Specially for cardiology and nuclear medicine doctor

1. Test for viable myocardiumTest for viable myocardium
Dr. Muhammad Bayazid
M.D Final part student, Cardiology, DMCH

3. Cell injuryCell injury
THE MYOCARDIAL RESPONSE TO ISCHEMICTHE MYOCARDIAL RESPONSE TO ISCHEMIC
INJURYINJURY
 Within secondsWithin seconds
 Decrease in the production of high-energyDecrease in the production of high-energy
phosphates, namely adenosine triphosphatephosphates, namely adenosine triphosphate
(ATP) and phosphocreatine (PCr)(ATP) and phosphocreatine (PCr)

4. Cell injuryCell injury
 Ultrastructural changes occur such as mitochondrialUltrastructural changes occur such as mitochondrial
swelling, loosening of intercellular attachments, theswelling, loosening of intercellular attachments, the
presence of small, lipid-rich amorphous mitochondrialpresence of small, lipid-rich amorphous mitochondrial
densities, dilation of the sarcoplasmic reticulum,densities, dilation of the sarcoplasmic reticulum,
disaggregation of SR polysomes, and myofibrillardisaggregation of SR polysomes, and myofibrillar
relaxationrelaxation
 within 1 min of acute onsetwithin 1 min of acute onset
 The myocardium is functionally sensitive to ischemiaThe myocardium is functionally sensitive to ischemia
and will exhibit marked contractile dysfunctionand will exhibit marked contractile dysfunction
 HOWEVER, these ultrastructural defects are entirelyHOWEVER, these ultrastructural defects are entirely
reversible if reperfusion occurs within 20– 40 min.reversible if reperfusion occurs within 20– 40 min.

5.  Irreversible InjuryIrreversible Injury
 Begins in the subendocardial tissue andBegins in the subendocardial tissue and
progresses towards the subepicardium.progresses towards the subepicardium.
 In humans, it may take as long as 6–12 hr forIn humans, it may take as long as 6–12 hr for
complete infarction of the myocardium, thecomplete infarction of the myocardium, the
necrotic changes are usually evident about 4–necrotic changes are usually evident about 4–
12 hr after onset12 hr after onset
 This may include the denaturation ofThis may include the denaturation of
cytoplasmic proteins, swelling, and enzymaticcytoplasmic proteins, swelling, and enzymatic
digestion of organelles and the sarcolemma.digestion of organelles and the sarcolemma.

7. Definition of viable myocardiumDefinition of viable myocardium
The most practical definition of viability is “myocardiumThe most practical definition of viability is “myocardium
that demonstrates contractile dysfunction that showsthat demonstrates contractile dysfunction that shows
functional improvement after revascularization”functional improvement after revascularization”
Viable myocardium must have the followingViable myocardium must have the following
characteristicscharacteristics
1.1. The ability to generate HEP (PCr and ATP)The ability to generate HEP (PCr and ATP)
2.2. Have an intact sarcolemma, in order to maintainHave an intact sarcolemma, in order to maintain
ionic/electrochemical gradients, andionic/electrochemical gradients, and
3.3. Have sufficient perfusion, both for the delivery ofHave sufficient perfusion, both for the delivery of
substrates and O2 and for the adequate washout ofsubstrates and O2 and for the adequate washout of
potentially noxious metabolitespotentially noxious metabolites

8.  If tissue is viable, restoration of normalIf tissue is viable, restoration of normal
blood flow, will improve the ventricularblood flow, will improve the ventricular
functionfunction
 Thus, the patient‘s prognosis will alsoThus, the patient‘s prognosis will also
improve, as a result of an increase inimprove, as a result of an increase in
ejection fraction, systolic and diastolicejection fraction, systolic and diastolic
performance, exercise capacity, and mostperformance, exercise capacity, and most
importantly, survival.importantly, survival.

