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Table 20.2 Summary of imaging modalities utilized in heart failure
Conditions where
Imaging modality Most useful in dening
Coronary
angiogram
Echocardiography Biventricular function,
Computed
tomography
(coronary CT)
Magnetic resonance
(CMR)
Cardiopulmonary
exercise testing
(CPET)
Nuclear imaging
Multigated
acquisition scan
(MUGA)
Positive emission
tomography (PET)
Single-photon
emission computed
tomography
(SPECT)
Adapted from Heart Failure: A Companion to Braunwald’s Heart Disease [10]. CMP cardiomyopathy
Gold standard for
evaluating coronary
artery disease (CAD)
wall motion, valvular
lesions, structural
abnormalities, pericardial
effusion, estimation of
right atrial and
pulmonary artery
pressures
Coronary disease,
biventricular function
and volumes, congenital
heart disease anatomy
Gold standard for EF
and volume assessment.
Etiology (ischemic
versus nonischemic
CMP) and
characterization of
nonischemic CMP,
myocardial viability,
biventricular volumes,
congenital heart disease
anatomy
Objective measurement
of functional limitation
in advanced HF
LV function and volumes Determining LVEF
Myocardial perfusion
and viability, LV function
and volumes, sarcoidosis
Myocardial perfusion,
amyloidosis
most helpful Advantages Disadvantages
Suspected CAD Can intervene at
time of diagnosis
Suspected CAD,
valvular disease,
pericardial
tamponade,
pulmonary
hypertension
Suspected CAD,
adult congenital
disease
Ischemic CMP:
Viability
Nonischemic CMP:
Diagnosis
Myocarditis,
sarcoidosis,
amyloidosis,
arrhythmogenic RV
cardiomyopathy, LV
non-compaction,
constrictive
pericarditis
Advanced HFrEF,
consideration for
advanced HF
therapies,
determining
pulmonary versus
cardiac etiology of
dyspnea
in patients with poor
acoustic windows
Suspected CAD,
“hibernating”
myocardium,
sarcoidosis
Suspected CAD,
amyloidosis
Noninvasive, no
radiation exposure,
ventricular function,
hemodynamic
information, good
for initial evaluation,
and monitoring of
treatment response
in HF
High negative
predictive value for
CAD with reliable
ejection fraction
(EF) measurement
No radiation
exposure, best
noninvasive
evaluation of
myocardial tissue
Noninvasive,
objective
measurement of
functional status,
monitoring of
functional decline
over time
Highly reproducible
measurement of
LVEF
Allows for
noninvasive
diagnosis of
sarcoidosis
Noninvasive
diagnosis of
amyloidosis
L. Eyadiel and B. Rasmussen
Invasive, radiation
exposure, risk for
contrast-induced
nephropathy
Difcult in patient
with poor acoustic
windows
Radiation exposure,
risk for contrastinduced nephropathy,
difcult with rapid
heart rate
Limited to magnet
compatible metals,
poor visualization in
the presence of
pacemakers or
implantable cardiac
debrillators,
difcult to evaluate
in arrhythmias
Orthopedic issues
that limit patient
ability to ride bike or
walk on treadmill,
can be affected by
beta blocker use and
obesity
Radiation exposure
Exposure to
radiation, variable
accuracy given
specic diet prior to
testing, may miss
three vessel CAD
Exposure to
radiation, may miss
three vessel CAD,
poor assessment of
ejection fraction
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Fig. 20.4 Cardiac chamber enlargement on echo due to
HFrEF
failure [11]. Transthoracic echocardiography
(TTE) is readily available, noninvasive, and provides information regarding the type of ventricular dysfunction (systolic versus diastolic), left
ventricular ejection fraction (LVEF), assessment of right ventricular function, dimensions
of the cardiac chambers, valvular function,
structural abnormalities, as well as the presence
or absence of a pericardial effusion. This information is useful at the time of diagnosis as well
as for monitoring treatment response and prognosis over time. Below are images that demonstrate HFrEF based on echocardiography
(Fig.20.4).
Cardiac Magnetic Resonance Imaging
Cardiac MRI (CMR) is considered to provide a
higher-quality image than TTE and has become
the noninvasive gold standard for determining
LV volume, LVEF, and LV mass [10, 12, 13].
