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19 Coronary Artery Disease
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Viability Imaging
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KevinEmeryBoczar, ChristianeWiefels,
AndrewM.Crean, RobertA.deKemp,
andRobBeanlands
20
Introduction
Ischemic cardiomyopathy is a leading cause of
morbidity and mortality worldwide [1]. It is a
far- reaching condition, with incidence and
prevalence that continue to rise. There were
over 6.2 million American adults living with
heart failure (HF) between the years of 2013
and 2016, compared with only 5.7 million
between 2009 and 2012 [1]. Based on these
data, projections show that there could be over
eight million people living with heart failure by
the year 2030 [1].
While medical advances continue to improve
the survival of those with a diagnosis of HF, it
unfortunately remains a disease with an extremely
poor prognosis. Data suggest that the associated
5-year mortality approaches 50% for patients
with this condition [2]. Thus, given the impact
K. E. Boczar (*)
Division of Cardiology, Department of Medicine,
National Cardiac PET Centre, University of Ottawa
Heart Institute, Ottawa, ON, Canada
Department of Medicine, School of Epidemiology
and Public Health, University of Ottawa,
Ottawa, ON, Canada
University of Pennsylvania, Philadelphia, PA, USA
e-mail: kboczar@ottawaheart.ca
C. Wiefels
Division of Cardiology, Department of Medicine,
National Cardiac PET Centre, University of Ottawa
Heart Institute, Ottawa, ON, Canada
that ischemic HF places on patients and the
health-care system, management strategies aimed
at improving outcomes have been a prominent
focus of research for many years. Specically,
the role that revascularization can play to improve
patient outcomes has been widely investigated. In
this regard, research on the utility of viability
imaging to indicate which patients may benet
most from revascularization has demonstrated
great potential in some studies, but not in others.
As such, data is not uniformly consistent toward
denitive conclusions on the role of viability
detection.
This chapter will discuss the concept of myocardial viability, the multimodality imaging tools
available to assess viable myocardium, the new
advances through research in this eld, the clinical applications of viability assessment, and
future directions in the area.
Department of Cardiovascular Sciences, Federal
Fluminense University, Niterói, Rio de Janeiro, Brazil
Division of Nuclear Medicine, Department of
Medicine, University of Ottawa, Ottawa, ON, Canada
A. M. Crean · R. A. deKemp · R. Beanlands
Division of Cardiology, Department of Medicine,
National Cardiac PET Centre, University of Ottawa
Heart Institute, Ottawa, ON, Canada
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022
M. Pelletier-Galarneau, P. Martineau (eds.), FDG-PET/CT and PET/MR in Cardiovascular
Diseases, https://doi.org/10.1007/978-3-031-09807-9_20
275
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K. E. Boczar et al.
Viability: Back toBasics:
Understanding theTerminology
The concept of myocardial viability and the
terms surrounding its use are often misused and
misunderstood. Thus, a discussion of viability
imaging modalities would not be complete without a brief discussion of the correct denitions
and understanding of these fundamental terms.
Myocardial ischemia is the result of an imbalance between myocardial oxygen supply and
demand; this can result either from an acute coronary syndrome, or alternatively, from chronic
ischemic heart disease. In patients with chronic
ischemic heart disease, persistent ventricular
dysfunction can result from repeated stressinduced ischemia—this dysfunction can either be
due to stunning of the myocardium, hibernating
myocardium, or scar. Prolonged ischemia-related
myocardial injury results in cell death whereby
scar replaces healthy myocardial tissue. To distill
it to its simplest form, the term “viable myocardium” encompasses all tissue that is not scarred
[3]. If the ischemia-related injury is not severe or
prolonged enough to cause cell death, the myocardial tissue is considered viable. Dysfunctional
myocardium that is viable has the potential to
recover from injury, if myocardial ow is either
maintained or restored [4–6]. However, there are
several subcategories of viable myocardium that
require clarication.