9. Stunned myocardium &Stunned myocardium &
Hibernating myocardiumHibernating myocardium
 There are two tissue states that exhibitThere are two tissue states that exhibit
sustained contractile dysfunction despitesustained contractile dysfunction despite
meeting the three criteriameeting the three criteria

10. Myocardial stunningMyocardial stunning
 Heyndrickx et al 1978Heyndrickx et al 1978
 Prolonged and fully reversible contractileProlonged and fully reversible contractile
dysfunction which is often caused by abruptdysfunction which is often caused by abrupt
cessation of flow that persists after reperfusioncessation of flow that persists after reperfusion
 Affected area responsive to inotropesAffected area responsive to inotropes
 Time course not altered by use of inotropes-Time course not altered by use of inotropes-
spontaneously resolve within a weekspontaneously resolve within a week
 Duration of stunning depends on the durationDuration of stunning depends on the duration
and severity of ischemia and the adequacy ofand severity of ischemia and the adequacy of
arterial flowarterial flow

11. MechanismMechanism
 Calcium hypothesis-decreaseCalcium hypothesis-decrease
responsiveness to calciumresponsiveness to calcium
 Oxy radical hypothesis-ROS duringOxy radical hypothesis-ROS during
reperfusion impairs calcium handlingreperfusion impairs calcium handling

12. Mechanism of stunningMechanism of stunning
 Normal cardiac contraction depends on the maintenance ofNormal cardiac contraction depends on the maintenance of
calcium cycling and homeostasis across the mitochondrialcalcium cycling and homeostasis across the mitochondrial
membrane and sarcoplasmic reticulum during each cardiacmembrane and sarcoplasmic reticulum during each cardiac
cycle.cycle.
 Brief ischemia followed by reperfusion accumulation of calciumBrief ischemia followed by reperfusion accumulation of calcium
and a partial failure of normal beat to beat calcium cyclingand a partial failure of normal beat to beat calcium cycling
damages Ca2+ pump and ion channels of the sarcoplasmicdamages Ca2+ pump and ion channels of the sarcoplasmic
reticulum.reticulum.
 Recent evidence suggests that calcium overload may activateRecent evidence suggests that calcium overload may activate
calpains, resulting in selective proteolysis of myofibrils; the timecalpains, resulting in selective proteolysis of myofibrils; the time
required for resynthesis of damaged proteins would explain inrequired for resynthesis of damaged proteins would explain in
part the delayed recovery of function in stunned myocardium.part the delayed recovery of function in stunned myocardium.
Increased free radical formation could cause cellular calciumIncreased free radical formation could cause cellular calcium
overload, which would damage the contractile apparatus of theoverload, which would damage the contractile apparatus of the
myocytes.myocytes.

13. HibernationHibernation
 Viable myocardium has altered itsViable myocardium has altered its
metabolism and thus reduced itsmetabolism and thus reduced its
contractile function as a mechanism tocontractile function as a mechanism to
cope with chronically inadequate bloodcope with chronically inadequate blood
supply (chronic stable angina) or repetitivesupply (chronic stable angina) or repetitive
ischemic injury.ischemic injury.

14. CriteriaCriteria
 Tissue ischemia and resultant remodelingTissue ischemia and resultant remodeling
without necrosiswithout necrosis
 Residual contractile reserve in response toResidual contractile reserve in response to
inotropic stimulation (in at least half of clinicalinotropic stimulation (in at least half of clinical
cases).cases).
 Recovery of contractile function after successfulRecovery of contractile function after successful
revascularizationrevascularization..

