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MYOCARDIAL

VIABILITY
ASSESSMENT IN
NUCLEAR AND MRI

I Made Indra
Prasetya

VIABILITY IN
NUCLEAR

NUCLEAR IN MEDICINE
The use of radioisotope or radionuclide for
medical assessment
The radionuclide is injected, uptaken by human
tissue, and scanned with a gamma camera

NUCLEAR CARDIOLOGY
non-invasive nuclear imaging
technique that uses radioactive
imaging agents to image the heart
Among the techniques of nuclear
cardiology, myocardial perfusion
imaging is the most widely used

NUCLEAR CARDIOLOGY
Myocardial perfusion imaging :
1. Identify inadequate blood supply as well as the
areas of scarred myocard
2. In addition to the localization of the coronary
artery with atherosclerosis quantify the
extent of the myocard with a limited blood fl ow
3. provide information about the pumping function
of the heart

MAIN CLINICAL INDICATION OF


NC
Detection of ischemic heart disease
Hemodynamic eff ect of coronary stenoses
Prognosis of patients with known CAD
Evaluation of revascularization eff ect and
detection of restenosis
Risk stratifi cation of patients after MI
Myocardial viability
Acute coronary syndromes
Cardiac risk in non-cardiac surgery

VIABILITY OF THE MYOCARDIUM


Viability
Determine the appropriateness of the (living and
healthy) tissue in the heart muscle
Limited or absent scarring
Potential for functional recovery
Reversible ischemic contractile dysfunction
Myocardial stunning
Myocardial hibernation

MYOCARDIAL STUNNING
Prolonged and fully reversible contractile dysfunction
of the ischemic heart that persists after reperfusion
Responsive to inotropes
Spontaneously resolve within a week
Duration of stunning depends on the duration and
severity of ischemia and the adequacy of arterial fl ow
Mechanism:
(1) a oxygen-free radical hypothesis and
(2) a calciumoverload hypothesis

MYOCARDIAL HIBERNATION
Episodic and/or chronically reduced blood fl ow,
which is directly responsible for the decrease in
the myocardial contractile function
Tissue ischemia and resultant remodeling without
necrosis, which causes prioritization of metabolic
process in the myocardial cell relative to
contractile function
Recovery of contractile function after successful
revascularization
Time to restoration:
Months to one year
Depend on duration and severity of fl ow reduction &
ultrastructural changes

Mechanism:
Myocardial function &metabolism reduced to match a
reduction in blood fl ow (Smart heart hypothesis)
Repetitive stunning hypothesis

TECHNIQUES FOR VIABILITY


ASSESSMENT
Myocardial glucose utilisation-PET FDG
SPECT Thallium (cell membrane integrity)
SPECT Tc (intact mitochondria)
Dob.echo and Dob.MRI (assess contractile reserve)
MRI with IV contrast (assess scar)

SPECT
Single Photon Emission
Computed Tomography

SPECT IMAGE QUANTIFICATION

TRACERS
Thallium 201

Introduced in the 1970s


Monovalent cation K+
Emits 80 keV
T 73h
First pass 85%
Transported by NaK ATPase &
facilitative diff usion
Redistribution image
Rest ischemia
Viable myocardium
False scar defect

Technetium 99m
Introduced 1990s
Lipid soluble cationic
comp.
Emits 140 keV
T 6h
First pass 60%
Passive distribution
Minimal redistribution

REST-THALLIUM IMAGING
HIBERNATING MYOCARDIUM
Principal and technique
Rest-redistribution exam presence or absence
myocardial viability
3-4 mCi injection of thallium image acquired at the
time and 3-4hours later

ABNORMALITIES CAN BE IDENTIFIED

1. Clearly reversible abnormalities


Severely ischemic but viable
myocardium (hibernating
myocardium)
LV dysfunction w/ myocardial
viability surgical
revascularization much better
prognosis than medical therapy

ABNORMALITIES CAN BE IDENTIFIED


2. Fixed defects w/ mild to moderate decreased
tracer activity
50% these regions improved wall motion following
revascularization
Contain mixed viable myocardial tissue and scar
Mild defect (30% reduction activity) viability with
better likelihood for improvement in wall motion
following revascularization
Fixed defect > 50% of peak activity indicates
myocardial viability contain subendocardial scar
tissue and may not improve in function following
revascularization

ABNORMALITIES CAN BE IDENTIFIED


3. Fixed defects w/ severely decreased

tracer activity
Rest perfusion defect that do not demonstrate
improved on delayed images represent scar
Defects w/ < 50% of peak activity low
likelihood improved LV after revascularization
Note: for fixed defects w/ activity < 50% of
maximal uptake, up to 25% have been shown
to be viable by FDG imaging

