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1 CT Angiography and CT Perfusion in the Management of Acute Stroke Stroke – past good outcome with IV good outcome with IV tPA(mRS tPA(mRS 0- 1): 1): 39% 39% vs. vs. 26% 26% 1 most patients arrive too late most patients arrive too late (>3 hrs for NINDS) (>3 hrs for NINDS) currently, only currently, only 0.6 0.6- 1.8% 1.8% of strokes get IV tPA of strokes get IV tPA 2,3 2,3 NINDS NEJM 1995 1 , Katzan JAMA 2000 Katzan JAMA 2000 2 , Qureshi NRS 2005 Qureshi NRS 2005 3 Stroke – present Odds Ratio for Favorable Outcome Odds Ratio for Favorable Outcome IV IV tPA tPA exclusions / contraindications exclusions / contraindications Stroke – present 1. > 3 hrs from stroke onset 2. 80 > age > 18 3. pregnancy (up to 10 days postpartum) 4. “symptoms suggestive of SAH” – despite negative CT 5. “rapidly improving or minor symptoms” 6. “seizure at onset of stroke” 7. ever: history of intracranial hemorrhage 8. within 3 mo: stroke, serious head trauma, intracranial surgery 9. within 21d: GI/urinary/pulmonary hemorrhage 10. within 14d: major surgery 11. within 7d: arterial puncture at a non-compressible site 12. SBP > 185 mmHg or DBP > 110 mmHg 13. aggressive treatment required to reduce BP to specified limits 14. current use of anticoagulants (or recent, with PT > 15s) 15. use of heparin within 48hrs and elevated PTT 16. platelets < 100,000 17. glucose < 50 or > 400 mg per deciliter 18. brain tumour, abscess, aneurysm, AVM 19. bacterial endocarditis 20. known bleeding diathesis – includes renal, hepatic insufficiency 21. etc… IV IV tPA tPA is less effective for severe strokes is less effective for severe strokes 1 NIHSS NIHSS 10: 75% decreased chance of good outcome 10: 75% decreased chance of good outcome NIHSS > 20: only 8% will attain NIHSS=1 after IV NIHSS > 20: only 8% will attain NIHSS=1 after IV tPA tPA IV IV tPA tPA is less effective for large vessel occlusions is less effective for large vessel occlusions 2,3 2,3 ICA recanalization rate is 1/3 that of MCA ICA recanalization rate is 1/3 that of MCA tandem ICA/MCA has poor recanalization & bad prognosis tandem ICA/MCA has poor recanalization & bad prognosis IV IV tPA tPA is relatively slow is relatively slow- acting acting 4,5 4,5 TCD over 6hrs TCD over 6hrs 30% 30% recan recan (of which (of which ¾ are within 1hr are within 1hr tpa tpa) angio 1hr after angio 1hr after tPA tPA 1/10 ICA/proximal MCA, 1/3 distal MCA 1/10 ICA/proximal MCA, 1/3 distal MCA 1: NINDS Stroke 1997; 28:2119–2125 2: LInfante Stroke 2002; 33:2066 2: LInfante Stroke 2002; 33:2066-2071 2071 3: 3: Rubiera Rubiera Stroke 2006; 37:2301 Stroke 2006; 37:2301-2305 2305 4: 4: Christou Christou Stroke 2000; 31:1812 Stroke 2000; 31:1812-1816 1816 5: Lee 5: Lee Stroke 2007; 38:192-3 Stroke – present Time is brain Time is brain” typical supratentorial large vessel stroke: ~54ml brain is typical supratentorial large vessel stroke: ~54ml brain is lost over ~10 hrs lost over ~10 hrs per hour: per hour: 830 billion synapses, 120 million neurons, 447 830 billion synapses, 120 million neurons, 447 miles of myelinated miles of myelinated fibre fibre lost lost each each hour hour, brain effectively ages 3.6 , brain effectively ages 3.6 years years Saver, Stroke 2006; 37:263

CT Angiography & CT Perfusion in Management of Acute Stroke

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Page 1: CT Angiography & CT Perfusion in Management of Acute Stroke

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CT Angiography and CT Perfusion in the

Management of Acute Stroke

Stroke – past

good outcome with IV good outcome with IV tPA(mRStPA(mRS 00--1): 1): 39%39% vs. vs. 26%26% 11

most patients arrive too late most patients arrive too late (>3 hrs for NINDS)(>3 hrs for NINDS)currently, only currently, only 0.60.6--1.8%1.8% of strokes get IV tPA of strokes get IV tPA 2,32,3