15. MechanismMechanism
3 mechanisms whereby this may occur3 mechanisms whereby this may occur
 Decreased flow at rest , decreased metabolism,Decreased flow at rest , decreased metabolism,
decreased function, Chronically depresseddecreased function, Chronically depressed
contractile function.contractile function.
 Demand ischemia ,Recovery, RepeatedDemand ischemia ,Recovery, Repeated
stunning Chronically depressed contractilestunning Chronically depressed contractile
function.function.
 Genomic trigger for cell survival, SurvivalGenomic trigger for cell survival, Survival
proteins produced by anti apoptotic,proteins produced by anti apoptotic,
cytoprotective, and growth-promoting genescytoprotective, and growth-promoting genes
Protection against apoptosisProtection against apoptosis
 All these mechanisms lead to cell survival in theAll these mechanisms lead to cell survival in the

16. Assessment of viabilityAssessment of viability

17. SymptomSymptom
 Chest pain :Chest pain :
Ischemic episodes release a collage ofIschemic episodes release a collage of
chemicals, including adenosine and bradykinin,chemicals, including adenosine and bradykinin,
that excites the receptors of the sympatheticthat excites the receptors of the sympathetic
and vagal afferent pathways.and vagal afferent pathways.

18. ECGECG
 Chronic pathological Q waves are usefulChronic pathological Q waves are useful
markers of myocardial scarring.markers of myocardial scarring.
 Preservation of R waves followingPreservation of R waves following
pathological Q waves is a marker forpathological Q waves is a marker for
hibernating myocardium.hibernating myocardium.
Can the surface electrocardiogram be used to predict myocardial viability? A Al-Mohammad, M Y Norton, I R Mahy, J C Patel, A E Welch, PCan the surface electrocardiogram be used to predict myocardial viability? A Al-Mohammad, M Y Norton, I R Mahy, J C Patel, A E Welch, P
Mikecz, S WaltonMikecz, S Walton
http://heart.bmj.com/ on June 16, 2017http://heart.bmj.com/ on June 16, 2017

19. EchocardiogramEchocardiogram
 Thin, echogenic, akinetic or dyskineticThin, echogenic, akinetic or dyskinetic
segment indicate transmural infarctionsegment indicate transmural infarction
and suggestive of non viable tissueand suggestive of non viable tissue
 Hypokinetic segment with preservation ofHypokinetic segment with preservation of
thickness may be partially infarcted orthickness may be partially infarcted or
viableviable
 Wall thickness less than 6 mm is lowWall thickness less than 6 mm is low
likelihood of recovery of functionlikelihood of recovery of function

20. Widely used viability testWidely used viability test
 MPIMPI
SPECTSPECT
Thalium (thallium is a potassium analogsThalium (thallium is a potassium analogs
that relies on the Na/K ATPase for uptake)that relies on the Na/K ATPase for uptake)
Technetium-99 m ( Relies on intactTechnetium-99 m ( Relies on intact
mitichondrial function)mitichondrial function)
PET-FDG ( Relies on intact metabolism)PET-FDG ( Relies on intact metabolism)
 Dobutamine strss echoDobutamine strss echo
 Delayed enhancement MRIDelayed enhancement MRI

21. MPI is a non-invasive nuclear imagingMPI is a non-invasive nuclear imaging
technique that uses radioactive imagingtechnique that uses radioactive imaging
agents to image the heart.agents to image the heart.
There are 2 techniques for MPI: There are 2 techniques for MPI:

Single photon emission computed tomographySingle photon emission computed tomography
Thallium - 201Thallium - 201
Technetium-99 m SestamibiTechnetium-99 m Sestamibi
Technetium-99 m TetrofosminTechnetium-99 m Tetrofosmin
 Positron emission tomography (PET).
What is Myocardial PerfusionWhat is Myocardial Perfusion
Imaging?Imaging?

