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MYOCARDITIS
215
immune response to the infectious agent. Molecular
mimicry plays a big role here, with the similarity
of the antigens on viral pathogen and myocytes; an
immune response to the former would cause dam-
age to the latter. Viral-induced myocyte damage can
provoke release of intracellular proteins and trigger
a host immune cascade in a genetically predisposed
individual.
14
Lastly, in the chronic phase, toxicity
occurs from exogenous chemicals or endotoxins pro-
duced by the agent.
15
In neonates, damage is thought
to be related to direct cytotoxicity from the offending
virus, whereas in adults, an exaggerated host response
plays a larger role.
8
Pathophysiology
It is believed that myocardial injury from myocarditis
occurs via three main mechanisms. In the beginning,
in the acute phase (0–3 days), cellular injury occurs
from direct invasion of the virus and its replication.
Myocyte antigens are released and cytokine induc-
tion follows with the release of tumor necrosis fac-
tor-alpha, interferons, and interleukins.
10
The body’s
immune response can limit the degree of viremia, but
if the response is insuffi cient, the virus may not be
eliminated, and further damage to myocardium can
occur.
11–13
Next, in the subacute phase (4–14 days),
destruction of cardiac tissue occurs due to host
Table 15-1. Causative agents of myocarditis
INFECTIOUS
Virus
Coxsackie
Adenovirus
Epstein-Barr
Infl uenza
Parainfl uenza
Human Immunodefi ciency
Virus
Mumps
Cytomegalovirus
Herpesvirus
Varicella zoster
Rubella
Rubeola
Rabies
Echovirus
Polio
Hepatitis A, B, C, and D
Bacteria
Borrelia burgdorferi (Lyme disease)
Legionella pneumophila
Mycoplasma pneumoniae
Corynebacterium diphtheriae
Mycobacterium tuberculosis
Chlamydia pneumoniae
Streptococcus
Parasite
Toxoplasmosis
Chagas disease
Trichinosis
Echinococcosis
Fungal
NONINFECTIOUS
Immunological
Vasculitis/Connective Tissue Infl ammatory Bowel Disease Postmyocardial injury Postviral
Systemic lupus erythematosis Crohn’s disease Churg-Strauss syndrome Acute rheumatic fever
Rheumatoid arthritis Ulcerative colitis Sarcoidosis Sjogren’s syndrome
Kawasaki disease
Postirradiation
Medication/chemical
Cocaine
Doxorubicin
Idiopathic
CHAPTER 15
216
disproportionate to the temperature or toxicity should
be a clinical clue to the diagnosis. The cardiac exami-
nation may be normal, or exhibit rales, an S3 gallop,
or a pericardial friction rub.
22
Failure is a common
manifestation of myocarditis, as are dysrhythmias, and
some patients will present in cardiogenic shock.
In children, physical examination fi ndings include
grunting respirations and intercostal retractions.
Some will have wheezing. On cardiac examination, an
S3 gallop and rales may be heard. Infants often have
a fulminant course characterized by fever, cyanosis,
respiratory distress, tachycardia, and cardiac failure.
22
New-onset wheezing in a child should prompt the cli-
nician to obtain a chest radiograph to exclude either
foreign body in the airway or pulmonary edema.
Special presentations
A history of a recent tick bite, arthritis, the classic rash
(erythema chronicum migrans), or fever, especially
when seen together with conduction abnormalities
(atrioventricular blocks), should make one consider
a Lyme myocarditis.
23
Myocarditis usually develops
within 2–4 weeks of onset of symptoms.
Mucocutaneous lymph node syndrome, also known
as Kawasaki disease, is an illness that affects young
children. Four out of fi ve features are required for
diagnosis: (1) fever greater than fi ve days duration, (2)
conjunctivitis without exudate, (3) lymphadenopathy
(4) erythematous exanthem with subsequent desqua-
mation, and (5) changes in lips and oral mucous mem-
branes. It is thought to be caused by an autoimmune
response to an infectious agent or toxin. Patients can
develop myocarditis as well as other complications,
including myocardial infarction, dysrthymias, CHF,
and coronary artery aneurysm formation. Look for
the diagnosis in children with prolonged fever, rash
and conjunctivitis.
Testing in myocarditis
Diagnostic studies can assist in confi rming a diagnosis
of myocarditis (Table 15-2). Commonly ordered tests
include an electrocardiogram (EKG), chest radio-
graph, and laboratory tests, including serum cardiac
markers and echocardiography. Additional specialized
testing studies are nuclear medicine imaging, MRI,
viral titers, coronary angiography, and endomyocar-
dial biopsy.
