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CHAPTER 18 Acute Heart Failure and Pulmonary Edema 198.e1
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OUTLINE
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Definition and Epidemiology, 199
Etiology, 199
Pathophysiology of Fulminant Myocarditis, 199
Diagnostic Evaluation of a Patient With Suspected
Myocarditis, 200
Laboratory Tests, 200
19
Acute Fulminant Myocarditis
Bettina Heidecker, Leslie T. Cooper Jr
Electrocardiographic Findings, 200
Echocardiography, 201
Indications for Endomyocardial Biopsy, 201
Magnetic Resonance Imaging, 201
Therapy, 202
DEFINITION AND EPIDEMIOLOGY
Myocarditis is defined as inflammation of the myocardium
generally following an injury such as infection, ischemia, or
trauma.1 Approximately 2.5 million cases of myocarditis and
cardiomyopathy were diagnosed globally in 2015.2 Most cases of
acute myocarditis present with chest pain or mild left ventricular
(LV) dysfunction. Fulminant myocarditis refers to a specific
clinicopathologic form of recent-onset myocarditis requiring
inotropic or mechanical circulatory support to maintain tissue
perfusion. The most commonly identified trigger of fulminant
myocarditis is a viral infection; however, giant cell myocarditis,
hypersensitivity, and toxic drug reactions can present with
identical clinical features.
This chapter focuses on myocarditis requiring cardiac intensive care unit (CICU) management. This includes myocarditis
complicated by severe LV or right ventricular (RV) failure as
well as myocarditis associated with sustained and symptomatic
arrhythmias. Fulminant myocarditis presenting in this manner
is uncommon, probably accounting for less than 10% of all
cases. The frequency of fulminant myocarditis is more commonly
described in case series of children than adults, possibly due
to a less robust immune response or different pathogens with
older age.
Etiology
Most commonly, fulminant myocarditis is caused by a viral
infection.4 While enteroviruses—in particular, coxsackievirus
strains in North America and Western Europe
frequently identified strains until the 1990s, parvovirus B19 has
become the most common cause in recent years.7 Although many
other viruses have been identified in endomyocardial biopsies
(EMBs), their role in fulminant disease is not yet established.
3
5,6
—were the most
Hypersensitivity myocarditis associated with dobutamine is
relevant to the CICU patient population.
diomyopathy related to methamphetamine can require inotropic
support. In the setting of acute physical or emotional stress,
typical or atypical takotsubo or stress-induced cardiomyopathy
should be considered. Giant cell and necrotizing eosinophilic
myocarditis are rapidly fatal causes of acute cardiomyopathy of
particular importance to the CICU physician as they frequently
respond to early immunosuppression in addition to guidelinedirected medical management.
8,9
Occasionally, car-
PATHOPHYSIOLOGY OF
FULMINANT MYOCARDITIS
The transitions from acute viral infection through active inflammation to chronic dilated cardiomyopathy can be conceptualized
as a multiphase model recently reviewed by Heymans et al.10
The initial acute injury can be caused by direct cytotoxicity to
the myocardium by pathogens such as viruses, while cytokines
released during the immune response lead to further cell death
and remodeling.11 Multiple cellular and extracellular components
of the myocardium and the immune system contribute to effector
and regulatory influences that shape the clinical presentation.
In models of fulminant myocarditis, cytokines with negative
inotropic influence, such as tumor necrosis factor α (TNF-α), are
expressed at high levels.12 T effector cells and proinflammatory
macrophages predominate in the inflammatory infiltrates and
contribute to myocardial depression. Within weeks, the regulatory immune elements increase and downregulate the acute
response in model systems. In clinical practice, the purpose of
mechanical circulatory support is to bridge patients through the
acute period of fulminant disease to the phase in what healing
factors predominate.
