuingmedical education for physicians.
9/8/2009
2
Accreditation
Medical Education Resources is an approvedprovider of continuing nursing education byColorado Nurses Association an accreditedColorado Nurses Association, an accreditedapprover by the American Nurses CredentialingCenter’s Commission on Accreditation.
Credit Designation
MER designates this educational activity for amaximum of 1.5 AMA PRA Category 1 CreditTM.Physicians should only claim credit commensurate
ith the e tent of their participation in thewith the extent of their participation in theactivity.
This CE activity provides 1.5 contact hours.Provider approval expires July 31, 2010.
Disclaimer
The content and views presented in thiseducational program are those of the authors andfaculty and do not necessarily reflect those ofMedical Education Resources or National StrokeAssociation. Before prescribing any medicine, primaryReferences and full prescribing information should beconsulted. All faculty members participating in continuingmedical education programs sponsored by MER areexpected to disclose any real or perceived conflict ofinterest related to the content of their presentations. Facultydisclosures are included in your program materials.
9/8/2009
3
Learning Objectives
At the conclusion of this activity, participants should be ableto:• Describe the incidence of ischemic stroke and the
opportunity to maximize patient outcomes.• Describe guidelines-based acute ischemic stroke treatment
strategies.• Identify clinically important recent advances in stroke
management and apply the latest guidelines into clinical practice.
• Access enduring resources to assist clinicians to educate themselves and make modifications to current practice and/or process.
The Critical First Hours in Acute Stroke:
The Emergency Department
Edward C. Jauch, MD MSAssociate Professor
Department of Emergency MedicineAssociate Professor
Department of NeurosciencesMedical University of South Carolina
Charleston, SC
Edward C. Jauch, MD MSAssociate Professor
Department of Emergency MedicineAssociate Professor
Department of NeurosciencesMedical University of South Carolina
Charleston, SC
Disclosures
• ConsultingGenentech (2008)
• Research supportNovo Nordisk
• National Institutes of Health supportIMS-III, SPOTRIAS, ALIAS2, FAST-MAG
9/8/2009
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Lecture Goals
• Briefly review the pathophysiology of brain ischemia
• Review treatment options for ischemic stroke
• Highlight critical steps in the Emergency Department
• Brief look at the future
Pathophysiology of Ischemic StrokeCerebral Blood Flow Thresholds
100
90
80
70min
Normal
70
60
50
40
30
20
10
0
CB
F m
l / 1
00 g
m /
Hypo-perfusion
Oligemia
IschemiaInfarct
Penumbra
(Muir, (Muir, Lancet Neurology,Lancet Neurology, 2005)2005)
Abnormal neuronal function documented by a correlation with acute
clinical deficit
Goals of Early ED Management
• Penumbra– Abnormal neuronal function documented by a
correlation with acute clinical deficit– Physiological and/or biochemical characteristics
consistent with cellular dysfunction but not deathconsistent with cellular dysfunction but not death– Uncertain fate but salvage is correlated with better
clinical recovery• Limit penumbral progression
– Physiologic optimization– Targeted neuroprotection– Global (pluripotential) neuroprotection
• Optimize blood flow– Restore flow and improve collateral flow
9/8/2009
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Altered Mental Status
Stroke / TIA
Coma / Cardiac A t
Other Time Dependent Neurologic Emergencies
TraumaWeak &Dizzy
Arrest
System Development: Learn from Trauma & Heart Attacks
• Protocol & center development• Increase public awareness• Rapid access to EMS• Prehospital notification triage• Prehospital notification, triage• Prehospital diagnosis, interventions• Confirmatory tests• Strong collaboration with specialists• Team and protocols in place in ED• “Door to Drug/Groin”