Myocarditis has been linked to the development of
chronic dilatated cardiomyopathy, and autoantigens
are often seen at this stage. This has led to the hypoth-
esis that cardiomyopathy postmyocarditis is due to
an abnormal host immune response, resulting from
either shared antigens or molecular mimicry.
16
The microscopic/pathologic diagnosis of myo-
carditis requires evidence of myocyte degeneration
or death with a surrounding infl ammatory response,
such as myocyte fi ber necrosis with an infi ltrate of
neutrophils and monocytes. Gross examination of
the heart often reveals myocardial hemorrhage with
degeneration or necrosis, and the subendocardium
and valves are spared. Biventricular dilatation is often
seen, with the left greater than right. Scar tissue is pro-
duced after the acute injury, and this reduces cardiac
contractility and ejection fraction. The conduction
system may be involved, with resulting brady- and
tachydysrhythmias.
17,18
Initial presentation: History and physical
In the early stages of viral myocarditis, the majority of
patients often have nonspecifi c fl u-like complaints.
19
Half of the patients will note a recent upper respi-
ratory or gastrointestinal infection.
20
Many cases are
probably subclinical and asymptomatic, and the car-
diac symptoms and signs are overshadowed by the
systemic manifestations of the viral infection (i.e.,
cough, dyspnea, dizziness, weakness, fever, emesis,
diarrhea, and myalgias). In general, onset of cardio-
respiratory symptoms usually appear 7–10 days after
infectious complaints develop, and include dyspnea,
orthopnea, paroxysmal nocturnal dyspnea, palpita-
tions, syncope, and pedal edema. Congestive heart
failure and dysrhythmia are the most frequent pre-
sentations in admitted patients. Pleuritic chest pain
is common when there is pericardial involvement,
and patients may additionally complain of fatigue,
decreased exercise capacity, and palpitations sec-
ondary to tachydysrhythmias or heart block.
20
Some
patients may describe a substernal chest pressure
or ache, similar to patients with an acute coronary
syndrome.
21
Myocarditis is frequently a diagnosis of
exclusion.
15
On physical examination, careful note of vital signs
should be made. Abnormal vital signs include fever
(found in half of the cases), tachycardia, tachypnea, and
hypotension.
3
Traditional teaching is that tachycardia
MYOCARDITIS
217
When present, ST-elevations are convex (dome-
shaped) mimicking acute myocardial infarction,
though generally the magnitude of the ST-elevations
is less than 5 mm. There can sometimes be reciprocal
changes. Additionally, new Q waves may appear, and
there may be PR depression. Prolongation of the PR
interval may also occur. Cardiac dysrhythmias are
common (up to 60%), and more often ventricular
than supraventricular.
3
Heart block is also common,
but usually transient, and rarely requires permanent
pacemaker placement.
Common EKG abnormalities include sinus tachy-
cardia (Figure 15-1) and low voltage. Other dys-
rhythmias seen include atrial fi brillation with bundle
branch block, complete atrioventricular block with
narrow (Figure 15-2) or wide QRS complex escape
rhythm, and ventricular tachycardia. Additional
changes can include a prolonged QT interval or a
pseudoinfarction pattern with the following abnor-
malities: ST-segment elevation or depression, T-wave
inversions, and pathologic Q-waves.
24
Twenty per-
cent of patients develop a left bundle branch block.
Table 15-2. Diagnostic studies for evaluation of myocarditis
Diagnostic Study Findings
Basic Tests
EKG Sinus tachycardia, atrioventricular and intraventricular blocks, ventricular tachycardia,
nonspecifi c ST-segment/T-wave changes, prolonged QT interval
ST-segment elevation and depression
Chest radiograph Normal
Cardiomegaly with clear lung fi elds
Pulmonary edema
Redistribution of blood fl ow (cephalization)
Interstitial edema
Alveolar edema
Pleural and pericardial effusions
Right ventricular failure
Right atrial enlargement
Prominent azygos vein
Superior vena cava enlargement
Serum cardiac markers
(troponin and CPK)
Elevation
Other laboratory tests Infl ammation (ESR, CRP, platelet count, WBC), multiorgan failure (AST/ALT, creatinine),
poor systemic perfusion (lactate)
Echocardiogram Multichamber dilatation, reduced left ventricular ejection fraction, pericardial fl uid, wall
motion hypokinesis (focal or global)
Additional Tests
Cardiac MRI Diffuse infl ammation, involves epicardial surface preferentially, can distinguish myocarditis
from AMI
Nuclear medicine imaging Indium-111: detects diffuse myocardial necrosis. Used with resting stress thallium showing
normal perfusion, can rule out AMI in favor of myocarditis
Viral/serologic testing Low yield, not helpful in the ED
Coronary angiography Normal coronary vessels
Endomyocardial biopsy Dallas Criteria: lymphocytic infi ltration with myocyte injury or death
Abbreviations: AST/ALT, aspartate aminotransferase/alanine aminotransferase; CPK, creatine phosphokinase;
CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; WBC, white blood cell count; ED, emergency
department.