Compared with TTE, it is felt that there is less
interrater variability. This imaging modality typically utilizes gadolinium contrast which assists
in differentiating tissue characteristics to guide
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management [13]. The presence of late gadolinium enhancement is representative of scar in the
myocardium, which is important for treatment
considerations, including placement of implantable cardiac debrillators. The pattern of
enhancement gives information regarding HF
etiology and can differentiate between dilated
cardiomyopathy, ischemia, hypertrophic cardiomyopathy, myocarditis, as well as more rare cardiomyopathies [10, 12]. This method is superior
in identication and characterization of left ventricular thrombi when compared with TTE [10].
In ischemic cardiomyopathy, CMR images can
assist in evaluating viability with and without
stress images [10].
Unfortunately, the presence of cardiac devices,
including cardiac resynchronization therapy
devices, can cause artifact, making the images
difcult or impossible to interpret. This may render the test inadequate; therefore, alternative
imaging methods are preferred in these patients.
In addition, CMR is contraindicated in patients
with metallic elements that are not MRI compatible. MRI can cause these metals to heat up during the test, can cause forces on magnetic metals,
or cause severe image degradation.
Pathology/Description
Ischemic Heart Failure
Despite advances in revascularization and treatment of coronary artery disease, myocardial
infarction (MI) is the most common cause of
heart failure. Heart failure development at the
time of MI, during index hospitalization, or following MI may manifest with different clinical
attributes and outcomes. Myocardial compromise secondary to necrosis, stunning, or structural rupture causes rapid structural changes,
myocyte edema, and progressive myocyte death
within three hours of ischemic time. Even revascularization causes insult through an oxidative
stress reaction and embolization of thrombotic
debris [14]. The incidence of heart failure at the
time of presentation has increased, possibly
because of improvement in prehospital care.
Conversely, heart failure development during
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hospitalization has fallen in the setting of
improvements in revascularization. However, the
incidence of heart failure with preserved ejection
fraction after myocardial infarction has increased.
Heart failure with reduced ejection fraction
(HFrEF) following hospitalization for MI is secondary to scar formation and cardiomyocyte
death triggering activation of neurohormonal and
sympathetic nervous system processes that initiate and perpetuate left ventricular remodeling.
Infarction size and location impact the risk for
development of HFrEF.Multivessel disease and
anterior MI pose the highest risk [14].
Comorbidities including hypertension, atrial
brillation, diabetes, and chronic kidney disease
further compound the risk for HFrEF development post MI.Female gender and older age also
increase the risk of heart failure.
Natriuretic peptide elevation, biphasic pattern
of BNP elevation, and glomerular ltration rate
are associated with HFrEF development post MI.
Troponin elevation can correspond to infarct size
on CMR, but association with HFrEF development is unclear [14].
Wall motion abnormalities on TTE predict
mortality in HFrEF more accurately than LV
ejection fraction alone. Right ventricular dysfunction seen on TTE also contributes to HFrEF
development. Left ventricular enlargement post
MI is more commonly seen in relation to transmural MI, larger infarct size, intramyocardial
hemorrhage, microvascular obstruction, and
advanced age and confers an increased risk of
HFrEF hospitalization [14]. CMR is the gold
standard imaging modality to dene infarct size
and scar formation.
Guideline-directed medical therapy including
beta blockers, ACEIs/ARBs, and mineralocorticoid receptor antagonists has shown mortality
benet following MI. Early administration of
statins within 24 h of MI is associated with a
reduction in heart failure hospitalization and inhospital mortality [15]. Patients should be risk
stratied for wearable debrillator prior to hospital discharge (see Chap. 13).
Nonischemic Cardiomyopathy (NICM)
Cardiomyopathy is a myocardial disorder in
which heart muscle structure and/or function is
abnormal in the absence of coronary artery disease, hypertension, valvular disease, or congenital
heart defect [16]. Non Ischemic Cardiomyopathy
categorization has evolved through advances in
imaging and knowledge. The American Heart
Association (AHA) dened cardiomyopathies as
primary, or conned to the heart, or secondary, as
part of generalized systemic disorders.
Three primary categories exist:
1. Genetic: channel disorders, arrhythmogenic
right ventricular cardiomyopathy (ARVC),
hypertrophic cardiomyopathy (HCM), left
ventricular non-compaction (LVNC), and glycogen storage disorders
2. Acquired: inammatory/myocarditis, stress
induced (Takotsubo), peripartum,
tachycardia-induced
3. Mixed acquired and genetic (dilated (DCM)
and restrictive (RCM) cardiomyopathy) [17]
The European Society of Cardiology 2008
position paper on cardiomyopathy classication
sought to group cardiomyopathies according to
functional and morphological phenotypes which
could be used to guide clinical practice [18].