or Golden hour of trauma
61 year old male, acute aphasia, right facial droop, and right sided weakness
• 12:30 Sudden onset while working in yard
• 12:45 Family calls 911
13 05 Ad d d• 13:05 Advanced squad evaluates, rapidly triages and transports
• 13:15 Squad notifies receiving hospital of possible stroke patient; hospital notifies team
9/8/2009
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61 year old male with possible stroke Arrives at Our Lady of Faint Hope
• 13:30 ED triage andphysician evaluation
• 13:45 Stroke Team respondsp
• 14:00 CT scan performed
• 14:15 Discuss with family and PMD
• 14:20 Critical data backFSBS gluc 97BP remains 150/70’s
• Detection Early recognition• Dispatch Early EMS activation• Delivery Transport & managementy g• Door ED triage• Data ED evaluation & management• Decision Neurology input, therapy
selection• Drug Thrombolytic & future agents• Disposition Admission or transfer
Dispatch: 911 Delivery: Transport & Management
• Public education• EMS education
– ABC’s– Stroke recognitionStroke recognition– Time of onset– Neurologic evaluation– Glucose– Early hospital notification– Rapid transport (Air?)– Transport family
• Triage to stroke centers
(Silliman Stroke. 2003;34:729 –733)
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Door: Emergent TriageData: ED Evaluation
61 yo male with possible stroke
• 14:20 CT reading: No hemorrhage or early ischemia
• 14:25 Checklist done: No exclusion criteria met
• 14:30 Decision time
61 yo male with acute strokeThe decision to treat
• 14:35 IV rt-PA givenPatient weight 90 kg 0.9 mg/kg total (90 mg max dose10% (8 mg) bolus10% (8 mg) bolusRemaining 90% (73 mg) over 1 hr
• 15:45 Patient goes to ICUReport personally given to ICU staff
• 15:50 Pathway actions begin(HOB, BP, aspiration precautions, carotid ultrasound)
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Decision: Team ApproachDrug: IV, IA, Mechanical, Other
Goal Directed Therapy for Cerebral Resuscitation• Like sepsis, early goal directed therapy will
improve stroke outcome
• Look to other forms of brain injury for guidance (post-cardiac arrest syndrome)– Limit ongoing injury– Organ support
(Nolan Resuscitation 2008; 79:350—379)
Goal Directed Therapy for Cerebral Resuscitation - Stroke
• Glucose control– Current goal 140-185 mg/dl– GRASP (GIK for glucose > 110 mg/dl)– Control by stroke subtype
• Temperature control– Hyperthermia prevention– Induced hypothermia
• Mild (35oC)• Moderate (33oC) CHILI, COAST-II
(Bruno Stroke. 200;39:384-389)
9/8/2009
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Goal Directed Therapy for Cerebral Resuscitation - Stroke
• Optimal oxygenation– Hypoxia is bad– Normobaric oxygen (45l/min)Normobaric oxygen (45l/min)
• Optimal BP management– Extremes associated with worse
outcomes– ICH studies will come first
(Leonardi-Bee Stroke 2002;33:1315-1320)(Singhal Stroke. 2005;36:797-802)
Current Recanalization Options
• No recanalization»
• Recanalization strategies– Intravenous rt-PA
• 0-3 hrs (I A)• 3-4.5 (I B) with specific patient selection
– Other “investigational” treatments• Intra-arterial thrombolysis (I B)• Embolectomy (IIb B)• Acute intracranial stenting (III C) (Stroke. 2007;XX)
Limitations of IV tPA
• Generalizability– 4% utilization of tPA – ~25% present within 3 hours; 29% eligible– 12323 screened for 180 in PROACT II
Big strokes are difficult• Big strokes are difficult– Baseline NIHSS >10 and a dense MCA sign
predicted poor clinical outcome– TTATS recanalization rate of no more than 30%
for large vessel occlusion
• Sustained recanalization in only 10-20%• Increased risk of sICH with larger strokes(Kleindorfer Stroke 2004; 35:27-29)(Tomsick. AJNR 1996; 17:79-85)(Genentech, Summary basis for Activase approval. NDA. PLA96-0350)(Alexandrov. NEJM 2004;10:1379-83)
9/8/2009
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Extending the Therapeutic Window• The optimal temporal window remains
elusive