CHAPTER 15
218
same leads in which ST-elevations had been present in
Stage One), followed by normalization of inversions
and return to baseline in Stage Four. The progression
through the various stages is variable and unpredict-
able, taking days to weeks. One may also see low
voltage and electrical alternans if a large pericardial
effusion is present.
When patients present with myopericarditis, their
EKGs are more typical of acute pericarditis, and
evolve through four stages. Stage One is notable for
generalized ST-segment elevation and PR depression
(Figure 15-3), followed by resolution of these changes
and T-wave fl attening in Stage Two. Stage Three is
characterized by T-wave inversion (usually in the
Figure 15.1 Extreme sinus tachycardia.
Figure 15.2 Myocarditis with complete heart block.
MYOCARDITIS
219
Echocardiography can be helpful, but is often nei-
ther specifi c nor diagnostic. It can be used to document
the presence of a pericardial effusion (uncommon in
acute myocarditis, more common in pericarditis),
ventricular systolic dysfunction (generally global, but
may be segmental), decreased ejection fraction, and
multichamber enlargement. Specifi c fi ndings on echo
include increased echogenicity/brightness of the peri-
cardium due to fi brin deposition and infl ammation of
the pericardial layers.
3
Left ventricular thrombi are
often seen. Additionally, right ventricle (RV) systolic
dysfunction is an independent predictor of death or
need for cardiac transplantation in acute myocardi-
tis.
31
This test is becoming increasingly available in
EDs as more emergency physicians perform bed-
side echocardiograms. A limited or focused bedside
echocardiogram can assess the presence or absence of
a pericardial effusion, as well as global left ventricular
function.
32–34
An additional imaging modality, cardiac MRI, has
the advantage of being able to distinguish a myo-
cardial infarction from myocarditis. The myocardial
infarction pattern involves enhancement of the sub-
endocardium, which becomes transmural in severe
cases, since necrosis begins in the subendocardium
and extends towards the epicardium. It is also limited
Chest radiography in myocarditis patients may be
entirely normal or show cardiac enlargement, pul-
monary venous blood fl ow redistribution, intersti-
tial and alveolar edema, and pleural and pericardial
effusions.
25
The chest radiograph may show a normal
cardiac silhouette with pulmonary edema. The X-ray
fi ndings of right ventricular failure include right atrial
enlargement, prominent azygos vein, and superior
vena cava enlargement. A normal chest radiograph,
however, does not exclude the diagnosis.
26
Laboratory abnormalities include elevations of
cardiac enzymes, which have been reported in both
myocarditis and pericarditis. Elevations in cardiac
troponin are more common than CK-MB in biopsy-
proven myocarditis.
27,28
The degree of troponin eleva-
tion seems to be related to the extent of myocardial
infl ammation, and does not carry an adverse prognosis
as it does in ACS.
29,30
Despite this, troponin levels may
be normal in half of the patients with biopsy-proven
myocarditis.
27,28
The white blood cell count, platelet
count, Erythrocyte Sedimentation Rate (ESR), and
C-Reactive Protein (CRP) are non-specifi c markers
of infl ammation, and are often elevated. An elevated
serum lactate can confi rm poor perfusion in a patient
in cardiogenic shock, and elevated transaminases and
serum creatinine are found in multiple organ failure.
Figure 15.3 Myopericarditis.
CHAPTER 15
220
present in only 5–30% of patients with a clinically
suspected myocarditis, 41% of patients with an acute
dilatated cardiomyopathy, and up to 63% of patients
with a chronic dilatated cardiomyopathy. Patients
who have virus present on biopsy tissue have a much
worse prognosis.
