TEXTBOOK READING
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“Any inflammation of the myocardium”
External Triggers :
1. Viruses
2. Bacteria
3. Parasites
4. Toxins
5. Drugs
6. Mechanical trauma
Internal Triggers :
1. Autoimmune activation
2. Ischemic damage
3. Genetic
cardiomyopathies
Cardiac injury
Immunologic response
Cardiac inflammation
Destroy heart tissue acutely
Persistent cardiac dysfunction
Cardiac remodeling
Dilated cardiomyopathy,
heart failure, death
Good news : most patients is self limited with proper support and follow up care
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Prevalence rate
Per 100.000
Global Burden of Disease Myocarditis
Higher in the 1st year of life
9.21
8.04
Estimated 0.42
deaths per 100.000
1-14 years, males = females
>15 years, males > females
1990
2019
Disability from
Myocarditis
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HEART FAILURE
DCM
SUDDEN CARDIOVASCULAR DEATH
2% of infants
5% of children
5-14% of young athletes
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GIT/respiratory
Mucosal
surface
Respiratory
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Mechanism:
1. Direct infection
2. Activation of inflammatory
myocardial dysfunction
3. Bloodstream infection
metastatic foci in myocardium
Pathogens:
1. Corynebacterium diphteriae
2. Streptococcal
3. Tuberculosis
4. Tropheryma whipplei
5. Borrelia burgdorferi
Trypanosoma cruzi :
Chagas disease
1. Trichinella
2. Echinococcus
1. Arsenicals and lithium myocyte necrosis
2. Physical agents: Radiation, excessive heat,
hypothermia
3. Drugs: antiepileptic, antimicrobial, allopurinol,
sulfa-based drugs, dobutamine,
corticosteroids, clozapine, smallpox
vaccination, chemotherapeutic
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Myocarditis has a wide- ranging array of potential clinical presentations
ASYMPTOMATIC
ECG/ECHO ABNORMALITY
Community viral
outbreaks/influenza
pandemics :
Transient ECG/
echocardiographic
abnormality
Mostly cardiac
asymptomatic  few
longterm squele
CHEST
PAIN
CARDIAC
DYSFUNCTION
ARRHYTMIAS/
HEART FAILURE
HEMODYNAMIC
COLLAPSE
Young children – teenagers  acute/fulminant
Chest pain in
Adult  subtle – insidious, DCM, HF
myocarditis may
resemble typical
B19V
: endothelial dysfunction
angina and
GCM : ventricular arrhythmias
accompanied by ECG
and heart block
changes including
STElevation. Also can
mimic in pericarditis Sarcoidosis : Enlarged LN, CXR hilar adenopathy
Drug/toxin : pruritic, maculopapular rash,
eosinophilia
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ACUTE MYOCARDITIS
Nonspecific symptoms related to
the Heart. Fatigue (82%), DOE
(81%), arrhythmias (55%),
palpitations (49%), and chest pain
at rest (26%). Fever, chills,
myalgias, and constitutional
symptoms occurs in 20%- 80%
FULMINANT MYOCARDITIS
Hemodynamic compromise and
hypotension. Abrupt onset,
usually within 2 weeks of a viral
illness. Echo: diffuse global
hypofunction, cardiac dilation,
thickening ventricular wall. EMB:
typical diffuse myuocarditis
GIANT CELL MYOCARDITIS
EOSINOPHILIC MYOCARDITIS
Heart failure, arrhythmia, or heart
block, with standard medical
therapy fails to improve. Improved
with the use of immunosuppressive
therapy. EMB: Giant cell, active
inflammation, scar tissue. Often
have other autoimmune:
thymoma/crohn disease
Allergic eosinophilic myocarditis :
caused by a hypersensitivity
reaction to a foreign antigen.
Löffler endocarditis : systemic
eosinophilic disorders, resulting in
myocardial, endocardial, and
Valvular involvement. Fulminant
necrotic myocarditis.
CHRONIC ACTIVE
MYOCARDITIS
PERIPARTUM
CARDIOMYOPATHY
Older adults. Insidious onset.
moderate ventricular dysfunction
(fatigue and dyspnea). EMB:
active myocarditis, or
borderline/fibrosis/myocyte
droput. 60% DCM of unknown
LV dysfunction in the last month of
pregnancy or within 5 months of
delivery, no preexisting cardiac
dysfunction and no recognized
cause of the cardiomyopathy.