199
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TABLE 19.1 Etiologies of Myocarditis
Infectious Myocarditis
Bacterial Staphylococcus, Streptococcus, Pneumococcus, Meningococcus, Gonococcus, Salmonella, Corynebacterium diphtheriae, Haemophilus
influenzae, Mycobacterium (tuberculosis), Mycoplasma pneumoniae, Brucella
Spirochaetal Borrelia (Lyme disease), Leptospira (Weil disease)
Fungal Aspergillus, Actinomyces, Blastomyces, Candida, Coccidioides, Cryptococcus, Histoplasma, Mucormycoses, Nocardia, Sporothrix
Parasitic Trichinella spiralis, Echinococcus granulosus, Taenia solium
Rickettsial Coxiella burnetii (Q fever), R. rickettsii (Rocky Mountain spotted fever), R. tsutsugamushi
Viral RNA viruses: coxsackieviruses A and B, echoviruses, polioviruses, influenza A and B viruses, respiratory syncytial virus, mumps virus,
measles virus, rubella virus, hepatitis C virus, dengue virus, yellow fever virus, Chikungunya virus, Junin virus, Lassa fever virus,
rabies virus, human immunodeficiency virus–1
DNA viruses: adenoviruses, parvovirus B19, cytomegalovirus, human herpes virus–6, Epstein-Barr virus, varicella-zoster virus, herpes
simplex virus, variola virus, vaccinia virus
Immune-Mediated Myocarditis
Allergens Tetanus toxoid, vaccines, serum sickness
Drugs: penicillin, cefaclor, colchicine, furosemide, isoniazid, lidocaine, tetracycline, sulfonamides, phenytoin, phenylbutazone,
methyldopa, thiazide diuretics, amitriptyline
Alloantigens Heart transplant rejection
Autoantigens Infection-negative lymphocytic, infection-negative giant cell
Associated with autoimmune or immune-oriented disorders: systemic lupus erythematosus, rheumatoid arthritis, Churg-Strauss
syndrome, Kawasaki disease, inflammatory bowel disease, scleroderma, polymyositis, myasthenia gravis, insulin-dependent
diabetes mellitus, thyrotoxicosis, sarcoidosis, Wegener granulomatosis, rheumatic heart disease (rheumatic fever)
Toxic Myocarditis
Drugs Amphetamines, anthracyclines, cocaine, cyclophosphamide, ethanol, fluorouracil, lithium, catecholamines, hemetine, interleukin-2,
trastuzumab, clozapine
Heavy metals Copper, iron, lead (rare, more commonly cause intramyocyte accumulation)
Miscellaneous Scorpion sting, snake, and spider bites; bee and wasp stings; carbon monoxide; inhalants; phosphorus, arsenic, sodium azide
Hormones Pheochromocytoma, vitamins: beri-beri
Physical agents Radiation, electric shock
From Caforio AL, Pankuweit S, Arbustini E, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis:
a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J.
2013;34:2636–2648.
The close temporal link between a well-defined viral prodrome
and the onset of fulminant myocarditis led to the hypothesis
that a robust immune response could clear viral infection at the
price of short-term myocardial depression and lead within weeks
to a high rate of recovery.13 Most recent clinical data support
this concept in that adults and children with fulminant myocarditis can frequently be bridged to recovery with mechanical
circulatory support.
14,15
Other causes of fulminant myocarditis, such as giant cell
myocarditis and necrotizing eosinophilic myocarditis, have illdefined triggers and unclear pathogenesis. Nonetheless, case series
support the use of mechanical circulatory support (MCS) as a
bridge to recovery or transplant in these scenarios, often in
combination with some form of immunosuppression.
16,17
DIAGNOSTIC EVALUATION OF A PATIENT
WITH SUSPECTED MYOCARDITIS
Laboratory Tests
Myocarditis should be suspected in all cases of acute nonischemic
cardiomyopathy according to the criteria suggested in the current
European Society of Cardiology (ESC) position statement on
the management of myocarditis (Table 19.1).18 Cardiac troponins
and creatine kinase levels are elevated in many cases of acute
myocarditis; however, cardiac enzymes are not specific for cardiac
inflammation and, in a large multicenter trial, troponin I was
elevated in only about a third of the subjects with histologically
19
active or borderline myocarditis.