47
Molecular genetic probes, such as polymerase chain
reaction (PCR), are used to supplement endomyocar-
dial biopsy. The preferred biopsy method is a trans-
venous endomyocardial biopsy of the right ventricular
septum, which carries a 1/250 risk of perforation,
and 1/1000 risk of death when performed with expe-
rienced hands.
48
Given the risks of biopsy and lim-
ited benefi ts, it tends to be used selectively in patients
with signifi cant myocardial involvement and severe
left ventricular dysfunction who are not responsive to
conventional medical management, for example prior
to cardiac transplantation.
49,50
Treatment of myocarditis
The treatment of acute myocarditis in the ED is gener-
ally supportive, and includes stabilization of abnor-
mal vital signs and the treatment of acute congestive
heart failure. There is general consensus for bed rest,
and avoidance of physical activity for these patients
since exercise can worsen dysrthymias.
8
These patients
should all be placed in a monitored bed where aggres-
sive resuscitation can be carried out, as nontoxic
patients may deteriorate rapidly. Additionally, myo-
carditis patients show more ectopy at rest, and are at
high risk for dysrhythmias. Immediate interventions
required may range from providing supplemental
oxygenation to securing an airway with endotracheal
intubation and mechanical ventilation. Perfusion sta-
tus needs to be evaluated, and if inadequate, increas-
ing preload with small fl uid boluses of normal saline,
and the use of vasopressors and inotropic support
may be required. Acute pulmonary edema should be
treated in the standard manner, assuming the patient
is not hypotensive. Use of preload agents such as
nitroglycerin (oral, topical, or parenteral) and intra-
venous furosemide is encouraged. Afterload reducers
may be used if the patient is hypertensive: angiotensin
converting enzyme inhibitors (orally or parenterally).
The bedside echocardiogram looking for the presence
of a pericardial effusion may be invaluable in certain
cases, as a large pericardial effusion or signs of tam-
ponade on echocardiography can signal the need for
to coronary perfusion territory. Acute myocarditis, on
the other hand, involves the epicardium, the mid-wall
of the left ventricular free wall, and the intraventricu-
lar septum.
35,36
The MRI abnormalities can persist for
at least 1 month after the onset of symptoms. Overall
diagnostic sensitivity is 86% with 95% specifi city in
one study.
37
An MRI may be diffi cult to obtain through
the ED, and is not suitable in the unstable patient or
in a patient with ferromagnetic contraindications.
Nuclear medicine imaging is another specialized
diagnostic modality. Gallium-67, one type of nuclear
medicine imaging, is considered to be an excellent
imaging study for chronic infl ammation, but is not
specifi c for an acute myocarditis.
5
However, its use
has decreased over time due to a lack of specifi city.
With Indium-111, antimyosin antibodies bind specifi -
cally to exposed myosin in damaged myocytes, and
in one study this test has a sensitivity of 100% and
specifi city of 58%.
38
It can be used to detect ongo-
ing myocardial necrosis in myocarditis, acute MI,
dilatated cardiomyopathy, and cardiac transplanta-
tion rejection.
39
Antimyosin scans, used together with
resting thallium imaging, can distinguish myocarditis
from acute MI. Acute myocarditis is suggested when
antimyosin scans show myocardial infl ammation in
the presence of normal perfusion on thallium scans.
40
Viral titers can be helpful, but the yield is low, and
not helpful to the emergency physician in the acute
phase of illness.
41
A small proportion of patients show
a signifi cant rise in titers for Coxsackie B virus, and
a fourfold rise in enteroviral IgG titers over a 4-week
period helps identify an acute viral infection.
42
In clinical cases where ACS is a major differential
or strong consideration, coronary angiography can be
useful to exclude ACS, as the young acute myocardi-
tis patient would be expected to have no clinically
signifi cant occlusions. Endomyocardial biopsy has
been considered to be the “gold standard,” but even
it has variable specifi city and sensitivity and is avail-
able only at specialized centers.
43
It was pioneered by
Richardson at King’s College Hospital (London) in
1974.
44
The Dallas Criteria for the histological diag-
nosis of myocarditis were introduced in 1986, and the
biopsy specimen criteria specifi es lymphocytic infi ltra-
tion associated with myocyte injury in the absence
of ischemia.
45
Unfortunately, it underestimates the
incidence of myocarditis because of patchy involve-
ment of the myocardium and large intraobserver
variability.
45,46
Histologic criteria for myocarditis are
MYOCARDITIS
221
The use of corticosteroids in the setting of viral
myocarditis has been found to be an independent
risk factor for recurrences, since they promote viral
replication, and therefore, they are not generally
recommended.