Cardiomyopathies were divided into ve categories which could have either familial or nonfamilial subclassications: HCM, DCM, ARVC,
RCM, and unclassied cardiomyopathies
(Fig.20.5).
Enlarged
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Heart Muscle
Diseases
Myocarditis
Inflammation of
heart muscle
Hypertrophic cardiomyopathy Dilated cardiomyopathy
Thickened
heart muscle
Weakened
heart
musc
ventricle
Fig. 20.5 ESC classication of myocarditis, dilated cardiomyopathy, and hypertrophic cardiomyopathy. (Used with
permission, Shutterstock)
Hypertrophic Cardiomyopathy
(HCM)
(particularly associated with exertion or dehydration) and SCD.Evaluation of family history for
unexplained SCD is imperative. A systolic mur-
HCM is an autosomal dominant sarcomere protein mutation cardiomyopathy in which nondilated left ventricular hypertrophy (LVH) is
present in the absence of a systemic or valvular
disease [16, 17]. There are greater than 30 genes
known that can be evaluated for by genetic testing for prognostic education of family members.
It is the most common cause of sudden cardiac
death (SCD) in athletes younger than 35years of
age [19]. It can be associated with congenital
syndromes and glycogen storage disease disorders or metabolic disorders such as
Anderson- Fabry disease. Presenting symptoms
characteristic of HCM include atypical chest pain
mur that increases with intensity during Valsalva
maneuver may be present [20].
Electrocardiographic T wave inversions, generally in the lateral leads, are the most common
electrocardiogram abnormality; ST segment
depression, pathological Q waves, and ventricular arrhythmias have also been observed, particularly after exercise [19, 20]. On TTE, small
ventricular chamber size with LVH is noted with
an irregular localization of septal or apical hypertrophy (Fig.20.6), which can result in left ventricular outow tract obstruction (LVOTO) or
mitral valve dysfunction (Fig. 20.7) (systolic
anterior motion of the mitral valve against the
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intraventricular septum causing dynamic
LVOTO) (Fig.20.8). In cases of mild LVH in athletes, CMR can help differentiate pathologic and
physiologic LVH [19]. Contrasted CMR studies
differentiate the extent of myocardial brosis
Fig. 20.6 Echocardiography of HCM. Arrow points to
asymmetric septal hypertrophy of HCM
which is associated with increased risk of ventricular arrhythmias [21].
Beta blockers are the initial therapy for symptomatic HCM, with non-dihydropyridine calcium
channel blockers used if beta blockers are not
well tolerated. These medications decrease myocardial oxygen demand of the hypertrophied
muscle, decrease the rate of brosis formation,
and reduce the severity of the obstruction. They
also can help prevent and treat potential arrhythmias. Reduction of symptoms and improvement
of the murmur is the goal of therapy. If LVOTO is
refractory to maximally tolerated medical therapy or hemodynamics are compromised, septal
reduction procedures such as surgical myomectomy or alcohol ablation should be considered.
Cardiac transplantation is reserved for end-stage
systolic dysfunction [21]. Regardless of medical
course, moderate or high intensity competitive
sports are prohibited. Shared decision-making
between the patient and physician is critical
Fig. 20.7 Dynamic outow tract gradient-induced MR.
Red arrow shows turbulent ow below the aortic valve
from a dynamic LVOT obstruction. The yellow arrow
demonstrates eccentric MR caused by abnormal anterior
leaet function
Normal
left atr
v
r
Hypertrophic Cardiomyopathy
normally
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arch of aorta
ium
aortic valve
right atrium
entricular septum
tricuspid valve
ight ventricle
Fig. 20.8 Structural differences in normal and hypertrophic heart. (Used with permission, Journal of Imaging, 8(4),
102. https://doi.org/10.3390/jimaging8040102)
regarding activity restriction. Patients should be
risk stratied for SCD and evaluated for implantable cardioverter-debrillator (ICD) placement.
This evaluation considers percentage of scar burden seen on MRI (>12–15%), frequency of nonsustained ventricular tachycardia on ambulatory
monitoring, the specic genetic defect, and family history of SCD.
blood flows easily
through vessels
mitral valve
left ventricle
heart pumping
thickened ventricular septum
small left ventricle
observed. A right-sided S3 or left ventricular S4
sound may be present, indicating rapid lling
within a stiffened ventricle [23] (see Chap. 1).