22. Myocardial Perfusion
Performed at rest & stress
Stress study options
• Treadmill exercise
• Pharmacologic stress agents
• Adenosine
• Dipyridamole
• Dobutamine

23. Myocardial Perfusion ImagingMyocardial Perfusion Imaging
MPI Basic PrinciplesMPI Basic Principles ––
 Radionuclides taken up by perfused myocytesRadionuclides taken up by perfused myocytes
 In ischemic segment delayed uptake and delayedIn ischemic segment delayed uptake and delayed
washout occur.washout occur.
 Identify areas of infarction or inducible ischaemia byIdentify areas of infarction or inducible ischaemia by
comparing perfusion in rest and stress statescomparing perfusion in rest and stress states
 Exercise or pharmacologically induced coronaryExercise or pharmacologically induced coronary
artery vasodilatation > proportionately less perfusionartery vasodilatation > proportionately less perfusion
distal to stenoses > relatively low radionuclidedistal to stenoses > relatively low radionuclide
uptake in myocardium distal to stenoses > relativelyuptake in myocardium distal to stenoses > relatively
low signal from areas of low perfusionlow signal from areas of low perfusion

24. Indications for MPIIndications for MPI
 Suspected false +veSuspected false +ve
or -ve ETTor -ve ETT
 Resting ST changesResting ST changes
 LBBB,LVH, digitalis,LBBB,LVH, digitalis,
pre-excitation orpre-excitation or
pacemakerpacemaker
 Women with +ve ETTWomen with +ve ETT
and low orand low or
intermediateintermediate
probability CADprobability CAD
 Inability to exerciseInability to exercise
 Prognosis of knownPrognosis of known
CADCAD
 Detecting post PTCADetecting post PTCA
or CABG ischaemiaor CABG ischaemia
 Assessing myocardialAssessing myocardial
viabilityviability
 Risk evaluation inRisk evaluation in
non-cardiac surgerynon-cardiac surgery
patientspatients
 Assessment ofAssessment of
functional significancefunctional significance
of documentedof documented
coronary stenosiscoronary stenosis

25. ContraindicationsContraindications
 PregnancyPregnancy
 Food within 4 hours of stress studyFood within 4 hours of stress study
 Caffeine within 24 hours (forCaffeine within 24 hours (for
pharmaceutical stress)pharmaceutical stress)
 Bronchospasm or severe obstructive lungBronchospasm or severe obstructive lung
disease (for pharmaceutical stress)disease (for pharmaceutical stress)
 Hypotension (SBP < 90 mm Hg)Hypotension (SBP < 90 mm Hg)
 Xanthine-containing drugsXanthine-containing drugs

26. Patient Prep MPI Stress TestPatient Prep MPI Stress Test
 NPO 4 hours prior to testNPO 4 hours prior to test
 No caffeine within 24 hoursNo caffeine within 24 hours
 Restrict cardiac medication if possibleRestrict cardiac medication if possible
 Consent for stressConsent for stress
 Skin prep/lead placement 12 lead ECGSkin prep/lead placement 12 lead ECG
 IV placementIV placement

27. SPECT by Thalium 201SPECT by Thalium 201
 Thalium 201 is a potassium analogue thatThalium 201 is a potassium analogue that
utilizes the Na/K ATP ase and relies on intactutilizes the Na/K ATP ase and relies on intact
cellcell
 Thalium201 have relatively long half life ( 73Thalium201 have relatively long half life ( 73
hours) which means that a small dose ( 2-4 mCi)hours) which means that a small dose ( 2-4 mCi)
must be usedmust be used
 It emits X-ray ( 68-80 keV) and gamma ray atIt emits X-ray ( 68-80 keV) and gamma ray at
135-167 keV135-167 keV
 There is a linear relationship between blood flowThere is a linear relationship between blood flow
and uptake of thalium at rest which is maintainedand uptake of thalium at rest which is maintained
during exercise making it reliable indicator ofduring exercise making it reliable indicator of

29. Exam Results
•Non viable
- perfusion defect on rest & stress
•Myocardial Ischemia/ Viable
- perfusion defect on stress only