Stunned myocardium refers to left ventricle
(LV) dysfunction that occurs after either one
acute episode or multiple repetitive episodes of
ischemia [3]. While the coronary blood ow was
reduced and restored so that it is preserved at rest,
the myocardial function remains impaired; with
the capacity to recover with time (assuming resolution of the ongoing ischemic insult).
Repetitive ischemic insult that is ongoing
over time can cause the myocardial tissue that
has been repeatedly “stunned” to adapt by
reducing its perfusion and contractile function
to preserve cellular integrity; this adaptation of
downregulation of ow and function is the socalled state of hibernating myocardium [3, 6]. If
blood ow can be adequately restored before
irreversible injury occurs, then LV function is
potentially recoverable (either in whole or in
part) [3]. This concept is central in the eld of
viability imaging and is illustrated in Table20.1
[4–6].
There are several imaging modalities that are
available to assess viability including cardiac
PET, single-photon emission computed tomography (SPECT), dobutamine echocardiography
(ECHO), dobutamine CMR, late gadolinium
enhancement CMR (LGE-CMR), late iodine
enhancement CT (LIE-CT) [4] and myocardial
contrast ECHO [17, 18]. The nuclear methods
and LGE-CMR techniques that are used clinically are summarized in more depth below.
20 Viability Imaging
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not persist or become repetitive;
revascularization can prevent recurrent
stunning
if adequate revascularization can be
achieved
prevent recurrent ischemia
revascularization
No May benet from revascularization to
277
Function/contractile
reserve Structural changes Potential to recover/clinical relevance
Reduced No Likely to recover if ischemic injury does
FDG)
18
Variable (normal, increased,
or reduced)
transitory ischemic
Viable
Stunning Preserved (after
Myocardium Flow/perfusion Glucose metabolism (
Table 20.1 Characteristics of viable and nonviable myocardium
Reduced Yes some May have partial/delayed or full recovery
insult)
Hibernation Reduced Preserved or increased
Preserved at rest,
impaired at stress
Normal at rest, increased at
(=perfusion-metabolism
stress
mismatch)
impaired at stress
Ischemia Preserved at rest,
Nonviable
Scar Reduced Reduced Absent Fibrosis Unlikely to recover with or without
FDG 18F-uorodeoxyglucose
Reproduced with permission from Kandolin etal., CJC 2019 [3]. Data obtained from multiple sources [3, 4, 7–16]
18
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K. E. Boczar et al.
Clinical Applications forViability
While it may be straightforward to understand the
potential clinical importance of viability as a general
concept, it can be less clear when viability imaging
should be applied in specic clinical scenarios.
Viability assessment is most useful when the decision to revascularize a patient is not “clear-cut”, and
where the treatment strategy is more nuanced. We
consider imaging for viability to offer the biggest
incremental value in patients with the following:
1. IHD (or where it is very strongly suspected).
2. Symptomatic heart failure (≥NYHA II).
3. Moderate to severe LV dysfunction (LVEF
<40%).
4. Moderate to large persistent perfusion defects
on stress perfusion imaging.
Of note, patients with LV dysfunction, should not
already have signicant ischemia identied, as
this would indicate that myocardium is viable and
they would likely benet from revascularization,
thus obviating the need for viability testing
Table 20.2 Characteristics to consider in decision
regarding which patients will benet from viability
imaging
Viability testing not
needed/unlikely to
add useful
information
Younger patients Older patients
HFrEF with > class II
angina
Proven moderate-to-
severe ischemia on
other testing
Higher LVEF (>40%) Lower LVEF (<40%)
Left main coronary
artery disease
No or limited
comorbidities
Reproduced with permission from Kandolin et al., CJC
2019 [3]. Data obtained from multiple sources [16,
19–21]
CABG coronary artery bypass graft, CAD coronary artery
disease, COPD chronic obstructive pulmonary disease,
HFrEF heart failure with reduced ejection fraction, LVEF
left ventricular ejection fraction
Viability testing may add
useful information
HFrEF without angina
No evidence of ischemia;
moderate to large persistent
perfusion defects suggesting
scar (but may be hibernating)
Chronic total occlusion
Severe/multiple comorbidities
(renal insufciency, COPD,
previous CABG)
There are certainly other factors that would modify the decision-making to pursue (or not) revascularization (and would thereby modify the
utility of viability imaging). Factors such as the
following will alter the incremental utility of viability assessment (Table20.2):
(a) Extensive patient comorbidities.