Diffuse reduced QRS voltage or prolonged PR
interval can be seen on electrocardiogram,
although their presence is unnecessary for diagnosis. Bi-atrial enlargement is often present with
restrictive physiology and is reected in widened
more prominent P waves on EKG.Atrial or ventricular dysrhythmia may also be present [23].
Restrictive Cardiomyopathy (RCM)
Common TTE ndings are bi-atrial enlargement
and diastolic dysfunction. Further imaging is
Unlike the anatomic basis for HCM, restrictive
cardiomyopathies are characterized by a functional pattern in which impaired myocardial
guided by disease suspicion. Laboratory nding
of elevated B-type natriuretic peptide (BNP)
marker is common.
compliance results in reduced ventricular lling
and increased ventricular pressure, diastolic dysfunction, and preserved ejection fraction [16].
Amyloidosis
Heterogeneity of culprit pathologies makes dening RCM difcult. RCM can be idiopathic, familial, or secondary to systemic disorders. It can
involve inltration of the myocardium with
abnormal proteins, glycogen, minerals, or other
substances or demonstrate restrictive physiology
without inltration. Common causes of RCM in
adults are amyloidosis, sarcoidosis, hemochromatosis, and sequelae of radiation therapy [22].
Diagnosis of RCM is based on clinical, laboratory, and imaging ndings. The primary clinical presentation is heart failure, particularly right
heart failure, with dyspnea on exertion and
fatigue being most common. Signs of right heart
failure, such as elevated jugular vein distention,
peripheral edema, and ascites are commonly
Amyloidosis is an inltrative RCM in which
amyloid, an abnormal brillar protein made up of
unstable precursor proteins, deposits in the heart
(or other organs) leading to functional organ loss
[24]. The most common types are immunoglobulin light chain amyloidosis (AL) or transthyretin
amyloidosis, further divided into “wild type”
(ATTR-wt) and mutant (ATTR-m) subtypes.
Patients present with differing organ involvement
patterns with disease course dependent on the
involved organs. In general, cardiac involvement
increases mortality [22]. History of bilateral carpal tunnel syndrome, peripheral neuropathy, or
syncope raises suspicion of disease presence.
Physical exam may be notable for macroglossia
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L. Eyadiel and B. Rasmussen
and periorbital purpura. Orthostatic hypotension
or baseline hypotension is often present.
In addition to the restrictive pattern ndings
above, TTE imaging is also signicant for LV,
right ventricular, and intra-atrial thickening, possibly with a “speckled” pattern seen on ultrasound imaging due to amyloid brils in the
myocardium. Pericardial effusion can be present.
Longitudinal strain imaging shows more signicant impairment in the left ventricular basal versus apical segments, producing a “cherry on top”
pattern [23] (Fig. 20.9). On CMR, amyloid
deposits produce a unique subendocardial late
gadolinium enhancement in the ventricles and
atria [22]. Nuclear imaging tracers (pyrophosphate scan) can detect ATTR with high sensitivity
and specicity differentiate between AL and
ATTR types.
High sensitivity cardiac troponin and BNP are
useful markers of disease progression but not
specic. After TTE, electrocardiogram, and clinical evaluation, laboratory markers of AL amyloidosis should be considered. These include serum
free light chains, serum, and urine immunoxation electrophoresis. While endomyocardial
biopsy (EMB) is the gold standard for cardiac
amyloidosis, it is invasive and not without complication risk. A negative biopsy cannot rule out
disease process because of patchy amyloid depo-
sition pattern. If EMB is pursued, Congo red
staining identies amyloid presence. A less invasive biopsy test is fat pad biopsy, which has a
higher yield in AL amyloid [22].
Heart failure treatment involves addressing
conduction blocks and managing volume overload with diuretics or aldosterone antagonists
[20]. AL amyloid is treated systemically with
chemotherapeutic agents and potentially stem
cell transplant. ATTR amyloid (both wild type
and mutant) can be treated with early initiation of tafamidis, which binds to transthyretin
and slows amyloid formation. Beta blockers
should be used cautiously since the cardiac
output in amyloid patients is often heart rate
dependent.
Cardiac Sarcoidosis
Sarcoidosis is a multi-organ granulomatous disease in which noncaseating granulomatous
inammation can lead to brosis in affected
organs. Cardiac sarcoidosis (CS) most commonly
presents as conduction abnormalities (including
ventricular abnormalities and atrioventricular
(AV) node blocks) and heart failure symptoms.
Patients may complain of palpitations, syncope,
presyncope, or even have SCD [25]. In clinically
ab
Fig. 20.9 (a) Typical echogenic ndings of cardiac amyloidosis with LV and septal thickening and (b) strain imaging.