SENSITIVITY AND SPECIFICITY


Determination of viability and improvements in wall
motion, sensitivity 67%-86% , specifi city 55%-77%
PET imaging NPV 76% 83%, PPV 84%-92%
Combine rest-thallium and dobu-echocardiography
accurate information than either technique
independently

TECHNETIUM OF HIBERNATING
MYOCARDIUM AND MYOCARD VIABILITIY
Thallium imaging with reinjection is superior to
Tc-sestamibi imaging in identfying viable
myocardium in patients with chronic CAD
Approximately 35% - 60% of reversible
myocardial regions on thallium reinjection
imaging will appear as fi xed defect on exerciserest images with Tc-sestamibi
Thallium is superior to technetium agents for
the assessments of myocardial viability

POSITRON EMISSION TOMOGRAPHY


Quantitative evaluation of metabolism and
myocardial perfusion
Using a positron emitting isotopes

TRACER
PRODUCED
Perfusion
Oxygen-15 Cyclotron
Nitrogen-13 Cyclotron
Rubidium-82 Generator
Metabolism
Carbon-11

Cyclotron

Fluorine-18

Cyclotron

HALF-LIFE

COMPOUND

2.1 minutes H2O


10 minutes NH3
76 seconds RbCl
20.4
minutes

Acetate,
palmitate
Deoxyglucos
110 minutes
e

PET SCAN METHODS AND IMAGES

PET SCAN INTERPRETATION


Normal perfusion-viability
Flow metabolism mismatch-reduced perfusion
with intact metabolism-hibernating viable
myocardium
Flow metabolism match-impaired FDG uptake
with reduced perfusion-scar
Gold standard for assessment of viability

PET FDG IMAGING


Enhanced LV function after revascularization is
associated w/ improving survival crucial to identify
areal of viable myocardial tissue
FDG remains the gold standard for the evaluation of
myocardial viability (up to 30-50% of segments
showing scar by delayed thallium FDG uptake
suggesting viability)
Severely decreased FDG uptake < 50% of normal
myocardial activity scar

VIABILITY IN MRI

MRI
MR determination of viability:
Based on visible changes in myocardial wall
thickness
Through the use of delayed contrast enhanced
imaging
Assessing inotropic reserve by low-dose Dob-MRI

MR advantages:
Excellent anatomic resolution that can be achieved
with rapid cardiac imaging sequence
Much higher spatial resolution
allow the detection of even a small areas of
subendocardial infarction that will be missed on
SPECT imaging
Delayed contrast (DE MR) can detect acute MIparticularly inferior infarcts and subendocardial scar
with greater sensitivity than SPECT

Resting thallium-201 SPECT images and corresponding DE MR images


in two patients with subendocardial MI. In this study comparing resting
thallium 201 SPECT and MRI in 91 patients with known or suspected
CAD. 13% (N=6) of patients with subendocardial infarction visible by
MRI had no abnormality detected on resting SPECT images.

MR limitation:
DE MR imaging spesifi c for acute MI and scar (not for
hibernating myocardium or repetitively stunned
myocardium) cannot distinguish hibernating myocardium
from normally perfused myocardium in regions of
nontransmural hyperenhancement

Reason of hibernating myocardium segments


failed/limited to demonstrate improved function:
Adjacent to infarcted segments
Related to mechanical tethering
Myocardium have hypertrophied myocytes that have
impaired contractile function

Had nontransmural wall thinning


Subendocardial infarct with preserved end diastolic
wall thickening

FUNCTIONAL MYOCARDIAL
EVALUATION
For functional MR Imaging: 6-8 short axis
Hypokinetic or akinetic segments demonstrate <
1mm of wall thickening
Segments EDWT < 5,5 mm recovery after
revascularization
Wall thinning can predict functional recovery
following revascularization:
Sensitivity: 55 95%
Specifi city: 41%

WALL THICKNESS

End-Diastolic Wall
Thickness

Systolic Wall
Thickening

Normal Myocardial

> 5,5 mm

> 1,5 mm

Hibernating
Myocardial

> 5,5 mm

< 1,5 mm

Infarcted Myocardial

< 5,5 mm

< 1,5 mm

Cut plane perpendicular to long axis on 2-C view, and parallel to


atrial-ventricular valves (between anterior & posterior grooves) &
almost perpendicular to interventricular septum on 4-C views.
Cover from atria to apex.

CONTRAST ENHANCED IMAGING


Gadolinium is retained by scar tissue
There is faster washout of the contrast from normal
myocardium

Delayed contrast enhanced MR (DE


MR)
imaging is very sensitive for
detecting
areas of myocardial infarction and
scar

DE MR
Delayed Enhacement MR (DE MR)
Kim et al. in 1999
use of an inversion-recovery prepared T1-weighted
gradient-echo sequence after the intravenous
administration of a Gadolinium-chelate (Gd)

Nonviable tissue as hyperenhanced or bright.