(b) Suitability of target vessels for coronary
artery bypass surgery (CABG).
(c) Presence of CCS II or greater anginal symp-
toms (which would thereby strongly point
toward the need for revascularization given
the proven symptom and outcome benet in
such patients).
Once it has been decided that a viability
assessment is the right test for the patient, the
next step is to decide on the correct means to
assess viability. Ultimately, several techniques
(18FDG PET, dobutamine echocardiography,
201
Tl-SPECT,
99m
Tc-SPECT, and CMR) can
be used for viability assessment, and each
modality carries its own strengths and limitations (Table20.3). Key factors that should be
weighed in selecting a modality include patient
contraindications to specic modalities (i.e.,
severe renal failure, pacemakers and implantable cardiac debrillators for CMR), local
center expertise, as well as availability of the
modality.
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279
Table 20.3
Modality Mechanism Findings indicative of viability Advantages/disadvantages
Dobutamine
echocardiography/CMR
SPECT Thallium-201 Perfusion:
SPECT
Technetium-99m-labelled
tracers
PET Perfusion/metabolism Perfusion: 13NH3,
CMR LGE
Reproduced with permission from Kandolin etal., CJC 2019 [3]
a
Biphasic response. Dobutamine low dose 5–10mg/kg/min leads to improved contractility in hibernating myocardium.
Dobutamine high dose up to 40mg/kg/min (+ atropine) leads to increased oxygen consumption, induced ischemia, and
decreased contractility
b
Risk of potentially life-threatening complications 0.2% [22]
Imaging methods for assessing viability
Contractile reserve
Sarcolemma
membrane integrity
(K+ analogue)
Mitochondrial
membrane integrity
82Rb, 15O-water
Myocyte glucose
utilization: FDG
Wall thickness
a
Improvement by visual or
strain rate imaging (echo)
Tracer uptake: >50%
maximum
Tracer uptake: >50–65% of
maximum
Flow-metabolism
mismatch=hibernation,
(Match=nonviable)
Scarring (LGE) <50% wall
thickness
Systolic thickening of a
dyskinetic segment
A: Specic, widely
available, without
radiation, can detect
ischemia, assess valvular
disease
D: interobserver
variability, risk related to
dobutamine
A: Widely available,
moderate cost
D: radiation dose,
moderate sensitivity with
low specicity
A: Widely available,
moderate cost
D: moderate accuracy
A: Highly sensitive
D: Limited availability,
high cost, need for glucose
load or insulin clamp in
patients with diabetes
A: Highly sensitive,
without radiation, assess
valvular disease
D: Limited availability,
high cost, risks in renal
failure, cannot use with
certain devices
b
Nuclear Methods forAssessing
Viability
SPECT
SPECT is a widely available imaging modality
and has been well validated from a clinical perspective [23]. Both Thallium-201 (
Technetium-99m-labelled agents (
used to assess myocardial viability [24].
99m
Tc-labelled agents
99m
The
99m
Tc-labelled agents,
Tc-tetrofosmin, have lipophilic properties that
enable them to enter cells passively [25]. Despite
this, their ability to remain within the cardiomyocyte is an active process that is reliant on the
201
Tl) and
99m
Tc) can be
99m
Tc-sestamibi and
integrity of the mitochondrial membrane; it is
this property which enables them to be utilized
for viability imaging.