The greater sensitivity of
third-generation troponin assays will improve the detection rate
for myocyte injury compared to the historical literature. The
current American Heart Association (AHA) scientific statement
and ESC position statements on the management of myocarditis
recommend that biomarkers of cardiac injury be drawn if
myocarditis is suspected.
18,19
Natriuretic peptides and soluble ST221 can be useful to assess
heart failure in patients with myocarditis.22 Transcriptomic
biomarkers of total
23–27
and microribonucleic acids
10,28,29
have
shown promise to improve diagnostic and prognostic assessment
of myocarditis in the future (Fig. 19.1).
Electrocardiographic Findings
The current AHA scientific statement and ESC position statements
on the management of myocarditis recommend that an electrocardiogram (ECG) be obtained in patients with suspected
CHAPTER 19 Acute Fulminant Myocarditis 201
PTPLAD1
MYO.
MYO.6MYO.8MYO.2MYO.9MYO.7MYO.3MYO.5MYO.
https://t.me/medicina_free
Unexplained Acute Cardiomyopathy*
LCE1E
SIGLEC1
MSI1
SWAP70
ITGB2
TLR1
MEGF9
FCER1G
TLR2
TLR7
ADCY7
IDIO.8
IDIO.9
IDIO.4
IDIO.5
CD14
1
MYO
4
IDIO
IDIO.1
IDIO.2
IDIO.3
IDIO.7
IDIO.6
Fig. 19.1 Transcriptomic biomarker that accurately distinguished
patients with lymphocytic myocarditis from idiopathic dilated
cardiomyopathy. The heatmap was created with an unsupervised
clustering approach based on euclidean distance using gene
expression levels from quantitative real-time polymerase chain
reaction (RT-PCR). RT-PCR was used as a confirmatory test for
a subset of genes or molecular signature that was discovered
with microarray analysis. Columns represent samples and rows
represent genes labeled with their corresponding symbol. This
biomarker identified lymphocytic myocarditis with greater accuracy
than standard histology. (From Heidecker B, Kittleson MM, Kasper
EK, et al. Transcriptomic biomarkers for the accurate diagnosis
of myocarditis. Circulation. 2011;123:1174–84.)
myocarditis despite relatively low sensitivity. ECG changes
suggestive of myocarditis are diffuse concave ST-T segment
elevations (rather than convex in myocardial ischemia) without
reciprocal changes.30 Conduction disturbances in the presence
of LV cardiomyopathy should raise suspicion for Lyme disease,
cardiac sarcoidosis, or giant cell myocarditis.30 Prolongation of
the QRS for 120 ms or longer is an independent predictor of
death or transplantation in case series from Europe and Asia.
31
Echocardiography
Echocardiography is useful to exclude pericardial and valvular
causes of heart failure and to define LV and RV function.
Myocarditis may present with dilated, hypertrophic, or restrictive
cardiomyopathy. Regional wall motion abnormalities may mimic
ischemic heart disease.
32,33
A thicker left ventricle with diminished
systolic function is more typical of fulminant myocarditis as
compared to acute disease without hemodynamic compromise.
32,33
34
Indications for Endomyocardial Biopsy
EMB should be performed in patients with new onset of unexplained cardiomyopathy with the following clinical risk factors:
(1) Heart failure requiring inotropic or mechanical circulatory
support, (2) Mobitz type 2 second-degree or higher heart block,
Requiring inotropic or mechanical circulatory
support, Mobitz type 2 second-degree or higher
heart block, sustained or symptomatic ventricular
tachycardia or failure to respond to guideline
based medical management within 1-2 weeks?
Yes: Endomyocardial Biopsy
COR I/LOE B
No: Cardiac MRI
COR 2B/LOE C
Fig. 19.2 Algorithm for the evaluation of suspected myocarditis
in the setting of unexplained acute cardiomyopathy. *Usually a
dilated cardiomyopathy. Fulminant myocarditis may have normal
end-diastolic diameter with mildly thickened walls. Exclude
ischemic, hemodynamic (valvular, hypertensive), metabolic, and
toxic causes of cardiomyopathy, as indicated clinically. COR,
Class of recommendation; LOE, level of evidence; MRI, magnetic
resonance imaging. (From Bozkurt B, Colvin M, Cook J, et al.