NINDS NEJM 19951,Katzan JAMA 2000Katzan JAMA 20002,,Qureshi NRS 2005Qureshi NRS 20053

Stroke – present

Odds Ratio for Favorable OutcomeOdds Ratio for Favorable Outcome

IV IV tPAtPA exclusions / contraindicationsexclusions / contraindications

Stroke – present

1. > 3 hrs from stroke onset2. 80 > age > 183. pregnancy (up to 10 days postpartum)4. “symptoms suggestive of SAH” – despite negative CT5. “rapidly improving or minor symptoms”6. “seizure at onset of stroke”7. ever: → history of intracranial hemorrhage 8. within 3 mo: → stroke, serious head trauma, intracranial surgery9. within 21d: → GI/urinary/pulmonary hemorrhage10. within 14d: → major surgery11. within 7d: → arterial puncture at a non-compressible site12. SBP > 185 mmHg or DBP > 110 mmHg13. aggressive treatment required to reduce BP to specified limits14. current use of anticoagulants (or recent, with PT > 15s)15. use of heparin within 48hrs and elevated PTT16. platelets < 100,00017. glucose < 50 or > 400 mg per deciliter18. brain tumour, abscess, aneurysm, AVM19. bacterial endocarditis20. known bleeding diathesis – includes renal, hepatic insufficiency21. etc…

IV IV tPAtPA is less effective for severe strokes is less effective for severe strokes 11NIHSS NIHSS ≥≥ 10: 75% decreased chance of good outcome10: 75% decreased chance of good outcomeNIHSS > 20: only 8% will attain NIHSS=1 after IV NIHSS > 20: only 8% will attain NIHSS=1 after IV tPAtPA

IV IV tPAtPA is less effective for large vessel occlusions is less effective for large vessel occlusions 2,32,3

ICA recanalization rate is 1/3 that of MCAICA recanalization rate is 1/3 that of MCAtandem ICA/MCA has poor recanalization & bad prognosistandem ICA/MCA has poor recanalization & bad prognosis

IV IV tPAtPA is relatively slowis relatively slow--acting acting 4,54,5

TCD over 6hrs TCD over 6hrs →→ 30% 30% recanrecan (of which (of which ¾¾ are within 1hr are within 1hr tpatpa))angio 1hr after angio 1hr after tPAtPA →→ 1/10 ICA/proximal MCA, 1/3 distal MCA1/10 ICA/proximal MCA, 1/3 distal MCA

1: NINDS Stroke 1997; 28:2119–21252: LInfante Stroke 2002; 33:20662: LInfante Stroke 2002; 33:2066--207120713: 3: RubieraRubiera Stroke 2006; 37:2301Stroke 2006; 37:2301--230523054: 4: ChristouChristou Stroke 2000; 31:1812Stroke 2000; 31:1812--181618165: Lee 5: Lee Stroke 2007; 38:192-3

Stroke – present ““Time is brainTime is brain””typical supratentorial large vessel stroke: ~54ml brain is typical supratentorial large vessel stroke: ~54ml brain is lost over ~10 hrslost over ~10 hrs

per hour:per hour: 830 billion synapses, 120 million neurons, 447 830 billion synapses, 120 million neurons, 447 miles of myelinated miles of myelinated fibrefibre lostlost

each each hourhour, brain effectively ages 3.6 , brain effectively ages 3.6 yearsyears

Saver, Stroke 2006; 37:263

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1987IV tPA

1996IV tPA

2000Stent

2003Cypher

1993PTCA

2004MERCI Retriever

1999PROACT II

Treatment of Acute Stroke

Treatment of Acute MI

???

MultimodalRevascularization

Stroke – future? now.

today

Thrombolytics:Thrombolytics: →→ Alteplase, RetavaseAlteplase, Retavase

GIIb/IIIa inhibitors:GIIb/IIIa inhibitors: →→ Reopro, IntegrilinReopro, Integrilin

Mechanical disruption:Mechanical disruption: →→ microwire / snaremicrowire / snare

Clot retrieval:Clot retrieval: →→ MERCI, PenumbraMERCI, Penumbra

Ultrasound Catheter:Ultrasound Catheter: →→ EKOSEKOS

Angioplasty / StentingAngioplasty / Stenting →→ Gateway / WingspanGateway / Wingspan

Stroke – new tools

Case example:

45 yo male

acute LMCA stroke

R paretic, R hemianopic, R facial droop, dysphasic, dysarthric.