(Used with permission, Biomedicines, 10 (4), 903. https://doi.org/10.3390/biomedicines10040903)
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Fig. 20.10 Late gadolinium enhancement in a patient
with pulmonary sarcoidosis and extensive cardiac involvement. There are several focal non-subendocardial based
evident disease, electrocardiogram abnormalities
in addition to conduction blocks can include QRS
complex fragmentation, pathological Q waves,
and ST changes. TTE ndings are not pathognomonic but may show basal interventricular thinning [26] (Fig.20.10). Endomyocardial biopsy is
felt to be low yield secondary to the patchy nature
of the CS.
CMR is the optimal study to determine the
presence of cardiac sarcoidosis. Late gadolinium
enhancement, seen in basal segments of the septal and lateral wall in a non-infarct pattern, commonly represents brosis although can also
indicate inammation. In active disease, inammation can be seen with uorodeoxyglucose
positron emission tomography (FDG-PET), with
FDG uptake patterns indicating active CS inammation [25], guiding treatment. These two
imaging modalities are complementary in the
diagnosis and management of CS.
LGE areas with inltration (arrows) in a variable pattern
of transmural distribution
Corticosteroids are the treatment of choice in
active disease, with methotrexate as a second-line
agent. Antiarrhythmic medication and possible
transcatheter ablation may be necessary in cases
of ventricular arrhythmia. Patients should be
risk-stratied for SCD and implantable cardiac
debrillator discussed. Cardiac resynchronization debrillator therapy is indicated for highgrade heart blocks.
Dilated Cardiomyopathy (DCM)
Dilated cardiomyopathy is dened as an enlargement of the left ventricle with contractile dysfunction. It is a common form of heart muscle
disease and the most frequent cause of heart
transplantation [17]. Familial cases account for
up to 35% of DCM [27]. Presentation can be
accompanied by thromboembolic events and
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arrhythmias. Pathophysiologic changes of ventricular remodeling and ventricular dilation are
discussed in detail above.
While heterogeneous in etiology (see
Table20.3), initial heart failure symptoms (lower
extremity swelling, orthopnea, fatigue after mild
exertion) are typically present and may be accompanied by nausea, abdominal fullness, early satiety, and anorexia. Physical exam can reveal
peripheral and generalized edema, elevated jugular vein pulsation, tachycardia, inferolateral displacement of apical pulse, S3 gallop, delayed
capillary rell, and crackles in lung eld
auscultation.
Electrocardiography is nonspecic but can
include tachyarrhythmias and bundle branch
blocks. Chest X-ray imaging will show cardiomegaly, often with pulmonary venous congestion.
Diagnosis is conrmed with echocardiography
which may include wall motion abnormalities,
right ventricular involvement, and functional
mitral regurgitation [27].
Table 20.3 Common causes of dilated cardiomyopathy
Genetic/familial Syndromic disease/inborn
Neuromuscular
disorders
Duchenne muscular
dystrophy
Becker muscular
dystrophy
Infection (myocarditis) Endocrine disorders
Viral
Bacterial
Fungal
Parasitic
Protozoal
Rickettsia
Autoimmune disorders Nutritional deciency
Giant cell myocarditis
Dermatomyositis
Systemic lupus
erythematosus
Peripartum
Toxicity and overload
Ethanol
Cocaine
Amphetamines
Anabolic steroids
Table adapted from Weintraub, R. et al. (2017). Dilated
Cardiomyopathy. The Lancet, 390(10092), 401–402 [27]
errors of metabolism
Drugs
Antineoplastic agents
Psychiatric drugs
Hypothyroidism
Hyperthyroidism
Cushing’s disease
Addison’s disease
Diabetes mellitus
Acromegaly
Selenium
Thiamine
Zinc
Copper
Myocarditis
Myocarditis is an inammatory disease of the
heart which can be a consequence of infection,
toxic substance exposure, or immune system
activation. It can exist along a continuum from
acute to chronic and is characterized by those
stages as well as etiology and severity. The initial
presentation can range from prodromal symptoms to fulminant myocarditis with circulatory
collapse [28, 29]. Myocarditis progresses from
acute inammation to interstitial edema to myocyte necrosis to brosis. Ventricular size may be
preserved in the early phase, but damage to the
myocardium over time leads to LV dilation [17].
Patients with acute myocarditis present with a
variety of signs and symptoms as seen in
Table20.4 [17, 28].
