Myocardial Viability Biplave.pptx

Dr Biplave Karki
DM resident
Department of Cardiology, BPKIHS

Viable myocardium ?
Viability assessment
• Invasive methods
• Non-invasive methods
Role of viability testing for revascularization
in ICMP ?

 Refers to cardiac muscle that is alive, not dead
• presence of cellular, metabolic, and microscopic contractile
function
 Clinically
• LV systolic dysfunction in ischemic heart disease does not
always represent irreversible damage and
• dysfunctional but viable myocardium has the potential to
improve its systolic function after revascularization
 Two basic mechanisms of reversible ischemic
dysfunction
• myocardial stunning
• myocardial hibernation

 Prolonged post-ischemic ventricular dysfunction that
occurs after brief episodes of non-lethal ischemia
 Transient LV dysfunction commonly observed following
an acute myocardial infarction treated with prompt
reperfusion.

 Myocardium downregulates its contractile function in
the presence of sustained reduced blood flow.
 Cardiac myocytes are depleted of their contractile
material and filled with glycogen (PAS-positive
staining)

Early
reperfusion
before
irreversible
damage
Repeated
episodes of
hypoperfusion
Longer
duration of
ischemia
Single
prolonged
period of
ischaemia

1. After a short period of ischaemia, which is alleviated before
irreversible damage has taken place,
• contractile dysfunction can persist for hours to days; this is termed stunning.
2. If the cell is exposed to repeated episodes of hypoperfusion,
• it can enter early- or ‘short-term’ hibernation with metabolic adaptation and early
histological changes becoming apparent:
• at this point, function remains persistently abnormal between episodes of
ischaemia, unless the stimulus is withdrawn for an extended period.
3. Over a longer duration,
• more extensive histological change occurs,
• some myocytes are lost with fibrotic replacement, whilst
• others enter advanced hibernation with cellular adaptations and remodelling.
4. Conversely, infarction, usually caused by a single prolonged period
of ischaemia, results in
• complete cellular necrosis and replacement of normal tissue with fibrous scar

Invasive methods
CAG
Non-invasive methods
Echocardiography
DSE
TMT
Nuclear Scintigraphy
• SPECT
• PET-FDG
CMR
CT

Myocardial viability
 Presence of high grade proximal stenosis, distal
TIMI-III flow
 Myocardial blush of contrast
 Collateral blood flow
 Improved contractility after IV NTG or inotropic
stimulation with low dose dobutamine
Simple but less accurate

 Resting LV size and function
 LV wall thinning and increased echo backscatter
are thought to be markers for scarring
 Increased LV end-systolic volume is associated
with worse clinical outcomes after
revascularization
 LV end-diastolic wall thickness (EDWT) of <6 mm
was initially reported to exclude viable myocardium
(results challenged by MRI based studies)

 An initial infusion of dobutamine at 2.5
μg/kg/min, with gradual increase to 5, 7.5, 10,
and 20 μg/kg/min.
 Wall thickness should be assessed on resting
images
• segments that are thinned (≤0.5 or 0.6 cm) and bright
(suggesting advanced fibrosis) rarely recover
 Sensitivity of 82% and Specificity of 79% for
predicting recovery of LV function after
reperfusion.

1. Biphasic response
• contractility improves in dysfunctional segments with low-dose
dobutamine and then becomes dysfunctional again at higher doses
due to ischemia.
2. Worsening contractile function as dobutamine doses
increase
• Hibernating myocardial tissue has no contractile reserve and
increases in demand result in ischemia and further worsens
contractility
3. Sustained improvement with increasing dobutamine dose
• Myocardial stunning
4. No response to dobutamine
• Lack of viability

End-systolic images
Biphasic response in the left anterior descending
artery territory (arrows).
At rest
Low-dose
High-dose
High-dose

End-systolic images
Biphasic response in midinferior wall (yellow arrows) and
A scar at the basal inferior wall (red arrows) in the same patient.
At rest
Low-dose
High-dose
High-dose

