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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
2
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
3
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
4
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
5
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
6
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
7
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)
8
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
9
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
10
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
11
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)
12
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!
13
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