EMB: high freq of myocarditis
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CLINICAL SUSPICION
LABORATORY
CRITERIA
LABORATORY TESTING
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Elevated cardiac troponin
Elevated creatine kinase–MB
In children with fulminant
myocarditis, higher serum
creatinine, lactate, and aspartate
transaminase (AST) levels are
associated with increased inhospital mortality rates.
NT- pro- BNP is predictably
elevated in children with acute
DCM due to myocarditis
HIgher interleukin-10 and soluble
Fas concentrations are associated
with an increased risk of death
IMAGING MODALITIES
ECG
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Nonspecific repolarization
changes and sinus
tachycardia are common
PR- segment depression and
diffuse ST- segment
elevation may accompany
a clinical presentation of
myopericarditis.
The presence of a QRS width
greater than 120 milliseconds
in duration and Q waves is
associated with a great risk
of cardiac death or need for
heart transplantation.
HISTOLOGIC
ECHOCARDIOGRAPHY
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Acute cardiomyopathy :
dilated, spherical ventricle with
reduced systolic function
Heart failure due to fulminant
myocarditis : small cardiac
chambers and mild and
reversible ventricular
hypertrophy from inflammation
Segmental wall motion
abnormalities often are
present early
A pericardial effusion usually
signifies myopericarditis.
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CLINICAL SUSPICION
LABORATORY
CRITERIA
IMAGING MODALITIES
HISTOLOGIC
CMR
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Myocardial necrosis can be
detected by late
gadolinium enhancement
(LGE)
T1- weighted, myocardialdelayed enhancement
technique can quantitate
regions of damage and
possibly predict the risk of
cardiovascular death and
ventricular arrhythmias after
myocarditis
T2- weighted imaging can
be used to detect
myocardial edema
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EMB
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Low sensitivity due to the patchy nature
of the inflammatory infiltrates in the
myocardium and the reluctance of
clinicians to perform an invasive
diagnostic procedure
GCM : diffuse or multifocal inflammatory
infiltrate of lymphocytes and
multinucleated giant cells in the
absence of granuloma. Eosinophi (+)
Cardiac sarcoidosis : giant cells are
located within the granuloma, at the
edges of the inflammation, where
myocyte damage is present. Fibrosis (+)
Acute myocarditis with widespread lymphocytic and histiocytic
infiltrate (arrow) and associated myocyte damage (arrowhead).
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Varies in relation to the clinical scenario and degree of left
ventricular dysfunction at presentation
15% of patients with myopericarditis may develop
recurrent myopericarditis
There is a risk of late heart failure due to diastolic
dysfunction years after the apparent resolution of acute
myocarditis
The presence of viral genomes on EMB may portend a
poor outcome
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The first- line therapy for all patients with myocarditis and
heart failure is supportive care
Routine treatment of mild to moderately severe acute
myocarditis with immunosuppressive drugs is not
recommended for adults
Treatment of viral infection may be helpful in the
management of posttransplantation viral heart
disease in children
adult patients with chronic DCM and viral genomes
detected by PCR in heart biopsy tissues, one trial series
suggests that 6 mIU of IFN- β three times per week
improves enteroviral or adenoviral heart infection
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Tailored Immunosuppression in Inflammatory Cardiomyopathy (TIMIC) trial, 85 patients with
chronic inflammatory cardiomyopathy without persistent viral infection were randomly assigned
to receive either prednisone and azathioprine or placebo. Immunosuppressive
treatment was associated with an increase in the left ventricular ejection fraction from 26% to
46% and an improved quality of life.
Patients with ventricular arrhythmias or heart block due to acute myocarditis should be
hospitalized for electrocardiographic monitoring. Arrhythmias usually resolve after several
weeks.
The indications for an implantable cardiac defibrillator (ICD) are the same as with nonischemic
DCM
Mechanical circulatory support or extracorporeal membrane oxygenation may allow a bridge
to transplantation or recovery in patients with cardiogenic shock despite optimal medical care.
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