30. Protocols usedProtocols used
 Rest / redistribution thaliumRest / redistribution thalium
 Imaging 30-60 minutes after an initialImaging 30-60 minutes after an initial
injection followed by reimaging 4 hoursinjection followed by reimaging 4 hours
laterlater
 Defects on initial image that improves in 4Defects on initial image that improves in 4
hour are considered viablehour are considered viable
 This protocol does not address ischemiaThis protocol does not address ischemia
and less sensitive than other protocolsand less sensitive than other protocols
and PETand PET

31. ContinueContinue
 Stress / redistributionStress / redistribution
 Pharmacologic or exercise induced stress withPharmacologic or exercise induced stress with
subsequent thalium injection and imaging immediatelysubsequent thalium injection and imaging immediately
followed by reimaging 4 hours laterfollowed by reimaging 4 hours later
Interpretation:Interpretation:
 Myocardium that has a defect on stress but improvesMyocardium that has a defect on stress but improves
with rest is considered to be ischemic and viablewith rest is considered to be ischemic and viable
 Myocardium that is not perfused at rest and stress isMyocardium that is not perfused at rest and stress is
considered to be scarconsidered to be scar
Disadvantage: Defects that do not improve in 4 hours mayDisadvantage: Defects that do not improve in 4 hours may
contain viable tissue , imaging 24 hours after stress maycontain viable tissue , imaging 24 hours after stress may
improve sensitivityimprove sensitivity

32.  Stress /redistribution/re injectionStress /redistribution/re injection
This protocol involve re injection of 1 mCi ofThis protocol involve re injection of 1 mCi of
thalium with subsequent re imaging of thethalium with subsequent re imaging of the
patient after 18-24 hourspatient after 18-24 hours
Interpretation:Interpretation:
Scar or non viable: defect on stress imagesScar or non viable: defect on stress images
and does not improve upon reinjectionand does not improve upon reinjection
and re imagingand re imaging
Viable myocardium: no uptake on stress butViable myocardium: no uptake on stress but
uptake on reinjection

33. Stress
NormalNo defect
Reversible
Perfusion Defect
MI/Scar
Ischemia
Rest
Fixed
Perfusion Defect

34. Tc99m labelled agentsTc99m labelled agents
 Rely on sarcolemmal integrity and mitochondrialRely on sarcolemmal integrity and mitochondrial
functionfunction
 Short half life( 6 hours) ,thus higher doses ( 10-Short half life( 6 hours) ,thus higher doses ( 10-
39mCi) , better image39mCi) , better image
 Redisribution less- so less helpful in assessingRedisribution less- so less helpful in assessing
viabilityviability
 The commonly used agents are Tc 99m sestamibi,The commonly used agents are Tc 99m sestamibi,
tc 99m tetrofosmin , Tc 99b furofosmin Tc 99mtc 99m tetrofosmin , Tc 99b furofosmin Tc 99m
NOET, Tc 99m NOET has -similar redistributionNOET, Tc 99m NOET has -similar redistribution
kinetics to Thalliumkinetics to Thallium
 Viability criterion is>50% tracer uptake inViability criterion is>50% tracer uptake in
dysfunctional segments.dysfunctional segments.

37. Comparing Perfusion AgentsComparing Perfusion Agents
Thallium-201Thallium-201
 K analogue, henceK analogue, hence
require intact cellrequire intact cell
membranemembrane
 Uptake proportional toUptake proportional to
blood flowblood flow
 Washes out slowly fromWashes out slowly from
myocardium-redistributionmyocardium-redistribution
phasephase
– defect normalizes =defect normalizes =
ischaemiaischaemia
– defect unchanged =defect unchanged =
scarscar
Tc 99m-SestamibiTc 99m-Sestamibi
 It is bound to innerIt is bound to inner
mitochondrial membrane,mitochondrial membrane,
hence require intacthence require intact
mitochondial functionmitochondial function
 Uptake proportional toUptake proportional to
blood flowblood flow
 Tissue uptake is fixedTissue uptake is fixed
– true perfusion agenttrue perfusion agent
 Higher energy/betterHigher energy/better
tissue penetration andtissue penetration and
imagesimages