With a stress–rest protocol, if there is a reversible defect present, it indicates ischemia, which if
moderate or severe, automatically negates the
need for further viability testing (as the tissue
must be viable and the patient may benet from
revascularization) [3]. However, the presence of a
persistent (“xed”) defect cannot distinguish scar
from hibernating myocardium—it is in this situation that viability imaging is sometimes
warranted.
While it is technically possible to utilize rest-
99m
only
Tc-based perfusion imaging for viability,
it has been shown that the use of nitrates can
improve detection [26–31]. Additionally, adding
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K. E. Boczar et al.
nitrates to
99m
Tc-based perfusion imaging better
correlates with recovery of left ventricular function following revascularization [26–31]. The
administration of nitrates prior to an additional
rest imaging has the capacity to increase blood
ow in the dilated epicardial and collateral vessels which can thereby increase the sensitivity to
detect viable myocardium. A protocol that combines rest perfusion imaging and rest perfusion
post-nitrate administration imaging (usually
10mg of oral isosorbide nitrate given 10–15min
before the image acquisition) can be used. While
dysfunctional myocardium that has normal perfusion is indicative of stunned myocardium (that
is likely to recover with time), segments with
reduced perfusion at rest that improve postnitrate administration suggest hibernating myocardium and thus viability. When persistent
defects with absence of tracer uptake are noted
on both rest and post-nitrate images, it suggests a
lack of viability; this is tissue that is unlikely to
recover with revascularization.
Thallium-201
201
Tl is the oldest radiopharmaceutical available
that is used to assess viability.
201
Tl is a potassium
analogue, and as such, its uptake is dependent on
membrane integrity. This is because it uses the
Na+/K+ ATPase pump to penetrate the cell. The
high rst-pass extraction and capacity to redistribute in the myocardium with time makes this
tracer suitable to assess both the presence of ischemia as well as the presence of hibernating
myocardium.
There are different protocols available for viability assessment with
protocol, similar to
201
Tl. The most common
99m
Tc-labelled agents, begins
with performing stress/rest imaging. In this case,
the protocol begins by giving one single injection
of 2.5–3.5mCi of
201
Tl during peak stress. Prompt
image acquisition, up to 15min post-stress will
demonstrate the rst distribution of the tracer,
proportional to blood ow. After 30 min the
redistribution phase starts, with a progressive
washout from the myocardium; this is due to a
concentration gradient between the myocyte and
the blood. The rst redistribution (rest) images
are then acquired 2.5–4h afterward. This allows
one to determine if there is a reversible or persistent defect. If rest perfusion thallium imaging
shows a persistent defect, the defect may indicate
scar or may still be viable. The options for distinguishing between these two include late redistribution or reinjection. In regions that initially had
low Tl-201 uptake, the redistribution of Tl-201
into the blood over time leads to gradient reversal
in tissues that initially had low Tl-201 uptake. If
this tissue is viable, then it will take up Tl-201
over time and will appear reversible.
If the defect is persistent (or xed) on both initial stress (or rest) and redistribution rest images,
then late redistribution images at 18–24h should
be acquired and interpreted [32]. If the defect
remains persistent on the late redistribution
images, this suggests the myocardium is nonviable scar and unlikely to recover after revascularization. However, if the defect is reversible on the
late redistribution images (or alternatively, on the
delayed images of a rest-redistribution protocol),
it indicates the presence of viable hibernating
myocardium which could potentially benet
from revascularization.
A reversible defect is described as an increase
in >10% of the maximum regional uptake, above
50–60% [33]. Viable hibernating cells have a
slower washout, and will therefore have a greater
relative uptake in delayed images when compared with viable nonischemic cells.
201
Tl redistribution is an ongoing, continuous process that
requires blood supply to the viable tissue. Thus,
its uptake is related both to perfusion as well as
the degree of coronary artery narrowing in the
vascular territory of interest [34]. Evidence has
shown that in viability imaging with
201
Tl, viable
myocardial tissue will show thallium redistribution (i.e., a reversible defect) on reinjection imaging after the 4 h redistribution images or late
imaging (8–72 h), while nonviable tissue will
appear as a persistent, or xed, defect with no
thallium uptake [34–37].