NIHSS = 15

CT: early left caudate head, basal ganglia infarct

CTP:↑↑MTT, ↓CBF, ↑CBV

Interpretation:small caudate andfrontopolar infarcts,surrounded by large(but salvageable)ischemic penumbra…

Flow

Volume

Transit Time

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CTA: LM1 occlusion (w/distal collateral) CTA: LCCA/inominate stenosis

AP: Sag:

LCCA origin severe stenosis, 5F sim2 finally pops in but is occlusive (static dye column) T-occlusion equivalent: proximal LA1, LM1 occluded, poor collateralization

All-star 0.014 wire maintains access to LCCA, pigtail arch run shows severe origin stenosis

1. Aviator 6x30mm over All-star wire, LCCA origin angioplastied

2. Sim2 back over All-star wire into distal LECA

3. All-star wire then exchanged for 0.035 stiff exchange glidewire

4. Sim2 swapped out for 7F concentric balloon guide over stiff exchange wire, parked in LCCA

5. Concentric guide catheter taken to distal cervical LICA

6. LMCA occlusion crossed with 18L Concentric microcatheter over Transend microwire…

Cross LM1 occlusion with MERIC 18L microcatheter over transend

AP Lateral

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Deploy MERCI L5 retriever

AP Lateral

Clot retreived, flow restored

AP Lateral

AP

Pre

Post

AP Lateral

Post – Arch MRA: LCCA stenosis better, inominate as before, will need tx later

Thrombolytics: Alteplase, RetavaseThrombolytics: Alteplase, RetavaseGIIb/IIIaGIIb/IIIa inhibitors: inhibitors: ReoproReopro, , IntegrilinIntegrilinMechanical disruption: microwire/snareMechanical disruption: microwire/snareClot retrieval: MERCI (X6, L5, variants)Clot retrieval: MERCI (X6, L5, variants)Ultrasound assisted Catheter: EKOSUltrasound assisted Catheter: EKOSBalloon AngioplastyBalloon AngioplastyPrimary StentingPrimary Stenting

IA Thrombolysis: New Tools

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To select out To select out patients with patients with viableviablebrain tissue at risk brain tissue at risk that can be treated that can be treated

with the with the optimaloptimaltool for tool for

revascularisationrevascularisation

GOAL:

HOW?

New-generation CTA/CTP = anatomy+physiology

1. faster: <5 min total acquisition time2. less motion artifact3. less dye (CTA+CTP <120ml) → <50ml with 320-slice!4. CTA (arch to vertex) :

• lesion presence/absence/location• lesion accessibility• a priori knowledge = no guessing!

5. CTP:• absolute numbers for CBF, CBV• 4-8 slices, + post-fossa coverage → full coverage with 320-slice!• CBF ≈ penumbra+core; CBV ≈ collateral supply• CBF/CBV mismatch = salvageable penumbra!

Imaging for stroke intervention

13.3±3.75 1.12±0.37

threshold=31.3

sensitivity=97.0%specificity=97.2%accuracy=97.1%

for CBFxCBV andsubsequent stroke

25.0±3.8237.3±5.01 2.15±0.431.78±0.30

FLOW VOLUME

CBFxCBV

Murphy, B. D. et al. Radiology 2008;247:818-825 Murphy, B. D. et al. Radiology 2008;247:818-825

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Figure 3: Scatterplot shows mean CBV versus mean CBF in penumbra and infarct regions in patients with acute stroke and confirmed recanalization at 24 hours (dashed line represents CBF×CBV = 8.14)

Murphy, B. D. et al. Radiology 2008;247:818-825

- 40 patients, median NIHSS=16, 19 received iv-tpa- compared initial CTP/CTA and day #3 postop MRI/MRP- reperfusion defined as normalization of ≥80% area with increased MTT

Regions with infarction (based upon DWI+ADC) at day #3 compared with CBV mapson initial CTP → in hypoperfused areas ( ↓↓CBF, ↑↑MTT), does CBV predicteventual infarction?

94% (go on to infarct)

63% (go on to infarct)

94% (go on to infarct)

No reperfusion

3% (go on to infarct)

41% (go on to infarct)

97% (go on to infarct)

With reperfusion

HighNormalLowCBV

rCBF prediction of symptomatic ICHfollowing IA treatment for MCA occlusion

Gupta 2006 Stroke 37:2526

~ 13 mlper 100g/min

~ 1/3 MCAterritory

CTP parameters can predict hemorrhage

CTP in posterior circulation!