• Two strategies to increase eligibility– Identifying a optimal subset using clinical
variables– Utilize advanced imaging to identify
salvageable tissue
CT and MRI: Core / Penumbra
A ↑CBV ↑MTT with recanalization → small stroke
E ↓CBV ↑MTT → big stroke(Majda Thurnher, Medical University of Vienna) (Parsons Neurology 2007;68:730–736)
61 year old male s/p t-PAHospital Course
• Carotid U/S shows 60 -80% stenosis left ICA
• Speech recommends swallowing II diet and dailyswallowing II diet and daily checks
• Physical therapy ongoing• CEA performed day 4• Patient discharged day 7
back to baseline except slight increase in golf handicap
9/8/2009
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The Future of Stroke Treatment• Prevention! Prevention! Prevention!• Increased public and medical education• Stroke systems Primary, comprehensive, enabled• New diagnostic tools Neuroimaging, markers• Thrombolytics TNK, rPA, Ancrod• Intra-arterial approaches IA, specialty catheters, stentspp , p y ,• Combination agents Antiplatelets, LMWH, GPIIbIIIa• Collateral augmentation Invasive, noninvasive• Cerebral protection Hypothermia, neuroprotection,
traditional Chinese medicine • Surgical Hemicraniectomy, cell transplant• Rehabilitation Constraint therapy
61 year old male s/p rt-PA 24 hour follow-up
• Initial NIHSS = 10• 24 hr NIHSS = 3
Mild facial palsyMild facial palsyRight arm driftMild dysarthria
• Repeat CT shows infarct
Selected Ongoing Clinical Reperfusion Trials
• Recanalization studies– New lytics (TNK stopped)– Multidrug approach
CLEARER, ROSIE, Argatroban, , g– Combined IV IA
IMS-III– Combined IV IA device
IMS-III, MR Rescue, registry– Patient selection IA
MR Rescue, PICS, EXTENDRETRIEVE, PISTE, DAWN (p)
– Intracranial stenting – Ultrasound enhanced thrombolysis
9/8/2009
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Collateral Enhancement and Flow Augmentation• Attempts to increase perfusion
via stenoses and collateral circulation– Willisian and leptomeningeal
collaterals• Medical approaches
– Rheologic (albumin, hemodilution)– Induced hypertension (CHIPPS)
• Device approaches – Intra-aortic obstruction (SENTIS)– Counter pulsation (CUFFS)– SPGS (ImpACT 24)
Ongoing Neuroprotective Studies
• Targeted– Prehospital magnesium (FAST-MAG)
• 1298 pts; 2o from onset– Minocycline to Improve Neurologic Outcomey p g– High dose albumin (ALIAS)– Citicoline (ICTUS)
• Global– Hypothermia
• Surface and intravenous• With and without tPA• With caffeinol
– PhotoThera “The laser”
Conclusions
• The burden of stroke will increase• In acute brain injury, time will remain brain• Goal to develop systems and teams to optimally p y p y
treat• Multiple approaches will likely be involved
– Reperfusion– Physiology optimization– Aggressive rehabilitation
• Ongoing trials will provide important guidance
9/8/2009
13
Acute Stroke TreatmentThe Therapeutic Window for Intravenous
Thrombolysis: An Update
Steven R. Levine, M.D., FAHA, FAANProfessor of NeurologyProfessor of Neurology
The Mount Sinai Stroke CenterThe Mount Sinai School of Medicine
New York, New York
Disclosure Statement•Research funded by NIH & GaismanFoundation•MEDLINK Associate Editor•NSA Acute Advisory Board•SAMMPRIS Executive Committee •External/Independent Monitor: IMS III, CLEAR-ER, FASTMAG, INSTINCT•Off-label application
–Intravenous rt-PA between 3-4.5 hours from stroke onset
Mrs. Smith• She is 76 with a history of hypertension, cigarette
smoking and hyperlipidemia. She has no prior stroke history. She is taking anti-hypertensive and statin therapy.
• At 10:15 a.m. she notices a “funny feeling” in her left arm and doesn’t seem to be moving as well asleft arm and doesn t seem to be moving as well as the right one. She doesn’t think much of this and continued to cook.
• Her husband comes home at 1:00 p.m. from a round of golf and notices her face seems somewhat crooked and she is slurring her words. He asks her how she feels and she says her left arm feels funny.