Current diagnostic and treatment strategies for specific dilated
cardiomyopathies: a scientific statement from the American
Heart Association. Circulation. 2016;134:e579-e646.)
(3) sustained or symptomatic ventricular tachycardia, or (4)
failure to respond to guideline-based medical management within
1 to 2 weeks (Class I, level of evidence B; Fig. 19.2).
19,35
Histologic
evaluation is required to categorize myocarditis into clinically
important subtypes with specific treatment algorithms: eosinophilic, lymphocytic, giant cell, and sarcoid (idiopathic granulomatous). If these additional risk factors are absent, further
diagnostic evaluation may be pursued with magnetic resonance
imaging (MRI; Class IIB, level of evidence C; see Fig. 19.2).19
Immunohistology with cell-specific secondary antibodies has a
greater sensitivity than histology with hematoxylin and eosin
for the diagnosis of myocarditis. Because of sampling error, a
mean of 17 samples per patient has been estimated to obtain a
sensitivity of 79% using blind RV septal biopsy and the Dallas
criteria, which is not feasible in clinical practice.
36
The right internal jugular vein or right femoral vein are
commonly used to access the interventricular septum of the
right ventricle. In the setting of isolated LV disease, EMB of the
left ventricle increases the sensitivity of EMB.37 Major complications occur in 0.64% of LV EMBs and 0.82% of RV EMBs. Minor
complications (including postprocedural pericardial effusion)
occurred in up to 2.89% of LV EMBs and 5.10% of RV EMBs.37
A subsequent study in an animal model suggested that the
diagnostic sensitivity of EMBs may be improved if combined
with real-time MRI.38 Therefore, MRI-guided EMB may be
considered but is not currently a standard procedure.
Magnetic Resonance Imaging
The AHA scientific statement recommends that in patients with
suspected myocarditis, MRI may be useful (Class IIBB, level of
evidence C; see Fig. 19.2). Patients with hemodynamic compromise
202 PART IV Noncoronary Diseases: Diagnosis and Management
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assist devices. Early transfer of those patients to a tertiary care
center with expertise in heart transplantation and destination
mechanical circulatory support is essential.
Intravenous amiodarone has been shown to be effective for
the management of ventricular arrhythmias.43 Digoxin is contraindicated, as the risk for atrioventricular (AV) block is increased
in myocarditis. Temporary pacing may be required if complete
AV block develops; some patients may require a Lifevest during
the acute phase if severe ventricular arrhythmias (ventricular
Fig. 19.3 T1-weighted magnetic resonance imaging of patient
with myocarditis. Apical and inferior late gadolinium enhancement
are consistent with myocarditis (1.5 T scan). (Courtesy Robert
Manka, MD, University Hospital Zurich.)
are frequently too unstable to lie flat and hold their breath for the
required sequences. As mentioned earlier, if patients also meet
criteria for EMB, cardiac MRI prior to biopsy may help target the
left ventricle.
37,38
Non–contrast-enhanced T2-weighted sequences
and early post-gadolinium T1-weighted sequences have been
used separately and in combination to diagnose myocarditis.19
An international consensus group for cardiovascular MRI in
myocarditis has established the Lake Louise criteria to define
the diagnosis of myocarditis on MRI.39 Diagnostic findings of
delayed gadolinium enhancement (DGE) can evolve from a focal
to a more diffuse pattern (Fig. 19.3) and then resolve over the
course of 2 to 4 weeks after symptom onset.40 The MyoRacer
Trial suggested that cardiac mapping techniques with T1- and
T2-weighted imaging outperform the Lake Louise criteria, and
that T1-weighted imaging was more accurate in acute myocarditis versus T2-weighted imaging, which was better for chronic
myocarditis.41 The presence of late gadolinium enhancement,
particularly in the anteroseptal region, is associated with a more
than doubled risk of major adverse cardiac events.
