Transcript Myocarditis & Pericarditis - Calgary Emergency Medicine

Myocarditis & Pericarditis
Resident Rounds
March 6, 2003
Aric Storck
Case 1
57 year old man
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previously healthy
No cardiac risk factors
One week history of
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General malaise, fever/chills, myalgias, coryza
Yesterday
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Gradual onset of 6/10 pleuritic chest pain
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Worst lying down
Better sitting forward
Not exacerbated by exertion
Slightly SOB
Physical exam
HR 105 RR 20 BP 130/80 T 38.2
H&N – some palpable lymph nodes
CVS – sounds like velcro
Chest – Normal
Abdo - Normal
Could this be a heart attack?
Should I call the cath lab?
What’s going on?
Pericardial Disease
Chest Pain - Ischemic vs
Pericarditis
pericarditis
Location
Quality
Precordium, L
trapezius ridge
Pleuritic
Duration
Hours to days
Exacerbation Lying down, chest
wall motion
Relief
Leaning forward
ischemic pain
Retrosternal, L
shoulder, arm
Pressure, tightness,
burning
1-15 minutes
exertion
Rest
Ischemic vs Pericarditis
Pericarditis
Ischemic Pain
Associated SSx
SOB, diaphoresis, N/V, diaphoresis,
no N/V
SOB
Vital signs
Often febrile
High fever rare
Pericardial Disease
Pericarditis
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Non-specific inflammation of pericardium
Rarely emergent
Pericardial effusion
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Accumulation of fluid in pericardial space
Serous, purulent, fibrinous, hemorrhagic
Cardiac tamponade
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Impairment of ventricular filling due to
fluid in pericardial space
Emergent
Pericardial physiology
Parietal layer
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Thick, collagenous, stiff
Adventitial attachments to sternum,
diaphragm, mediastinum
Visceral layer
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Thin
Closely adherent to epicardial surface
Pericardial fluid
Potential space between layers
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Normally 15-60 cc fluid
Functions
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Reduces friction
Prevention of infection
Augmentation of atrial filling
Maintains normal pressure-volume
relationship of chambers
No physiological consequence to absent
pericardium
Pericardial innervation
Parasympathetic
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Vagus
Left-recurrent laryngeal nerve
Sympathetic
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Stellate
First thoracic ganglia
Little somatic sensory innvervation
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Thus visceral nature of chest pain
Pericarditis - etiology
Viral
Bacterial
Traumatic
Malignant
Post-irradiation
Post-MI
Drug-induced
Collagen vascular disease
Viral Pericarditis
Most common cause
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Enteroviruses
 Coxsackie A & B
 Echovirus
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HIV
Mechanism of injury
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Direct viral cytotoxicity
Indirect auto-antibody mediated effects
Viral Pericarditis - SSx
Syndrome may be immediate or
develop 2-4 weeks post viral illness
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Chest pain
Pericardial friction rub
 Heard with diaphragm over LLSB, leaning
forward, breath held
 Scratchy
 Triphasic (presystolic, systolic, diastolic)
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Fever
Tachycardia
Tachypnea,dyspnea
diaphoresis
Bacterial Pericarditis
Common in less developed countries
More commonly associated with
tamonade
Higher mortality than viral
Streptococcus, staphylococcus, gram
negs, anaerobes
TB
Lyme disease
Concomitant pneumonia / empyema
Often not diagnosed until tamponade
Definitive Dx requires pericardiocentesis
Treatment Abx
ICU admission indicated
Uremic Pericarditis
ESRD / Underdialysis
Bloody pericardial effusions
ECG often normal (little epicardial involvement)
Cardiac tamponade common
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Often loculated - therapeutic pericardiocentesis
difficult
Treatment
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ICU admission
NSAIDS (caution b/c bleeding diathesis of uremia)
Post-MI Pericarditis
May occur within days of MI
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Direct extension of myocardial inflammation
Presents as “different” chest pain
Must distinguish from reinfarction
Incidence 7-16%
Tx: NSAIDs
Dressler’s syndrome
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Thought to be autoimmune
Weeks to months
Fever, chest pain, leukocytosis, pleuritis,
pericardial/pleural effusions
Tx: NSAIDs, steroids for resistant cases
Collagen Vascular Disease
Pericarditis
Common in many CVDs
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RA
 Incidence 30-50% - many clinically silent
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SLE
 50% incidence
Dx: CP, R CHF, echo
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ECG/CXR often normal
Tx: steroids
Commonly progress to constrictive
pericarditis
Malignant pericarditis
Primary tumours rare
Metastatic disease common
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Incidence 10% in cancer patients
Lung, breast, lymphoma, leukemia, MM
Children – Hodgkin’s, leukemia,
lymphosarcoma