A rest-only viability assessment can also be
performed with the injection of 2.5–3.5mCi of
201
Tl injected at rest, followed by redistribution
imaging either 3–4h later or 18–24h later; this
eliminates the stress-imaging component altogether. An alternative to the late redistribution
20 Viability Imaging
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Thallium-201 Rest
Thallium-201 Reinjection
Thallium-201 Rest
Thallium-201 Reinjection
281
Short axis
HLA
Fig. 20.1 Example of rest and reinjection short-axis and
horizontal long-axis thallium tomogram images in a
patient with known coronary artery disease. An apparently
image is a reinjection of 1mCi of
201
Tl after the
rest redistribution at 4 h, followed by prompt
image reacquisition (Figs.20.1, 20.2, and 20.3).
PET
Fluorine-18-uorodeoxyglucose (18FDG) is a glucose analogue and is used clinically to assess and
quantify myocardial glucose utilization [3]. The
18
use of
on the underlying principles of myocardial metabolic function. Cardiomyocytes can utilize many
different substrates for energy metabolism including free fatty acids (FFA), glucose, lactate, pyruvate, and ketones; however, FFA and glucose form
the primary energy substrates of choice of cardiomyocytes [39–41]. Adrenergic stimulation, ischemia and insulin can all shift the body’s myocardial
energy substrate-use toward the preferential utilization of glucose, whereas fasting shifts energy
metabolite use toward FFA utilization [42–45].
increased plasma insulin levels, glucose transporters 1 and 4 (GLUT 1 and 4) are transported
FDG PET for viability assessment relies
During periods of ischemia or states with
irreversible distal anterior defect on rest images improves
after reinjection indicating viable myocardium
from intracellular storage to the plasma membrane, and lead to increased glucose uptake (and
the preferential utilization of glucose as an energy
substrate) by the cardiomyocyte [46, 47].
Furthermore, conditions of adrenergic stimulation or myocardial ischemia cause the process of
FFA oxidation to decrease or even stop; hence,
under these states, anaerobic glycolysis facilitates the use of glucose as the main substrate of
myocardial energy [42, 44]. Thus, in hibernating
myocardium, glucose is preferentially used as the
primary energy substrate of choice, and forms the
basis of our ability to utilize 18FDG PET for viability assessment.
While 18FDG PET is often thought of as an
assessment of myocardial glucose metabolism,
more accurately, it is a surrogate marker for
exogenous glucose uptake [48]. Once 18FDG is
transported into the cardiomyocyte, it is converted into 18FDG-6-phosphate as part of the cellular metabolic pathway [49]. After this step
occurs, the metabolite is then trapped and cannot
continue further down the metabolic pathway,
and the tracer thereby remains trapped within the
cardiomyocyte [49].
282
Inject
Inject
Interpretation of the Images
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K. E. Boczar et al.
TI-201
Rest
TI-201
Rest
15 min.
Time
Day 1Day 2
Imaging
ReviewRest
Optional, Depending on Physician’s
24 hour
Redistribution
Imaging
Interpretation of the Images
Review
Fig. 20.2
15 min.
Time
201
Tl rest-redistribution protocol for viability assessment, with permission from Henzlova etal. [38]. Tl-201
Imaging
Thallium-201
FDG PET Imaging Protocols
The imaging protocols to assess myocardial viability using PET are normally composed of two
distinct and important components: (1) rest perfusion imaging performed with either nitrogen-
ReviewRest
3-4 hour
Delay
Optional, Depending on Physician’s
3-4 hour
Redistribution
Imaging
Review
13- ammonia (13NH3) or rubidium-82 (82Rb) in
North America; (oxygen-15-water is also used in
Europe and Asia) and (2) metabolic imaging with
18
FDG [3]. Notably, if PET perfusion tracers are
not available, then SPECT rest perfusion images
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