41a,41b
THERAPY
Fulminant myocarditis should be managed in accordance
with the current guidelines for systolic heart failure (HF), as
outlined by the AHA/American College of Cardiology (ACC)
and the ESC.
experience, as clinical trials of heart failure therapy specifically
in myocarditis have not been done. Patients with fulminant
myocarditis require hemodynamic support with vasopressors or
MCS, such as intraaortic balloon pump, extracorporeal membrane
oxygenation, or percutaneous or surgically placed ventricular
19,30,42
These recommendations are based on clinical
tachycardia or fibrillation) persist until the patient is otherwise
ready for discharge.
verter defibrillator should be deferred, as there is a significant
rate of LV recovery.
In myocarditis related to systemic autoimmune disease—such
as sarcoidosis, systemic lupus erythematosus, or a specific
vasculitis—treatment is based on the underlying disorder and
often includes immunosuppression.
pressive, antiviral, and intravenous immunoglobulin therapies
in myocarditis patients requiring MCS has not been systematically
investigated. The major treatment trials of immunosuppression
either excluded patients on MCS or enrolled very few of these
patients.45 Treatment of mild to moderately severe acute myocarditis with immunosuppressive drugs is not recommended in
adults, as immunosuppression with prednisone and either
azathioprine or cyclosporine has been shown to lead to similar
changes in LV ejection fraction and transplant-free survival as
placebo.46 Two randomized trials of immunosuppression in
chronic (>6 months’ duration) inflammatory cardiomyopathy
without an identifiable pathogen showed favorable results with
prednisone and combinations of prednisone and azathioprine
or cyclosporine.
Nonsteroidal antiinflammatory drugs (NSAIDs) should be
avoided because of the risk of increased inflammation and
mortality in experimental models.50 Interferon, high-dose
immunoglobulin, and immunoadsorption are currently not
recommended in adults with myocarditis due to limited data.
Giant cell myocarditis can deteriorate rapidly into cardiogenic
shock and multiorgan failure, with a rate of death or cardiac
transplantation of 89%.51 Retrospective and prospective studies
have shown relatively favorable outcome at 1 year in patients
treated with prednisone and cyclosporine with or without
anti-T-cell antibodies.46 Repeat EMB may be considered in select
cases to monitor the histologic response if the clinical response is
incomplete. If a transplant is required, the recurrence rate of giant
cell myocarditis is approximately 20% to 25% in the allograft.
Eosinophilic necrotizing myocarditis is the most fulminant
form of eosinophilic myocarditis and is characterized by rapidly
progressing heart failure. Eosinophilic myocarditis can be a
manifestation of hypersensitivity to certain medications, such
as sumatriptans.53 Case reports describe success with high-dose
steroid therapy in addition to guideline-directed medical manage-
53,54
ment.
In summary, the clinical trajectory of myocarditis requiring CICU care is variable. Approximately 50% of patients improve
within 2 to 4 weeks, 25% develop persistent cardiac dysfunction,
and about 12% to 25% will potentially require a transplant
or long-term MCS. The average rate of survival after cardiac
transplantation for adults with myocarditis is similar to survival
30,44
Implantation of an implantable cardio-
45,47–49
30,45
The role of immunosup-
30
52
CHAPTER 19 Acute Fulminant Myocarditis 203
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after transplantation for other types of cardiomyopathy. However,
recent data in children suggest that the post-transplantation risk
is higher if active myocarditis was detected in the explanted
heart, raising the possibility that preexisting inflammation or
viral infection may adversely affect graft survival.
55
In those patients who recover, competitive sport participation
should be avoided for a minimum of 3 to 6 months after the
diagnosis of myocarditis. Reassessment with clinical evaluation
and functional testing is indicated before competitive sport
participation is resumed.
The full reference list for this chapter is available at
ExpertConsult.com.
CHAPTER 19 Acute Fulminant Myocarditis 203.e1
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