Progress to tamponade in 50-85%
Dx: pericardiocentesis / cytology
Tx: symptomatic
Post-Irradiation Pericarditis
Early (days – months)
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Dose related pericardial effusion
Must distinguish from malignant effusion
SSx:
 SOBOE
 can mimic infectious pericarditis (fever, CP, friction rub)
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Tx:
 Often resolves spontaneously
 NSAIDs, steroids, pericardiocentesis
Late (years)
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Constrictive pericarditis
Tx:
 Often requires pericardiectomy
Drug-induced pericarditis
SLE-like syndrome
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Procainamide
Hydralazine
Isoniazid
Methyldopa
Reserpine
Hypersensitivity
reaction
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Penicillin
Cromolyn sodium
Methysergide
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constrictive pericarditis
/ generalized
mediastinal fibrosis
Doxorubicin
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Chemotherapy
Pericarditis /
cardiomyopathy
Back to our case
You order an ECG on your
patient
His ECG
•STE – I, II, aVF, V2-V6
•Reciprocal STD – aVR
•PR depression
Pericarditis – ECG
4 Stages
Evolution over 3-4 weeks
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Only 50% have all 4 phases
Stage 1
Hours to days
Diffuse ST elevation
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ventricular subepicardial injury
I, II, III, aVL, aVF, V2 to V6
 Concave upwards
 No distinct J-point
 No T-wave inversions
Reciprocal ST depression
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aVR, V1
Diffuse PR depression
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atrial injury
Stage 2
Variable timeline
ECG transiently normal
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ST / PR return to baseline
Some T-wave flattening
Stage 3
Variable timeline
T-wave inversion
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Deep, uniform
Stage 4
Weeks to months
Return to normal
Some patients will have residual T-wave
inversion
ECG – ECG vs Pericarditis
Pericarditis
Ischemia/Infarction
ST elevation
Diffuse, concave
Anatomical, convex
ST changes
few reciprocal
changes
Reciprocal changes
PR segment
Depression
No depression
Q-T
prolongation
Evolution
Rarely without
myocarditis
Normalization in
stage 2
More commonly seen
Electrical
Alternans
Present with
tamponade
absent
MI progression with
development of Qwaves
What if your patient was an
18 year old male athlete with
burning chest discomfort after
one too many seven-layer
burritos?
His ECG
BER vs Pericarditis
Pericarditis – Ancillary tests
Most useful for ruling out other
diagnoses
Troponin / CK-MB
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Normal to mildly elevated (damage of
subepicardial myocardium)
ESR – elevated or normal
WBC – elevated or normal
Echocardiogram
Gold standard for pericarditis with
effusion
Can also evaluate
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Pericardial thickness
Tamponade
Tumours / cysts
Constrictive pericarditis
Trans-thoracic echocardiogram
•Large pericardial
effusion
•RV compressed
You suspect a viral
pericarditis.
How are you going to treat it?
Viral Pericarditis - treatment
All need to be followed to monitor for
effusion
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Effusion suspected if:
 Dyspnea, fatigue, findings of tamponade
 Must distinguish between purulent & viral
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May need diagnostic pericardiocentesis
NSAIDS – good relief of pain & fever
Colchicine – 1-2mg po od
Steroids – only if NSAID resistant
Admit if: cannot rule out MI, pain control
Pericardial Effusion
Collection of fluid in indistensible pericardium
Secondary to pericarditis
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infectious, uremic, malignant, post irradiation
Secondary to hemorrhage / trauma
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aortic dissection, penetrating trauma
Symptoms related to size and acuity of
collection
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80-100cc required before decompensation begins
(15-60cc fluid normal)
Chronic effusions rarely progress to tamponade
Pericardial tamponade
Physiologic decompensation due to pericardial
effusion
Acute surgical tamponade
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Penetrating injury
aortic dissection
Iatrogenic (central line insertion)
Medical tamponade
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Due to pericardial effusions due to pericarditis
Low-pressure tamponade
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Due to severe dehydration
LV pressure lowered to equilibrate with RV
pressure
Pericardial tamponade
Early
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<200cc,  CVP, tachycardia
Moderate
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~200cc,  CVP, tachycardia,  cardiac
output,  BP
Severe
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>200cc,  CVP (unless hypovolemic), 
BP,   cardiac output, +/- bradycardia
Traumatic Tamponade
2% of penetrating thoracic trauma
80-90% of stab wounds to heart
20% of GSW to heart
Large instruments cause exsanguination
Foreign bodies, rib fractures
Iatrogenic – cardiac catheterization,
pacemaker insertion, pericardiocentesis,
cardiac surgery
Clinical features
Beck’s triad:
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hypotension