38. PET-FDGPET-FDG
 Uses positron emitting isotope capable ofUses positron emitting isotope capable of
releasing 2 high energy ( 511 keV ) photons atreleasing 2 high energy ( 511 keV ) photons at
an angle of 180 degree. The PET camera canan angle of 180 degree. The PET camera can
detect these higher energy raysdetect these higher energy rays
 Uses separate agents to measure perfusion andUses separate agents to measure perfusion and
viability .viability .
 Perfusion agents are Rubidium 82, -Nitrogen 13Perfusion agents are Rubidium 82, -Nitrogen 13
ammonia, Oxygen15 waterammonia, Oxygen15 water
 Metabolic tracers- 18 FDG( 18 fluro de oxyMetabolic tracers- 18 FDG( 18 fluro de oxy
glucose), C11acetate, C11 palmitate,glucose), C11acetate, C11 palmitate,

39.  FDG is glucose analogue and it is takenFDG is glucose analogue and it is taken
up by viable cells and then phoshorylatedup by viable cells and then phoshorylated
so, that it can not be metabolized furtherso, that it can not be metabolized further
& trapped inside the cell& trapped inside the cell
 In normal myocardium , free fatty acidsIn normal myocardium , free fatty acids
are prferentially used. During periods ofare prferentially used. During periods of
ischemia , metabolism is altered , so thatischemia , metabolism is altered , so that
primarily glucose is utilized.primarily glucose is utilized.
 Poor uptake in diabeticsPoor uptake in diabetics

40. InterpretationInterpretation
 Normal perfusion-viabilityNormal perfusion-viability
 Flow metabolism mismatch-reducedFlow metabolism mismatch-reduced
perfusion with intact metabolism-perfusion with intact metabolism-
hibernating viable myocardiumhibernating viable myocardium
 Flow metabolism match-impaired FDGFlow metabolism match-impaired FDG
uptake with reduced perfusion-scar or nonuptake with reduced perfusion-scar or non
viable tissueviable tissue
 Gold standard for assessment of viabilityGold standard for assessment of viability

41. Perfusion metabolism mismatch-apex,Perfusion metabolism mismatch-apex,
anterior anterolateral wallanterior anterolateral wall

43.  Strengths-Strengths-
– Perfusion &metabolismPerfusion &metabolism
– More sensitiveMore sensitive
– No attenuationNo attenuation
– Absolute blood flow can be measuredAbsolute blood flow can be measured
– Predictive of outcomesPredictive of outcomes

44.  LimitationLimitation
– Lower specificity to dobutamine echo & MRILower specificity to dobutamine echo & MRI
– Cannot differentiate between endocardialCannot differentiate between endocardial
and epicardial viabilityand epicardial viability
– High costHigh cost
– Limited availabilityLimited availability

45. Dobutamine stress echoDobutamine stress echo
 Myocardial contractility ceases when 20% orMyocardial contractility ceases when 20% or
more of the trans mural thickness is ischemic ormore of the trans mural thickness is ischemic or
infarcted.infarcted.
 Dobutamine SE can be used to detect viableDobutamine SE can be used to detect viable
myocardium whether stunned or hibernatingmyocardium whether stunned or hibernating
 Myocardial stunning: Viable non ischemic nonMyocardial stunning: Viable non ischemic non
contractile myocardiumcontractile myocardium
 Myocardial hibernation : Viable chronic ischemicMyocardial hibernation : Viable chronic ischemic
non contractile myocardium.non contractile myocardium.
 These viable myocardium regain contractileThese viable myocardium regain contractile
function in response to inotropes and predictivefunction in response to inotropes and predictive
of recovery of function after revascularization.of recovery of function after revascularization.