58,59
A Cochrane review shows no evi-
dence of benefi t from use of corticosteroids for viral
myo carditis.
60
Nevertheless, there are case reports that
show a benefi t in postvaccinal myocarditis and infl am-
matory myopathy-related myocarditis, which are both
thought to be autoimmune mediated.
61–64
Specifi c therapies in certain populations
Patients with Lyme myocarditis may require atropine,
isoproterenol, and cardiac pacing for treatment of con-
duction abnormalities. Antibiotic therapy is also indi-
cated (ceftriaxone, tetracycline, or erythromycin). A
tapering course of corticosteroids is also recommended.
Children with Kawasaki disease will require high-dose
aspirin therapy, as well as treatment with intravenous
gamma globulin.
Prognosis
The clinical course of myocarditis is variable, and
the prognosis is diffi cult to determine upon initial
presentation. The majority of patients recover within
weeks to months following diagnosis.
8,65
Most of the
survivors are symptom-free, and do not require fur-
ther medical care; some need ongoing medical ther-
apy, and a proportion of those will require cardiac
transplantation.
An initial presentation involving acute CHF or
dysrhythmias portends a higher mortality. In these
patients, the 1-year mortality ranges between 15 and
20%; at 4 years, mortality rates of 50% are found
despite optimal management in the NIH myocarditis
trial.
66
The ejection fraction and RV function 1 year
after presentation may be the best predictor of subse-
quent survival.
54
Some patients develop a fulminant,
rapidly progressing form of myocarditis. Prognostic
factors associated with a fulminant course of myo-
carditis include prolongation of QRS complex and
depressed left ventricular ejection fraction. These fac-
tors predict inhospital mortality of 45%.
67
A clinicopathologic classifi cation was developed
by Lieberman et al.
68
subdividing patients into differ-
ent disease course categories and prognosis based on
the biopsy and clinical presentation. Four categories
acute intervention with pericardiocentesis. Additional
measures, such as correcting anemia, treating dys-
rhythmias, and reducing fevers, can help by decreas-
ing myocardial oxygen demand.
For those patients presenting in extremis and car-
diogenic shock, aggressive cardiac and pulmonary
resuscitation measures can be life saving. In addi-
tion to the measures mentioned above, these patients
may require ventricular assist devices, intraaortic
balloon counterpulsation and even cardiopulmonary
bypass as a bridge while awaiting recovery or car-
diac transplantation. These devices have been used
successfully over extended periods of time (up to 70
days), allowing time for some patients to recover
without the need for cardiac transplantation.
51
The
decision to initiate heparin therapy is controversial,
needs to be individualized to each patient, and is
usually made by the consultant cardiologist follow-
ing the results of a bedside echocardiogram. On the
one hand, myocarditis patients have compromised
left ventricular function and are at higher risk for
thromboembolic complications. On the other hand,
they are also at risk for hemopericardium with car-
diac tamponade.
High dose gamma globulin (IVIG) therapy
Additional therapies may be utilized in patients once
they have been admitted; they generally do not have
a role in the acute resuscitation in the ED. These
include immunologic agents (including antiviral
agents), immunosuppressants, and immunoglobulin.
Antiviral agents have been utilized in the early stage
of acute myocarditis following studies showing repli-
cating enterovirus RNA in the myocardium.
52,53
There
is some evidence of benefi t in uncontrolled studies
using immunosuppressive therapy in the later stages
of myocarditis, but the National Institutes of Health
(NIH)-sponsored multicenter trial for myocarditis
treatment does not establish benefi t in using immu-
nosuppressive therapy; however, using cyclosporine
or azathioprine has been studied in a pediatric pop-
ulation, and is associated with improvement in LV
function and increased survival after a year.
20,53–55
Nevertheless, a systematic review concludes there is
insuffi cient data to recommend routine IVIG therapy
in patients with acute myocarditis, and another sys-
temic review shows no benefi t to immunosuppresive
therapy in children.
56,57
CHAPTER 15
222
respiratory or gastrointestinal symptoms, and it takes
an astute clinician to tease out historical features of
CHF (exertional dyspnea, nonproductive cough,
weakness). Abnormal vital signs, especially tachycar-
dia, are red fl ags, and patients (especially infants and
children) with tachycardia out of proportion to fever
should be suspected of having myocarditis.