ECJ1
Slide 39
ECJ1 This is a lot of text. Several slides have >9 lines of text which may be hard to read depending on the viewing circumstancesEdward Jauch, 8/7/2009
9/8/2009
14
Mrs. Smith - 2• He is concerned and calls 911 and EMS brings her
to the local ED where the stroke team is called “stat” after the EP finds at 1:20 p.m. dysarthria & left-sided weakness and orders a “stat” head CT scan & blood work. He establishes time of stroke onset at 10:15 a.m. BP = 164/94. EKG shows NSR.Th l i t i th h it l d d fi d• The neurologist, in the hospital, responds and finds an NIHSS of 8:
–2 points for LUE motor–1 point for LLE motor–1 point for facial asymmetry–1 point for partial visual field impairment–1 point for dysarthria–1 point for partial sensory loss–1 point for extinction/neglect
Mrs. Smith - 3
• Mrs. Smith is back from head CT at 1:50 p.m. & the CT is read as normal except for possibly subtle EIC in the right parietal lobe; labs are normal.Th l i t h tl h d & d• The neurologist has recently heard & read about treatment with IV t-PA up until 4.5 hours with some benefit but knows it is not currently FDA-approved. She discusses with Mrs. Smith & her husband the potential risks and benefits for “off-label” use.
Mrs. Smith - 4• Given the couple’s tremendous fear of a
disabling stroke and being dependent, they readily request treatment, even though it is now 2:05 p.m.
• The neurologist documents her discussion with gthe patient and her husband in the chart, and has a witness sign, time, & date the note.
• t-PA is ordered & mixed, per the NINDS t-PA protocol* and the IV bolus is started at2:25 p.m.
*NINDS rt-PA Stroke Study Group: Tissue plasminogen activator for acute ischemic stroke. New Engl J Med 1995;333:1581-1587.
9/8/2009
15
Mrs. Smith - 5• 2 hours after the t-PA bolus, Mrs. Smith NIHSS is
6:–1 point for LUE motor–1 point for LLE motor–1 point for facial asymmetry
1 point for dysarthria–1 point for dysarthria–1 point for partial sensory loss–1 point for extinction/neglect
• 24 hours after t-PA, her NIHSS is 4:–1 point for LUE motor–1 point for facial asymmetry–1 point for dysarthria–1 point for partial sensory loss
Mrs. Smith - 6• 24 hours after t-PA, Mrs. Smith was placed on
325 mg/d of enteric coated aspirin, her dose of statin was raised as her LDL-cholesterol was 160. She was provided with smoking cessation counseling, information & medication, & a physiatry consult.
• Mrs. Smith was evaluated for the etiology of her stroke and was found to have a 2 cm right parietal infarct on DWI MRI and a high-grade right extracranial ICA stenosis for which she underwent CEA 2 weeks later.
LDL = low density lipoprotein; DWI MRI = diffusion-weighted imaging magnetic resonance imaging; CEA = carotid endarterectomy
Favorable Outcome (mRS 0-1, BI 95-100, NIHSS 0-1) at Day 90
Adjusted odds ratio with 95% confidence interval by stroke onset to treatment time (OTT) ITT population (N=2,776)
ECASS, ATLANTIS, and NINDS rt-PA Stroke Trial Investigators: Combined A l i L t 2004 363 768 74Analysis, Lancet 2004;363:768-74
Basis for ECASS 3
mRS = modified Rankin Scale; BI = Barthel Index; ITT = intention-to-treat
9/8/2009
16
ECASS 3:Thrombolysis with Alteplase 3 to 4.5 Hours after Acute Ischemic Stroke
Hacke W, et al NEJM 2008;359:1317-1329
• A phase III RCT to test the efficacy of IV rt-PA in AIS patients treated between 3 - 4.5 hrs after stroke onset
• NINDS rt-PA protocol (but DVT tx) but excluding:p ( ) g– Age > 80 years– On oral anticoagulation (independent of INR)– Baseline NIH Stroke Scale score > 25– A history of stroke & diabetes
