no-reflow phenomenon€¦ · no-reflow phenomenon. back in history. from bench to bedside....
TRANSCRIPT
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Jan BogaertRadiology & Medical Imaging Research Centre
Working Group on Magnetic ResonanceLoutraki, Greece February 17-19, 2011
No-Reflow Phenomenon
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Back in History
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From Bench to Bedside
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Mechanisms responsible for No-Reflow
Niccoli G et al. J Am Coll Cardiol 2009;54:281-292
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Ischemia Time
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Ischemia Time – No-Reflow
Francone M et al. J Am Coll Cardiol 2009;54:2145-53
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Infarct Size
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Diagnosis of No-Reflow
• Coronary angiography (TIMI flow grade – Myocardial Blush Grade)
• ECG (STR 1h after PPCI)
• Myocardial contrast echocardiography (MCE)
• Cardiac MRI
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MR Sequence Arsenal
• Morphology (T1w-SE MRI / cine MRI)
• Myocardial edema (T2w-STIR-SE MRI)
• Cardiac function – Systolic (cine MRI / tagging)– Diastolic function: (VENC cine MRI)
• Myocardial perfusion imaging (MPI)
• Tissue Characterization– late or delayed (gadolinium) enhancement– T2* sequences
• Flow & Motion imaging – b-SSFP cine MRI– velocity-encoded cine MRI
• Vessel (coronary artery imaging)– b-SSFP 3D MR(C)A– contrast-enhanced 3D MR(C)A
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MRI Approach
J Am Coll Cardiol 2008;52:181-189
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• extensive infarct with low EF LV (28%)• day 3 post-infarct
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No-Reflow Phenomenon
• increases with the duration of ischemia time (TARANTINI et al. 2005; FRANCONE et al. 2009)
• is related to more severe myocardial damage (BOGAERT et al. 2007)
• ….. together with other parameters such as intramyocardial hemorrhage (GANAME et al. 2009; MATHER et al. 2010).
• and is independently associated with lack of functional recovery, adverse ventricular remodeling and worse patient outcome (ITO et al. 1992; ITO et al. 1996; WU et al. 1998a; ROGERS et al. 1999; KRAMER et al. 2000; GERBER et al. 2000; TAYLOR et al. 2004; HOMBACH et al. 2005; BAKS et al. 2006; FUNARO et al. 2009; NIJVELDT et al. 2008; ORN et al. 2009)
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Therapeutic Approaches
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Conclusions
• shift from open coronary artery to open microvessel theory
• microvascular obstruction is frequently present in both STEMI and non- STEMI infarcts
• contrast-enhanced MRI probably the best technique => detection of MVO can be seen as a “free bonus” in infarct imaging– first pass perfusion– early ceMRI – late ceMRI
• unresolved issues are exact timing post contrast administration and post PCI
• novel strategies are targeted toward reduction of microvascular damage
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Coronary artery disease – related pathology
• angor/angina pectoris– stable– Unstable
• myocardial infarction– non-STEMI– STEMI
• ischemia-related heart failure
• sudden cardiac death
myocardialischemiaimaging
myocardialinfarct
imaging
heart failure
imaging
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Imaging in Ischemic Heart Disease
“functionality”(inducible ischemia)
CA anatomy(stenosis detection/exclusion)
consequencesof CA disease
stress perfusionstress functionCTCA / MRCA infarct/viability
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Myocardial Ischemia Imaging
• Morphology (T1w-SE MRI / cine MRI)
• Myocardial edema (T2w-STIR-SE MRI)
• Cardiac function– Systolic (cine MRI / tagging)– Diastolic function: (VENC cine MRI)
• Myocardial perfusion imaging (MPI)
• Tissue Characterization– late or delayed (gadolinium) enhancement– T2* sequences
• Flow & Motion imaging – b-SSFP cine MRI– velocity-encoded cine MRI
• Vessel (coronary artery imaging)– b-SSFP 3D MR(C)A– contrast-enhanced 3D MR(C)A
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Coronary occlusion 20 min. 60 min. 3hrs. >3-6hrs.