distended neck veins (>15mm H20 with
hypotension is diagnostic)
muffled heart sounds (unlikely to be heard
in trauma room)
pulsus paradoxus – difficult to measure
during resuscitation
no response to vigorous fluid
resuscitation
Diagnosis
Echocardiography
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available at some centres, but difficult to
perform during resuscitation
TTE better than TEE
98.1% sensitive, 99.9% specific
Also useful for evaluation of valves and
wall motion
Diagnosis
Ultrasound
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Features include
 fluid in pericardial sac
 dilated IVC
 Compression of RA
 Collapse of RV during diastole
Diagnosis
ECG
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Generalized low voltage
 R-wave height <1cm in all leads
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Electrical alternans
 specific but not sensitive
 more likely seen in chronic than acute effusions
 Morphology/amplitude of P, QRS, ST-T wave
alternate every beat in any single lead
 Likely due to inability of heart to return to a
single position following each beat because of
pericardial fluid
Diagnosis
CXR
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May show enlarged cardiac shadow if lots
of fluid (>200-250cc)
Generally not useful for acute early
tamponade as only a small amount of fluid
is required to create significant
hemodynamic compromise
Large Pericardial
Effusion
•Loss of customary
heart borders
•“water-bottle” heart
Management
Prehospital care
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Same as any trauma patient
Consider tension pneumothorax and needle
thoracostomy
Management
Emergency Department
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vigorous fluid resuscitation
CVP monitoring
Treat concomitant injuries
Pericardiocentesis
ED thoracotomy
Pericardiocentesis
Pericardiocentesis
Diagnostic and therapeutic
Many false positives / false negatives (clotted
blood)
Improvement possible with small volume of
blood removed
Complications
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Pericardial tamponade
Laceration of coronary artery / lung
Induction of dysrhythmia
Continued deterioration may necessitate
thoracotomy
Pericardiocentesis
Technique
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18 gauge, 10 cm spinal needle, 20 cc
syringe
Continuous ECG monitoring
Needle enters subxyphoid area
Aim for left scapula
Aspirate every 1-2 mm
Stop if blood aspirated, cardiac pulsations
felt, ECG changes
NB: if more than 20 cc blood is removed
easily you are probably in the RV (ooops!)
Case 2
28 year old man
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previously healthy
8 day history
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Fever
Fatigue
Myalgias
Progressive SOBOE
Vague chest discomfort
Physical examination
HR 140 RR 20 BP 100/70 T 38.3 SaO2 91%
diaphoretic
H&N
 Some cervical lymphadenopathy
Chest
 Coarse crackles in bases bilaterally
CVS
 Apex inferolaterally displaced
 No murmurs
 No friction rub
 Is that an S4?????
ECG
Sinus tachycardia
Frequent premature atrial and
ventricular beats
Non-specific ST & T wave changes
CXR
Troponin
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0.05
CBC
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WBC 13
Some atypical lymphocytes
No left shift
ESR 29
Echocardiogram
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Dilated chambers
Global wall motion abnormalities
Decreased LV and RV function
Mild tricuspid and mitral insufficiency
No pericardial effusion
Cardiac Catheterization
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Totally normal coronary arteries
What’s going on?
What are you going to do
about it?
Myocarditis
Etiology
Viral – most common
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Mostly enteroviruses – esp. Coxsackie B
Adenovirus
Influenza A/B
CMV / EBV / VZV
Bacterial
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S. aureus, Streptococcus
Mycoplasma
Diphtheria
Spirochetal
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Lyme disease
Mycotic
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Candida
Aspergillus
Rickettsial
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Rocky Mountain Spotted Fever
Helminthic
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Trichinosis
Schistosomiasis
Protozoal
Chagas disease
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most common cause
worldwide
Trypanosoma cruzi
Insect vector
Dx:
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Demonstration of serum
parasites
Tx:
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Nifurtimox
(antitrypanosomal)
HIV and myocarditis
Myocarditis in 46% on autopsy
Multifactorial
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HIV, CMV, toxoplasma, TB, aspergillus
Kaposi’s sarcoma- may involve myocardium
Cardiac B-cell lymphoma
Treatment toxicity
 Pentamidine, zidovudine, dideoxyinosine
Drugs
Cocaine
Emetine
Doxorubicin
HIV treatment
Systemic Diseases
Collagen Vascular Disease
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SLE
PAN
RA
Dermatomyositis
Sarcoidosis
Kawasaki’s Disease
Pathophysiology
Three major mechanisms
1. Myocardial necrosis from direct invasion
2. Autoimmune destruction
•
Beta myosin chain & coxsackie B share 50%
same amino acid sequences
3. Endotoxins produced by pathogens
Clinical Features
VERY NON-SPECIFIC!