• Primary endpoint: 0-1 mRS at 3 mos.• 821 patients: 418 rt-PA & 403 placebo• Median time to tx: 3 hrs 59 min
IV rt-PA now shown to be beneficial if given within 3-4.5 hours of stroke onsetIncreases t-PA treatment window by 50%
Endpoint tPA Placebo Odds Ratio (95% CI) PFavorable 52.4 45.2 1.34 (1.02 - 1.76) .04Outcome(mRS 0 or 1) Global favorable outcome OR 1.28 (mRS 0 or 1) at 90 Days (%)
Endpoint tPA Placebo PAny ICH 27.0 17.6 .001 Symptomatic ICH 2.4/7.9 0.2/3.5 .008 Mortality 7.7 8.4 .68
(1.00-1.65) vs. 1.9 (1.2-2.9) in NINDS t-PA Trial
Hacke W, et al NEJM 2008;359:1317-1329
ECASS 3 Results
Hacke W, et al NEJM 2008;359:1317-29
9/8/2009
17
Recommendations: An Advisory Statement from the Stroke Council, American Heart Association & American Stroke
Association - del Zoppo et al: Stroke 2009;40:2945-8
• rt-PA should be administered to eligible pts within 3.0-4.5 hrs after stroke (Class I Recommendation, LOE B)
• Eligibility criteria in this time period similar to those for persons treated at earlier time periods with the following additional exclusion criteria:
Age > 80 years; Oral anticoagulant use with INR ≤ 1 7*; baseline NIHSSS > 25;– Age > 80 years; Oral anticoagulant use with INR ≤ 1.7*; baseline NIHSSS > 25; a history of stroke and diabetes
– (*For the 3.0 – 4.5 hr window all pts receiving oral anticoagulant are excluded whatever their INR).
• The efficacy of IV rt-PA within 3.0 – 4.5 hrs after stroke in pts with these exclusion criteria is not well-established & requires further study. (Class IIb Recommendation, LOE C)
• Delays in evaluation & initiation of rt-PA should be avoided because the opportunity for improvement is greater with earlier treatment
Safe Implementation of Thrombolysis in Stroke-International Stroke Treatment Registry 3-4.5 hour Study
(SITS-ISTR 3-to-4.5 hour)
• Post hoc sampling of limited data from Dec 2002 – Nov 2007 from the ongoing International Registry
• 11,865 patients treated with t-PA within 3 hrs compared with 664 patients treated with t-PA within 3-4.5 hours (Walgren et al L t 2008 372 1303 9)Lancet 2008;372:1303-9)
• 72% treated after 3 hours were between 3-3.5 hours
• While there were several weaknesses in this study, no differences were found between the 2 groups for:
• Symptomatic ICH
• Mortality
• mRS 0-2 at 3 months
Number needed to treat to benefit and to harm for IV t-PA in the 3-4.5 hours window - Saver et al Stroke 2009;40:2433-37
Number of Patients Benefited and Harmed Per 100 Patients Treated With Intravenous t-PA in Different Time Windows
1–3 Hours 3–4.5 Hours
NINDS t-PA Trials ECASS 3 Trial
For transitions across all 7 levels of the mRS
NNTB = 6.1NNTH = 37.5
Benefit per 100 32.3 16.4Harm per 100 3.3 2.7For individual dichotomizations of the mRS
Net BPH 0 vs 1–6 7.7 5.7
Net BPH 0–1 vs 2–6 16.1 7.3
Net BPH 0–2 vs 3–6 11.9 5.0Mean mRS difference in NINDS tPA trials was 0.53 and in ECASS 3 trial it was 0.21. BPH indicates benefit per 100.
9/8/2009
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Why do we need a “Bridging Protocol”?Recanalization & Reocclusion post IV rt-PA:63 Patients with MCAOUT-Houston TCD Data, Courtesy of James Grotta
• No recanalization = 27%• Partial recanalization = 33%• Partial recanalization = 33%• Complete recanalization = 18%• Reocclusion = 22%• Sustained recanalization rates:
12% at 60 & 120 min w/o ultrasound
Beyond IV or IA rt-PA Treatment Alone
• More effective acute recanalizationstrategies are needed
• IA seems to help more severe strokes and larger clot burdens better than IVand larger clot burdens better than IV
• How to get the best of both worlds – IV and IA rt-PA?