The differential diagnosis in these patients includes
acute coronary syndrome (unstable angina or acute
MI), acute pulmonary edema, pulmonary embolism,
pneumonia, aortic dissection, and esophageal rup-
ture. Even if the diagnosis is correctly and appropri-
ately considered, the next challenge in these patients
is to differentiate myocarditis from ACS, as both
sets of patients may have severe chest pain, EKG
changes, elevated cardiac biomarkers, and conges-
tive heart failure. Features that may distinguish myo-
carditis from ischemia include younger age and an
absence of risk factors for coronary artery disease.
The EKG abnormalities in myocarditis are often dif-
fuse, rather than limited to coronary anatomy. They
should also not evolve with ongoing chest pain,
as one may expect with ACS. Echocardiographic
abnormalities are often global, rather than segmen-
tal as seen in ACS.
69
Nevertheless, the EKG fi ndings
in myocarditis may be localized to coronary artery
anatomy, and the echocardiography may show
segmental wall-motion abnormalities, making dif-
ferentiation of myocarditis from ACS very diffi cult
clinically.
70
Normal coronary angiography in the presence of
an elevated cardiac troponin should prompt consider-
ation of myocarditis rather than coronary vasospasm.
Up to 78% of patients who present with possible
ACS, and who have a normal coronary angiogram,
have evidence of myocarditis on further imaging.
40
Antimyosin scintigraphy (Indium-111 scanning) can
be employed. Myocarditis is characterized by a faint,
diffuse uptake of antimyosin antibody caused by
widespread myocardial necrosis. In contrast, acute
MI is seen as an intense, localized uptake of antibody
in the region of the occluded artery. A normal antimy-
osin scan excludes both acute MI and myocarditis.
71
When used with the results of a normal resting per-
fusion scan, a positive antimyosin scan is diagnostic
of acute myocarditis. If there is still clinical doubt, a
cardiac MRI and an endomyocardial biopsy may be
employed.
are described: fulminant, acute, chronic active, and
chronic persistent.
Fulminant: these patients have abrupt onset of 1
symptoms and usually present with cardiogenic
shock and pulmonary edema. Disease progression
is rapid, with either a full recovery or death within
30 days. Endomyocardial biopsy typically shows
widespread infl ammation with necrosis.
Active: these patients have a less distinct onset 2
of symptoms, with gradual progression and slow
recovery. They often have persistent left ventricular
dysfunction, and some patients develop dilatated
cardiomyopathy. Biopsy shows infl ammation with
scattered necrosis.
Chronic active: onset of symptoms is indistinct and 3
there is a slow progressive course leading to dilatated
cardiomyopathy and LV dysfunction. Biopsy typi-
cally shows a lesser degree of infl ammation.
Chronic persistent: these patients have atypical or 4
few symptoms, and minimal or no LV dysfunction.
Biopsy shows a mild persistent infl ammation.
Disposition of patients with myocarditis
All patients with suspected myocarditis should be
admitted to a monitored hospital bed; in most cases,
this should be a critical care unit. Invasive monitor-
ing with central venous catheters, arterial line cath-
eters, and pulmonary artery catheters may be required,
depending on the clinical status of the patient and
whether vasopressors and inotropic medications are
required. A multispecialty approach to these patients
is often needed, and consultations from critical care,
cardiology, cardiovascular surgery, and infectious dis-
ease physicians should be obtained at the discretion of
the admitting physician. Complications of myocarditis
include ventricular dysrhythmia, LV dysfunction, and
cardiac failure.
Summary
The fi rst major challenge is to consider myocarditis in
the differential diagnosis of these patients, especially
if the patient is young and previously healthy. These
patients will be seen intermixed with the large num-
bers of patients being evaluated for chest pain or viral
syndrome, and it is easy to overlook the possibility of
myocarditis in the differential diagnosis. Additionally,
these patients often have pronounced infectious
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Section IV: Decision making
There are three major pitfalls clinicians should try to
avoid:
Failure to seek the diagnosis in a patient presenting •
with mainly infectious symptoms or new onset
CHF in an otherwise young or healthy patient in
the setting of a viral syndrome.
Failure to admit to the hospital a well-appearing •
patient with suspected myocarditis, instead
arranging an outpatient follow-up and testing. This
occurs when the clinician does not appreciate the
rapid downhill course some myocarditis patients
can take when complications develop, which can
include dysrhythmias, thromboembolism, and
cardiogenic shock.
Administering the wrong therapy: giving a •
myocarditis patient thrombolytics for an EKG
with a pseudoinfarction pattern. This could be
potentially catastrophic, as these patients are at
higher risk for hemopericardium and tamponade.
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