LV
Normal myocardium
Myocardium at risk
Necrosis
Reversible injury Irreversible injury
Reperfusion
Consequences of ischemia/reperfusion
• Stunning• Preconditioning• Tissue viability(no necrosis)
• Subendocardial necrosis(salvage of outer layers)
• Necrosis extends intomidmyocardium, subepicardium
• Near transmural infarction (no salvage oftissue but may lead to negative LV remodeling)
LV
Transmural Wave Front of Necrosis
Each 30 min increase in time-to-treatment resulted ina 21-24% risk increase in transmurality (Thiele et al. Eur Heart J 2007;28:1433)
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Myocardial Infarct Imaging
• Morphology (T1w-SE MRI / cine MRI)
• Myocardial edema (T2w-STIR-SE MRI)
• Cardiac function– Systolic (cine MRI / tagging)– Diastolic function: (VENC cine MRI)
• Myocardial perfusion imaging (MPI)
• Tissue Characterization– late or delayed (gadolinium) enhancement– T2* sequences
• Flow & Motion imaging – b-SSFP cine MRI– velocity-encoded cine MRI
• Vessel (coronary artery imaging)– b-SSFP 3D MR(C)A– contrast-enhanced 3D MR(C)A
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Myocardial Edema
T2w-STIR MRI (triple IR sequence)
200020009393
myocardiumblood
Non-selective +Selective 180° pulse pair Readout
Mz Data acquisition
fat
Selective 180°Inversion pulse
ECG
TI1 TI2
‘edema-weighted MRI’
relaxation times in ‘infarcted’ myocardium are different from that in normal myocardium (related to increase in free water) (Mc.Namara et al. Circulation 71: 717, 1985)
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Francone M et al. J Am Coll Cardiol 2009
Wright J et al. J Am Coll Cardiol Cardiovascular Imaging
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Role of Edema Imaging
• increased (free) water content => hyperintense appearance• abnormalities occur very early and persist > 1 week• reflect : area-at-risk (overestimation of true necrotic area)(Dymarkowski et al. Invest. Radiol 2003)
• myocardial salvage (ratio LGE / AAR)– decreases with increasing time to reperfusion (Francone M et al JACC in press)
– reflect ST segment resolution – LV remodeling (Masci PG et al JACCi in press)
• useful to differentiate between acute – chronic infarcts
• findings are non-specific – not necessarily reflect myocardial necrosis (e.g. myocarditis)
• adjacent slow moving/stagnant blood: hyperintense
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Aborted Myocardial Infarction
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Necrosis / Fibrosis Imaging
• prolonged coronary occlusion leads to irreversible myocardial damage (necrosis)
• infarct healing and scar formation• paramagnetic contrast agents (gadolinium) enhance necrotic / fibrotic
myocardium• new sequences allow improved differentation between normal and
abnormal myocardium
timetime
contrastinjection
infarctedinfarcted myocardiummyocardium
ischemicischemic myocardiummyocardium
firstfirst--passpass delayed delayed enhancementenhancement
bloodblood poolpool
nono--reflowreflow--zonezone
normal normal myocardiummyocardium
33’’ 77’’
1010’’ 2525’’
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Contrast-Enhanced Inversion Recovery MRI
Mz
Mxy
180
TI or inversion time
null point (tissue specific)
scarred myocardium
normalmyocardium
Simonetti et al. Radiology 2001Delayed (Contrast) Enhancement (DE / DCE) MRILate (Gadolinium) Enhancement (LE/LGE) MRI
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Patterns of enhancement
• 1) subendocardial enhancement• 2) uniform, diffuse (ie transmural) enhancement• 3) centrally dark areas in reperfused infarcts• 4) doughnut pattern in occlusive infarcts
enhancement patterns - reflect infarct severity- related to peak serum enzyme levels- regional functional parameters- prognostically important (3)(4)=> infarct expansion / LV remodeling /
worser outcome
• 5) hemorrhagic infarction• 6) myocardial edema without infarction
(aborted infarction)
de Roos et al. Radiology 1989
(1) Subendocardial (2) Transmural
(3) No-Reflow (4) Occlusive
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Post-Reperfusion Myocardial Hemorrhage
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Microvascular Obstruction
• lack of reperfusion at tissue level– severe edema compressing intramural vessels or– extensive myocardial necrosis and – microcirculatory damage in center of a large infarction
• no-reflow zone may increase (x 3-fold) first 2d reperfusion (Rochitte et al. Circulation 1998)
– progressive microvascular and myocardial injury after reperfusion• area of no-reflow is a better predictor of LV remodeling than infarct size
(Gerber et al. Circulation 2000)
• MVO independent predictor of adverse remodeling and patient outcome (Hombach et al. Eur Heart J 2006)
3 minutes 20 minutes
Acute phase FU (4 months)
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Noninvasive Gold for Infarct Imaging ?
A. Wagner et al. Lancet 2003
necrosis as small as 1g can be detected with CE-IR-MRI <=> 10 g with SPECT
Ibrahim T et al. J Am Coll Cardiol 2007;49:208
CE-IR MRI is superior to SPECT in detecting myocardial necrosisafter reperfused AMI because MRI detects small infarcts that were missed by SPECT independent of the infarct location
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Infarct Imaging
– area-at-risk– myocardial necrosis
• location (perfusion territory)• circumferential and transmural extent• tissue characteristics
– microvascular obstruction– postreperfusion myocardial hemorrhage
– impact on regional and global ventricular function– associated findings – complications
• valve regurgitation (papillary muscle necrosis – ventricular dilation)• thrombus formation• myocardial rupture• pericardial inflammation
– baseline exam to evaluate• infarct healing• (adverse) LV remodeling
comprehensive MRI exam in acute MI
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LCx Infarction
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Infarct Healing – Ventricular Remodeling
Jugdutt B Circulation 2003;108:1395
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Integration of DSMRI in Cardiac MRI Protocol
ScoutViews
FunctionalImaging at Rest
Delayed EnhancementMRI
DSMRIlow-dose
DSMRIhigh-dose
Viability
Ischemia