• “Bridge” with IV during preparation for IA–What dose?
IMS Bridging Studies: Results• 3-month mortality in IMS patients was lower, but not statistically different from historical controls (placebo & IV arms of NINDS trial)S ICH i IMS i il t IV f• Sx ICH in IMS similar to IV arm of NINDS trial & higher than placebo arm (p = 0.018)
• IMS patients: better outcomes at 3 mo. than placebo arm of NINDS trial (all measures) IMS I: Stroke 2004;35: 904–911
IMS II: Stroke 2007;38:2127-2135
9/8/2009
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Comparison of StudiesShaltoni et al Stroke 2007: UT-Houston experience
Shaltoni n=69
IMS-I n=80
IMS-II n=73
NINDS rt-PA n=182
Median age, yrs 60 65 66 68Median baseline NIHSSS
18 18 19 17
Median time from onset →IV tx,min
120 140 141 90
Median time from 285 215 241 N/AMedian time from onset →IA tx,min
285 215 241 N/A
% SxICH≤ 36hrs 5.8 6.3 11 6.6 % ASxICH≤ 36hrs 28.9 49 28.8 6.0% PH-2 7.2 7.5 8.8 3.4% TICI 2 or 3 72.5 56 61 N/A
NA indicates not applicable. IA = intra-arterial; SxICH = symptomatic intracerebral hemorrhage; ASxICH = asymptomatic ICH; PH-2 =
parenchymal hemorrhage type 2; TICI = thrombolysis in cerebral ischemia recanalization grading scheme
Acute Stroke TreatmentEndovascular Interventions
Philip M. Meyers, MD, FAHAAssociate Professor, Radiology and Neurological
SurgeryColumbia University, College of Physicians & Surgeons
9/8/2009
20
Disclosure Statement
• No Financial Disclosure• External Monitor: IMS-III Trial• Off-label applications
– Intra-arterial application of fibrinolytic agents to treat acute ischemic stroke
– Wingspan™ cerebral stent applied to treat acute ischemic stroke
Topics
• Limitations of intravenous fibrinolysis• Intra-arterial fibrinolysis• Mechanical thrombectomy• Other experimental revascularization
– Balloon angioplasty– Stent revascularization
Intravenous Fibrinolysis
• FDA Approved• Treatment window 0-3 hours from
symptom onsetNINDS h d 30% i i f bl• NINDS showed 30% increase in favorable outcomes at 90 days versus placebo
• Limited efficacy:– IV t-PA opens 30 – 50% of major occluded
intracranial vessels within 1 – 2 hours
9/8/2009
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Recanalization Rates: IV tPA ≤ 8 hrs
40
35
M3 4t
26
8
M3, 4
M2M1
ICA
Percen
t
del Zoppo Ann Neurol 32: 78, 1992
Anterior Cerebral Circulation
M4
M3
M2 M1
Small Distal Blockage
40% probability40% probabilityof revascularization
Area at Risk
9/8/2009
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Large Proximal Blockage
8% probability8% probabilityof revascularization
Area at Risk
Intra-arterial ThrombolysisPROACT II – Study Design
• Treatment group:– 9 mg dose of Pro-urokinase + 3000 units
Heparin IV• Control group:g p
– Placebo + Heparin • Patients presenting with MCA M1 or M2
occlusion• Treatment window: 6 hours from symptom
onset
Furlan JAMA 282:2003, 1999
Intra-arterial ThrombolysisPROACT II - Results
Mean time to treat: 5.3 hoursIA pro-UK(n = 121)
Placebo(n = 59)
Modified Rankin 0-2 at 3 months 40% 25%
TIMI 2 – 3 67% 2%
Intracerebral Hemorrhage 10% 2%
Furlan JAMA 282:2003, 1999
9/8/2009
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PROACT II Summary
Provides proof of principle in a worst-case scenario:– Late time to treatment (5.3 hours)
Limited manipulation no mechanical– Limited manipulation, no mechanical maceration of clot
– Patient selection, NIHSS=17
Bridging Protocols: Outcome Rankin 0-2% vs Time
62IMS
66EMS
4050
60
70
80
t
PROA25
Contr
0
10
20
30
40
3.3 4.2 5.3 >6
Percen
Time in hours
Thrombectomy for Acute Stroke
Courtesy of Concentric Medical, Inc.