Over a quarter of presentations represent fulminant myocarditis presenting with ventricular
arrhythmias and cardiogenic shock (Table20.5).
More commonly, symptoms are accompanied by
abnormal electrocardiogram with ST elevation,
frequently in the inferior and lateral leads [28].
Endomyocardial biopsy is necessary in
arrhythmogenic or fulminant presentation with
cardiogenic shock [29]. EMB is recommended in
the following settings:
• Other causes of HF have been excluded or
when it may inuence treatment (Table20.5).
• For patients with unexplained fulminant HF
(new-onset HF of less than 2weeks duration
associated with hemodynamic compromise).
• Unexplained new-onset HF of 2 weeks to
3 months duration associated with a dilated
LV and new ventricular arrhythmias, Mobitz
type II second-degree AV block, third-degree
AV block, or failure to respond to usual care
within 1–2weeks.
CMR is recommended in clinically suspected
acute myocarditis within 2–3weeks from onset of
symptoms to evaluate for myocardial inammation. Hyperemia is suggested with early gadolinium enhancement, tissue edema seen with increased
T2-weighted imaging, and necrosis/brosis seen
with late gadolinium enhancement. These are the
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Table 20.4 Presentation of myocarditis
Signs and symptoms Clinical features Differential cause
New or worsening heart failure/
cardiomegaly
Chest pain/ACS-like presentation Ischemic features on EKG such ST depression or
Acute pericarditis Pleuritic chest pain. PR depression/diffuse ST elevation
Cardiac arrhythmias or EKG
changes
Cardiogenic shock May see rapid decompensation with or without associated
Nonspecic myalgias or recent
viral illness/URI
Sudden cardiac death All causes
Excessive fatigue or exercise intolerance
Pulmonary edema, S3 gallop
elevation/T-wave inversion
Sinus tachycardia. Atrial or ventricular arrhythmia; new
bundle branch block, heart block
multisystem organ failure
All causes
All causes
Giant cell
myocarditis
Cardiac sarcoidosis
Giant cell
myocarditis
Cardiac sarcoidosis
Viral myocarditis
Eosinophilic
myocarditis
established cardinal ndings to support myocardi-
Table 20.5 Clinical criteria for myocarditis
Clinical
presentation: at
least one or
more of the
following
Acute chest
pain
(pericarditis)
New onset or
worsening
dyspnea at rest
or exercise,
and/or fatigue,
with or without
left and/or right
HF signs
Palpitations or
unexplained
arrhythmia
symptoms and/
or syncope and/
or sudden
cardiac death
Unexplained
cardiogenic
shock
Adapted from Cooper, Leslie. Up to date. Clinical manifestations and diagnosis of myocarditis in adults. Jul 13,
2021
Diagnostic criteria:
at least one or more
of the following
New EKG ndings
of any of the
following:
First-third degree
AV block or BBB;
ST/T wave changes;
sinus arrest; VT;
VF; asystole; Ab;
IVCD; low voltage;
SVT
Elevated troponin Prior clinical
LV or RV
dysfunction
Tissue
characterization by
CMR
Ancillary
supportive
ndings
Fever ≥38.0°C
at presentation
or within prior
30days
+/− associated
symptoms such
as chills,
myalgias, HA,
N/V/D
suspected or
denite
myocarditis
Exposure to
toxic agents
Extra-cardiac
autoimmune
disease
tis. PET imaging can be considered as alternative
imaging if CMR is not possible or if other organs or
a systemic process is suspected [28].
One specic consideration is giant cell myocarditis. This disease presents as a rapidly progressive necrotizing myocarditis with generally
fulminant presentation and involving refractory
ventricular arrhythmias. It should be diagnosed
promptly with endomyocardial biopsy, and
immunosuppressive therapy should be initiated
as soon as possible. Even with early and aggressive therapy, mortality and need for cardiac transplantation are very high in this cohort of critically
ill patients. There should be early consideration
of extracorporeal membrane oxygenation and
mechanical support.
Immune checkpoint inhibitor inammation is
another specic disease. Patients on this class of
chemotherapeutic agents can have a rapidly progressive decompensation resulting in death. This
type of myocarditis needs an early diagnosis, and
high-dose corticosteroids are necessary to avoid
cardiogenic shock and death. Fortunately, early
intervention results in normalization of the ventricular function.
Treatment is directed at underlying cause and
therapies aimed at clinical presentation. Inotropic
and advanced mechanical support may be needed
in severe disease. The immune modulation therapies are reserved for a small subset of acute myocarditis (Table20.6).
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