CBF CBV MTT DWI

Acute Stroke

CTA / CTP

large vessel occl. (ICA, M1/M2, A1, VA/BA)large ischemic penumbra > infarctlarge stroke (NIHSS≥10)

0-3 hr

IV tPA IA TxIA Tx ± bridging IV tPA no acute thrombolysis, later medical or surgical stroke prophylaxis

>3 hr

large vessel occl. (ICA, M1/M2, A1,VA/BA)large ischemic penumbra > infarctlarge stroke (NIHSS≥10)

yes no yes no

Stroke Algorithm

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SUMMARY

CTP is available and powerful:

Transit time = very sensitive (but not specific)

Flow = penumbra plus core

Volume = penumbra vs core (collateral supply)

preserved → penumbra (still salvageable)

decreased → core (dead)

CBF/CBV = crude “risk/reward” ratio

onset often unclear → CT perfusion = more accurate physiological data

perfusion beats onset

POD#1 DWI: frontopolar, caudate, basal ganglia infarcts (predicted by CTP), butlarge LMCA territory salvaged

POD#1 FLAIR: smallcaudate head, basalganglia, frontopolarinfarcts

POD#2 CT

Case example:

83 yo male

acute right hemisphere stroke

left plegic, R gaze preference, L facial droop, dysarthric

NIHSS > 10

last normal > 14hrs ago

past medical history = paroxysmal atrial fibrillation (discovered on this admission)

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preop CBF preop CBV

EmergencyCT perfusion:

Low CBF but preserved CBV → stroke is still salvageable.

residualclot

thrombectomy and lytics → inferior division open, residual clot in superior divisionballoon angioplasty → superior division now also open

PostPre

preop CBF preop CBV

Case example:

33 yo female

acute right carotid stroke

left hemiplegia, facial droop, dysarthria, hemianopia, neglect, decreased left body sensation, drowsy, fixed gaze deviation to right.

NIHSS = 16

onset > 4 hrs

past medical history = smoker, oral contraceptive pills

CBF CBVTTP

INITIAL CTP:-Very low blood flow-Very slow blood flow-Preserved blood volume

-BUT: > 4hrs onset

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Complete right internal carotid artery occlusion → no intracranial blood flow microcatheter run shows distal blood vessels remains patent

MERCI thrombectomy opens distal carotid and proximal middle cerebral artery,balloon angioplasty opens distal middle cerebral artery

MRIfewdayslater…

Case example:

76 year old female

Found 2:30 am at outside institution with stroke, onset unknown

Rapidly transferred to tertiary-care institution.

When seen, unable to move anything except eyes

rapidly loosing consciousness → crash intubated in ED

NIHSS = 30

Mid-BA occlusion

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Big Problem…

Bigger Problem…?

Access is going to be tough!!!

arm

arm

Pooled NASCET, ECST, VA309 results Lancet 2003,361(9352):107

Case example #1:

70 yo male

acute LMCA stroke

driving → swerved off road → min. responsive on scene

right plegic, aphasic, fixed gaze to left in ED

NIHSS = 22

onset <1.5 hrs

PMH = HTN, NIDDM, dyslipidemia, atrial flutter, on ASA

hyperdense sign

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CBF CBV TTP

13.6 x 0.9 = 12.2

CBV reduction matchesreduction in CBF → nocollateral reserve, nopenumbra, infarct alreadywell established.

Case example #5:

70 yo male

acute RMCA stroke

initial NIHSS=12 in ED, worsened to > 18 → intubated

onset > 6 hrs

PMH = MI, CABG, PVD, HTN, NIDDM, previous L parietal subcortical stroke

CT (pre)

CBF CBV TTP

CTP (pre)

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Treatment:

Angio = RMCA bifurcation occlusion, ant. temporal open

Retavase 2mg M1

Retavase 1mg M2inf

wire both M2’s

Merci M2sup x2 Pre Post

CT (POD#1)

Outcome:

TIMI-3 M1/M2’s

distal branch of inferior M2 remained occluded

R basal ganglia ICH, R parietal infarct

rest of MCA territory spared

discharged 17 days later to rehab, NIHSS=16

return w/urosepsis one month later → no sig improvement

CT 44 days later…NIHSS still 16.

CTP keypoints:1. TTP/MTT is very sensitive – but not specific2. CBV distinguishes infarction vs. ischemic penumbra (dead vs. salvageable brain)3. Areas at risk for hemorrhage post-thrombolysis can be predicted4. Crude risk/benefit ratio = CBV / CBF deficitBottom line = physiological imaging is real and powerful…CTP does not lie!

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SUMMARY

CTP is available and powerful:

Transit time = very sensitive (but not specific)

Flow = penumbra plus core

Volume = penumbra vs core (collateral supply)

preserved → penumbra (still salvageable)

decreased → core (dead)

CBF/CBV = crude “risk/reward” ratio

onset often unclear → CT perfusion = more accurate physiological data

perfusion beats onset