9/8/2009
24
Case #1
• 75 year old woman• New onset atrial fibrillation• Evaluation for elective cardioversion• During echocardiogram, she develops
acute neurological changes– Aphasia– Right hemiplegia– Gaze deviation
Concentric Merci TrialMechanical Thrombectomy
Concentric Merci TrialMechanical Thrombectomy
9/8/2009
25
60%70%80%90%
100% rt-PA alone
Multi MERCI (Part I) Revascularization by VesselMerci WITHOUT Adjunctive Therapy
0%10%20%30%40%50%60%
Carotid MCA Vert/Bas Overall PROACT
52% 54% 60% 54%67%
N=121
Multi MERCI (Part I) Revascularization by VesselMerci WITH Adjunctive Therapy
70%80%90%
100%
15%20%
15%
rt-PA alone
Addtl. Revasc with Adjunctive Tx
0%10%20%30%40%50%60%
Carotid MCA Vert/BasOverallPROACT
52% 54% 60% 54%
15% 15% 15%
67%
N=33 N=68 N=10 N=111 N=121
40
50
60
70
49.151.9
Recanalized Not Recanalized
Multi MERCI Clinical Outcomes
0
10
20
30
Good Outcome Mortality (90 day)
24.8
9.6
Perc
ent
Smith ISC 2007
9/8/2009
26
Recanalization and Outcome - IACases with Reperfusion (p=0.02)
95% Prediction Bands
Cases without Reperfusion
Time from stroke onset to reperfusion minutes
Khatri P, ISC 2008, New Orleans, LA Courtesy of Ed Jauch, MD
Penumbra
Courtesy of Penumbra, Inc.
Case #2
• 72 year old man• Intermittent dizziness for several weeks• Rapid onset of nausea, vomiting,
l d l ft id d ksomnolence, and left-sided weakness
9/8/2009
27
9/8/2009
28
Comparison of Stroke Techniques
0 6
0.7
0.8
0.9
1
15%
ThrombolyticsAddtl. Revasc with Adjunctive TxPenumbra Device
on, %
0
0.1
0.2
0.3
0.4
0.5
0.6
IV TPA IA TPA MERCI PENUMBRA
80%
54%
15%
40%
66%
Recana
lizati
Intracranial Revascularization with Stent-Angioplasty
Courtesy of Boston Scientific, Inc.
9/8/2009
29
Case #3• 67 year old man• Sudden onset aphasia and confusion,
followed by onset of dense right hemiparesis.• ED evaluation shows NIHSS=23.• Patient receives 0.9 mg/kg rtPA at 2 hours
from stroke onset.• For presumed large artery occlusion, patient
was taken to angiography for possible endovascular treatment.
9/8/2009
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Future of Stroke InterventionTreatment Class and Level of EvidenceIntravenous fibrinolysis Class I LOE A
Intra-arterial fibrinolysis Class I LOE B
Mechanical embolectomy Class IIb LOE B
Stenting Class III LOE C
Meyers Circulation 119 (16): 2235‐49, 2009
9/8/2009
31
Conclusion
• Stroke is an important public health problem• Ongoing efforts by the medical community to
meet this growing need• Intravenous fibrinolysis remains the FDA• Intravenous fibrinolysis remains the FDA
approved treatment for acute ischemic stroke within 3 (possibly up to4.5) hours onset
• Endovascular stroke treatment is an area of active, ongoing research but remains experimental.
To receive CME and CE, please complete the program evaluation.
Upcoming CME EventRegister Today for Preventing RecurrentStroke: Targets for Managing Risk, a livewebcast presented by Philip Gorelick, MDand Fernando Testai, MDand Fernando Testai, MD
September 23, 2009; 12:00 PM Eastern
Visit www.stroke.org for more information onthis and other educational offerings.
9/8/2009
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For more information regarding National Stroke Association’s Acute Stroke Resource Center and other professional programs go to www.stroke.org.p g g g