 Echo contrast perfusion volume and velocity to the
myocardium
• Detects cardiac microvascular integrity as an assessment
of myocardial viability in akinetic segments
 Tissue Doppler imaging and speckle tracking
echocardiography
• Assess myocardial deformation in the evaluation of viable
myocardium
• More sensitive in detecting viability in ischemic
cardiomyopathy
• In a preliminary study, its diagnostic accuracy was reported
to be similar to that of LGE-CMR

Exercise induced ST elevation in infarct
related area was a/w residual tissue
viability
• Margonoto et al; JACC 1995
Sensitivity and specificity of 84% and
100% respectively
• Nakano A et al; JACC 1999

 SPECT utilizes radionuclide-labeled tracer (99mTc-sestamibi or
201Tl) to measure regional tracer concentration in the myocardium
• percentage of peak uptake of the tracer within myocytes with intact cell
membrane
 Rest images only or with a stress/rest testing protocol
 99mTc-sestamibi (Sensitivity of 84% and Specificity of 77%)
• much shorter protocol duration with rest imaging occurring approximately
1 hour after tracer administration.
 201TI (Sensitivity of 86% and Specificity of 59%)
• Redistribution of 201Tl in the myocardium
• 4-hour and 24-hour delayed imaged

 A cutoff of
>50% tracer
activity
 Large region
of infarct
apical to mid
anterior,
anteroseptal
and
inferoseptal
segments.
Quantitative
polar plot
Viability in all
coronary
territories except
in segments of the
apex.

 Normal, infarcted, stunned, and hibernating myocardium
 Better spatial resolution than SPECT
 Rest perfusion can be assessed with multiple tracers
• 13N-ammonia or 82Rb
 At rest the myocardium will generally oxidize free fatty acids to
produce ATP.
 However, in the setting of myocardial ischemia, there is a shift
to glucose metabolism with up-regulation of glucose
transporters. When fasting, FDG is taken up mainly by
ischemic myocardium
 Scar tissue and normal myocardium do not take up FDG

A large fixed
perfusion defect
with akinesia in the
anterior and septal
segments of the
LAD territory.
No FDG uptake is
seen in this territory
suggesting no
viability.

 Hibernating myocardium
• perfusion-metabolism mismatch
• decreased 13N-ammonia uptake and increased or preserved
FDG uptake
 Myocardial scar
• reduction in blood flow and metabolism
 Stunned myocardium
• normal perfusion in an area of regional contractile dysfunction.
 One limitation to PET is the variability of FDG uptake
which can be impacted by cardiac output, heart failure,
degree of ischemia, and sympathetic activity.

A meta-analysis of 20 studies with 598
patients undergoing viability with FDG
before revascularization
• high sensitivity (93%) but low specificity (58%) for
identifying LV recovery
Sensitivity was higher than other nuclear
imaging techniques and dobutamine
echocardiography.

 Global left ventricular function and regional
wall motion
 Viability can be assessed using
• LV end-diastolic wall thickness (EDWT)
• Response to dobutamine stress similar to DSE
• Gadolinium enhancement (LGE) imaging (m/c)
 Benefits of CMR over DSE and SPECT
• excellent spatial imaging
• ability to determine transmural variations in viability.

A) Anterior left ventricle was noted to be thinned and akinetic, with evidence of a subendocardial
myocardial infarction that spanned <50% of the transmural extent.
B) The thinned segments recovered contractile function after coronary revascularization
A B

Left
Thinned and
akinetic
segments are
noted in the
anterior and
anteroseptal
walls.
Infarction was
transmural.
Right
Late gadolinium
enhancement
imaging
demonstrating
≈50%
transmural
extent of
infarction in the
anterolateral
and
anteroseptal
segments.

 EDWT alone has limited prediction for functional recovery after
revascularization
• Baer et al reported that EDWT cutoff of 5.5 mm has 94% sensitivity but
only 52% specificity for predicting segmental functional recovery after
revascularization
 Gadolinium-based contrast agents (GBCAs)
 In normal state, gadolinium enters the extracellular space readily
after intravascular injection, but
 it is unable to cross the cell membrane of a normal myocyte.
 When the myocyte cell membrane is damaged or if there is an
increase in the extracellular space between myocytes (eg, acute
interstitial edema or chronic fibrosis or MI),
 GBCA accumulates in the extracellular space, and its washout is
delayed after the injection.