Wide spectrum of disease
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Subclinical (most)
 overshadowed by other manifestations of
illness
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Fulminant cardiac failure +/- death
History
Fever
Fatigue
Myalgias (**suggestics myotropic virus)
Vomiting / diarrhea
Chest pain
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May mimic ischemic or pericardial pain
Physical Exam
Cardiac exam may be normal
Tachycardia disproportionate to fever
Cardiomegaly
Atrial or ventricular dysrhythmias
S3, S4, TR/MR
+/- pericardial rub
CHF
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Usually biventricular
SSx of RV dysfunction (JVD, edema, hepatic
congestion, etc.)
SSx of LV dysfunction if predominant LV
involvement
Children
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Respiratory distress (grunting respirations,
intercostal retractions)
Lungs clear / wheeze
Ventricular dysrhythmias
Infants
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Often fulminant syndrome
 Fever, cyanosis, respiratory distress,
tachycardia, cardiac failure
ECG
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NON-SPECIFIC!
Sinus tachycardia
Low voltages
Prolonged QTc
AV block
AMI patterns
ST changes
T wave inversions
CXR
Often normal
Cardiomegaly
+/- pulmonary congestion
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Depends on relative RV vs LV dysfunction
Laboratory
Cardiac enzymes
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May or may not be elevated
Troponin
 elevated in 34% of patients with biopsy proven
myocarditis
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CK-MB
 Elevated in 5.7% of patients with biopsy proven
myocarditis
Bottom Line …. Not really very helpful
WBC
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Normal to elevated
ESR
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Normal to elevated
Viral titres
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May suggest a viral infection, but don’t
confirm etiology of cardiac disease
Echocardiography
Non-specific
May mimic AMI
Usually multichamber dysfunction
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Reduced LVEF
Global hypokinesis
Wall motion abnormalities
Can evaluate for thrombi and pericardial
involvement
That all sounds pretty nonspecific…
I’m confused?
When should I suspect
myocarditis?
Suspect myocarditis if …
Systemic infection is associated with
new cardiovascular problems.
Young patient with few coronary RF’s
Tachycardia out of proportion to fever
Severe myalgias

Suggests myotropic pathogen
Non-anatomical ECG changes
Continued pain with no ECG evolution
Global (vs segmental) wall motion
abnormalities on echo
Unexplained CHF / dysrhythmias in
previously healthy patient
I suspect myocarditis.
How do I confirm the
diagnosis?
MRI
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Contrast enhanced (gadopentate dimeglumine)
shown to be useful
Maybe the future?
Antimyosin scintigraphy (Indium-111)
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Binds to exposed myosin in damaged myocardium
Diffuse, faint uptake of antimyosin antibody
(AMI typically has intense, localized uptake)
Normal antimyosin scan excludes AMI and
myocarditis
Endomyocardial biopsy
Gold standard
One report …
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Sensitivity 79%, Specificity 63%
Dallas criteria used to standardize diagnosis
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Histologic criteria for myocarditis
 5-30% of patients with suspected myocarditis
 41% of patients with acute dilated cardiomyopathy
 63% of patients with chronic dilated cardiomyopathy
Worse prognosis for patients with histological
changes
I’m pretty sure it’s myocarditis
…. How do I treat it?
Treatment
ED treatment
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Bed rest
Cardiac monitoring
Management of arrhythmias
 No treatment of PAC’s, PVC’s
 Electrical cardioversion for supraventricular
arrhythmias with rapid ventricular response
 Drugs for serious ventricular ectopy /
arrhythmias
 Pacing for high grade conduction blocks
CHF
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Treat very cautiously
Aggressive preload or afterload reduction
may cause cardiogenic shock
Anticoagulation
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If intracardiac thrombi detected on echo
Definitive Treatment
Treat specific cause if possible
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Eg: Chagas disease, Lyme disease, etc.
Anti-viral agents & immunosuppression
are controversial
IVIG may be helpful in certain subsets
Cardiac transplantation if fulminant
Disposition
Admission to monitored bed
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All patients with symptomatic suspected
myocarditis
ICU / CCU
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All hemodynamically unstable patients
Prognosis
Many cases subclinical and benign
Wide spectrum

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Complete recovery to any of many
permanent cardiac problems
Dilated cardiomyopathy common sequelae
NIH myocarditis trial
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20% mortality at 1 year
56% mortality at 4.3 years
LVEF & RV function 1 year after
presentation best predictor of outcome
The End