46. InterpretationInterpretation
 Dobutamine started at 5mcg/kg/min and increment every 3Dobutamine started at 5mcg/kg/min and increment every 3
minutesminutes
 Low-dose dobutamine (5–10Low-dose dobutamine (5–10 μμg/kg/min)g/kg/min)
 High-dose dobutamine(upto 40High-dose dobutamine(upto 40 μμg/kg/min)g/kg/min)
– Biphasic response : Improvement of WMA at low low doses (5–10Biphasic response : Improvement of WMA at low low doses (5–10
μμg/kg/min) followed by worsening at high dose (upto 40g/kg/min) followed by worsening at high dose (upto 40 μμg/kg/min)–g/kg/min)–
underperfused but viable tissue-most specific sign of improvementunderperfused but viable tissue-most specific sign of improvement
after revascularization.after revascularization.
– Uniphasic response-sustained improvement both at low and highUniphasic response-sustained improvement both at low and high
doses -less predictive of improvement after revascularizationdoses -less predictive of improvement after revascularization
– Deterioration of wall motion without initial improvement-severeDeterioration of wall motion without initial improvement-severe
ischemiaischemia
– No change in wall motion-scarNo change in wall motion-scar
 Sensitivity(84%),specificity(81%)for recovery of functionSensitivity(84%),specificity(81%)for recovery of function

47.  Strengths-Strengths-
– Higher specificityHigher specificity
– Viability & ischemia assessedViability & ischemia assessed
– Good spatial resolutionGood spatial resolution
– Widely availableWidely available
– Lower costLower cost
– Predictive of clinical outcomesPredictive of clinical outcomes

48.  LimitationsLimitations
– Poor window in 30%Poor window in 30%
– Lower sensitivityLower sensitivity
– Reliance on visual assessmentReliance on visual assessment

49. Cardiac MRICardiac MRI
 Delayed enhancement cardiac MRI usesDelayed enhancement cardiac MRI uses
Gadolinium based contrast agents whichGadolinium based contrast agents which
are extra cellular compound, given IVare extra cellular compound, given IV
( 0.2mmol/kg)( 0.2mmol/kg)
 Areas of myocardial scar or fibrosis have aAreas of myocardial scar or fibrosis have a
larger extracellular space with a greaterlarger extracellular space with a greater
accumulation and slower washout .accumulation and slower washout .
Therefore appear bright compare toTherefore appear bright compare to
normal myocardiumnormal myocardium

50. InterpretationInterpretation
 Segments with 0 to 25 % transmural extent ofSegments with 0 to 25 % transmural extent of
hyperenhancement represent viable tissue with mostlyhyperenhancement represent viable tissue with mostly
normal myocardium and minimal fibrosis.normal myocardium and minimal fibrosis.
 Segments with more than 75 % transmural extent ofSegments with more than 75 % transmural extent of
hyperenhancement represent scared non viablehyperenhancement represent scared non viable
myocardiummyocardium
 Areas between 25-75 % have intermidiate viabilityAreas between 25-75 % have intermidiate viability
 Finally the areas of hyperenhancement can beFinally the areas of hyperenhancement can be
correlate with segmental wall function and rest/stresscorrelate with segmental wall function and rest/stress
perfusion to determine ischemia and viabilityperfusion to determine ischemia and viability

53. Ischemic cascadeIschemic cascade
 The ischemic cascade is a sequence ofThe ischemic cascade is a sequence of
hemodynamic and cardiachemodynamic and cardiac
electrophysiologic changes that culminateelectrophysiologic changes that culminate
in anginain angina
 It is initiated by an imbalance betweenIt is initiated by an imbalance between
myocardial oxygen supply and demandmyocardial oxygen supply and demand
 Abnormal myocardial perfusion is the firstAbnormal myocardial perfusion is the first
detectable event in the ischemic cascadedetectable event in the ischemic cascade

54. Ischemic cascadeIschemic cascade

55. Ischemic cascadeIschemic cascade

56. THANK YOU