 The most common current protocols use a GBCA at 0.1
mmol/kg patient weight and then perform LGE imaging at 10
minutes after GBCA injection.
• Latest GBCAs, LGE imaging as early as 5 minutes.
 Akinetic segments with no or minimal subendocardial
infarction
• >90% chance of segmental recovery after reperfusion
 > 50% transmural extent of infarction
• <10% chance of segmental contractile recovery
 <50% transmural extent of infarction
• functional recovery is not well predicted by the criteria using LGE
transmural extent alone, and
• it can benefit from assessment by inotropic contractile reserve.

 Iodinated contrast agents accumulate
in infarcted myocardium
 Absence of hyper-enhancement or
involvement of <50% myocardial wall
thickness indicates viability.
 High spatial resolution with possible
differentiation of transmural and
subendocardial infarction
 Old infarcts have low CT densities
than recent infarcts.
 Similar corelation with CMR
Hyper-enhancement of
posterior wall

Db-CMR indicates dobutamine cardiovascular magnetic resonance; Db-Echo, dobutamine echocardiography; LGE-
CMR, late gadolinium-enhanced cardiovascular magnetic resonance; PET-18F-FDG, positron emission tomography–
fluorodeoxyglucose; NPV, negative-predictive value; PPV, positive predictive value; 99mTc, technetium-99m; and
201Tl, thallium-201.
Data derived from Romero et al and Schinkel et al

 Surgical Treatment for Ischemic Heart Failure
• The 10-year results of this multicenter randomized trial
demonstrated improved long-term all-cause and
cardiovascular mortality with surgical revascularization of
patients with ischemic cardiomyopathy (LVEF ≤35%)
compared with patients receiving guideline-directed medical
therapy (GDMT)
• However, this late survival benefit was achieved at the
expense of higher short term 30-day mortality after CABG

 Prespecified viability substudy of STICH
• Assessed baseline myocardial viability with SPECT imaging or dobutamine
echocardiography in 618 of the1212 enrolled STICH patients
• Patients with myocardial viability had lower 5-year mortality rate (33% versus
50%)
• Viability status by these methods did not discriminate patients who would derive a
mortality benefit from CABG plus GDMT compared with GDMT alone
 Although an increase in LVEF was observed only among patients
with myocardial viability,
• The increase was similar in magnitude in patients treated with GDMT and with
CABG
• Survival was not related to whether LVEF increased

 Previous retrospective data in metaanalysis and
systematic reviews
• improved survival with revascularization compared with medical
therapy in patients with viable but dysfunctional myocardium
 Samady et al, 20 years earlier
• survival after CABG in patients with LV systolic dysfunction (mean
EF, 24%) did not depend on whether EF increased
postoperatively.
 PARR-2 trial
• patients randomized to PET viability imaging did not demonstrate
improved survival after CABG compared with standard care

Occluded Artery Trial (OAT)
 lack of benefit of PCI versus medical therapy in patients with an
occluded infarct-related artery
 these results can only apply to patients with an occluded infarct
related artery 3–28 days after an acute myocardial infarction and PCI
was not guided by ischemia nor myocardial viability testing
Baks et al.
 27 patients underwent successful CTO recanalization with DES and
whom had CMR before and after intervention
 segmental wall thickening (SWT) improved most significantly in
segments with <25% transmural extent of infarction by LGE CMR

 Kirschbaum et al.
• evaluated LV function recovery with CMR pre-procedure, 5
months, and 3 years after CTO PCI
 At 5-months follow-up
• SWT significantly improved in those with < 25% transmural infarct
but not in those with 25% to 75% transmural infarct
 At 3 years
• improvement in SWT in those with 25% to 75% transmural infarct
 Recovery time of dysfunctional myocardium was
related to the extent of damage on a cellular level

Myocardial Viability Biplave.pptx

Myocardial Viability Biplave.pptx

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