Areas of myocardial infarction (acute & chronic)


demonstrate LATE contrast enhacement in these
region following administration of Gadolinium
Secondary to edema & an increase in the extracellular
space at the site of infarction (scar) with delayed
washout of contrast as a consequence of reduced
capillary density

Infarction always involves the


subendocardium
which is most vulnerable to
ischemia

Mechanism of hyperenhancement of myocardial scar:

Presence of fibrotic tissue & loss of sarcomere membrane


integrity
Increased interstitial
space
Increased volume of distribution of Gd in infarcted
myocardium
Increased concentrations of Gd per unit volume of
tissue
Hyperenhancement relative to viable
myocardium

DE MR in the short axis projection demonstrate transmural


hyperenhacement of LAD distribution. Representative HE-stained
pathology sections reveal replacement fibrosis and normal myocardium.

Delayed hyperenhancement:
regions of increased signal intensity on T-1 weighted
images acquired more than 5 minutes after IV
Gadolinium administration
refl ects irreversibly injured myocardium or
replacement fi brosis

MR exam delayed inversion-recovery:


Fast low-angle shot contrast-enhanced imaging in short
axis plane 15 minutes following IV administration of
0.15 mmol/kg BW Gadolinium

AMI is illustrated in 4-chamber projection (end diastole on the left and end
systole in the middle). There is akinesis of the distal LAD distribution
arrowhead) closely corresponding with the transmural hyperenhacement of
the apex (arrow) and subendocardial hyperenhacement of the
distal interventricular septum.

Other conditions associated with delayed


enhacement
Hypertrophic cardiomyopathy
Dilated nonischemic cardiomyopathy
Arrythmogenic right ventricular dysplasia
Myocarditis
Sarcoid
Amyloid
Trauma
Hypereosinophilic syndrome
Post radiofrequency ablation

In the mid wall of the myocardium


(rather than subendocardial or
transmural)
Does not correspond to coronary vascular
teritories

Central dark core within areas of


hyperenhancement:
Associated with acutely infarcted myocardium
Secondary to no refl ow phenomenon defi ned
histopathologically as evidence of microvascular damage
and low myocardial perfusion
Associated with advanced myocardial damage and impaired
functional recovery

Midventricular short-axis DE MR demonstrating acute transmural infarction of the


lateral wall (arrowhead). There is also dense rim of subendocardial signal void
(black arrow) corresponding to the region of no-reflow or microvascular
obstruction. Because Gd is unable to reach this portion of the myocardium,
there is no T1shortening, and therefore, no hyperenhancement can be visualized

The no-reflow phenomenon revealed by DE MR. The no reflow zones are


almost completely surounded by larger regions of hyperenhancement
and, importantly, slowly become hyperenhanced as repeated images are
acquired at the same location over time. Labels refer to time (in minutes)
after administration of contrast media.

Gd-DTPA concentration will change in the normal


myocardium over time TI (Inversion Time) require
adjustment to avoid underestimation of infarct size:
Acquire series of images after the inversion prepulse using
a central shot axis slice
Visual or ROI analysis is performed to select TI that
produces the lowest signal from normal myocardium

PROGNOSIS MRI
Transmural extent of hyperenhancement within 1st
week after MI predict late improvement in
contractile function
Lack of delayed enhancement is highly predictive for
functional improvement after surgical
revascularization
Regions with greater transmural enhancement are
less likely to demonstrate improved wall motion

Prognosis MRI:
Segments >75% transmural of delayed hyperenhancement
unlikely to recover function
Segments 51-75% hyperenhancement
only 10% will demonstrate functional recovery
with revascularization
Segments <25%
recover function following revascularization

LOW DOSE DOB-MRI


Baer et al (1995,2000) compared with:
Dob-TEE: PPV 85% vs 92%, NPV 80% vs 85%
(for prediction of LV function after revascularization)
PET: sensitivity 88%, specifi city 87%
(viability after myocardial infarction: EDWT >5,5mm and
dob-induced systolic wall thickening >1mm)

Direct comparison low dose Dob-echo & low dose Dob-MRI study to assess
viability in septal & lateral wall after MI in the same patient. Both techniques
are capable of visualizing an improvement of wall motion after dobutamine
infusion (see arrows) as a sign of residual viability in the areas of interest.

ow-dose Dob-MR (left) and corresponding midventricular short-axis DE MR


(right). Low dose Dob-MRI demonstrates persistent akinesis of the inferior
Wall despite increasing dobutamine dose, consistent with lack of viability.
e corresponding DE MR is similarly able to demonstrate nonviable transmural
myocardial infarction, though without requiring pharmacological stress.

THANK YOU

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