Myocarditis

Zainal Safri, MD, FIHA / Refli Hasan,

MD, FIHA
Dept. Cardiology, Fac. of Medicine USU
Adam Malik Hospital
Myocarditis :
defined as inflammatory
changes in
the heart muscle and is
characterized by myocyte
necrosis.
 Background
Myocarditis is collection of diseases of infectious,
toxic, and autoimmune etiologies characterized by
inflammation of the heart. Subsequent myocardial
destruction can lead to dilated cardiomyopathy.

Myocarditis : the clinical presentation may range from

nearly asymptomatic to overt heart failure requiring
transplantation, and it is occasionally the
unrecognized culprit in cases of sudden death .
 Sex and Age
Sex
The male-to-female ratio is 1.5 : 1
Age
The average age of patients with
myocarditis is 42 years. It is a
prominent cause of sudden cardiac
death in young adults, accounting
for 8-12% of such deaths.
 Clinical Manifestations
An antecedent viral syndrome is present in more than
one half of patients with myocarditis.
Fever is present in 20% of patients.
Other symptoms include fatigue, myalgias and
arthralgias, and malaise.
Chest pain
Chest discomfort is reported in 35% of patients.
The pain is most commonly described as a pleuritic,
sharp, stabbing precordial pain.
It may be substernal and squeezing and, therefore,
difficult to distinguish from that typical of ischemic
pain.
Dyspnea on exertion is common.
 Clinical Manifestations
Orthopnea and shortness of breath at rest may be
noted if CHF is present.
Palpitations are common. Syncope in a patient with a
presentation consistent with myocarditis should be
carefully approached because it may signal high-
grade atrioventricular (AV) block or risk for sudden
death.
Pediatric patients, particularly infants, present with
nonspecific symptoms, including the following:
Respiratory distress
Poor feeding or, in cases with CHF, sweating while
feeding
Cyanosis in severe cases
 Physical Examinations
Physical findings can range from nearly
normal examination findings to signs of
fulminant CHF.
Patients with mild cases of myocarditis have

a non- toxic appearance and simply may

appear to have a viral syndrome.
Tachypnea and tachycardia are common.

Tachycardia is often out of proportion to fever.

More acutely ill patients have signs of

circulatory impairment due to left

ventricular failure.
 Physical Examinations
A widely inflamed heart shows the classic
signs of ventricular dysfunction including
the following:
Jugular venous distention
Bibasilar crackles
Ascites
Peripheral edema
S3 or a summation gallop may be noted
with significant biventricular involvement.
Intensity of S1 may be diminished.
Cyanosis may occur.
 Physical Examinations
Hypotension caused by left ventricular
dysfunction is uncommon in the acute setting
and indicates a poor prognosis when present.
Murmurs of mitral or tricuspid regurgitation
may be present due to ventricular dilation.
In cases where a dilated cardiomyopathy has
developed, signs of peripheral or pulmonary
thromboembolism may be found.
Diffuse inflammation may develop leading to
pericardial effusion, without tamponade, and
pericardial and pleural friction rub as the
inflammatory process involves surrounding
structures.
 Causes (1)
The causes of myocarditis are
numerous and can be roughly
divided into:
infectious,
toxic, and

immunologic etiologies, with viral

etiologies.
 Causes (2)
Amongst the infectious causes, viral acute
myocarditis is by far the most common .

Identification of the coxsackie-adenovirus receptor protein

explains the prevalence of these viruses as a frequent
cause. The receptor is the common target of coxsackievirus
B

Other viruses implicated in myocarditis include influenza

virus, echovirus, herpes simplex virus, varicella-zoster
virus, hepatitis, Epstein-Barr virus, and cytomegalovirus.
Hepatitis C

Human immunodeficiency virus (HIV) deserves special

mention because it seems to function differently than other
viruses. Although some evidence indicates that HIV directly
invades myocytes
 Causes (3)
Toxic myocarditis has a number of etiologies
including both medical agents and environmental
agents.
Among the most common drugs that cause
hypersensitivity reactions are clozapine, penicillin,
ampicillin, hydrochlorothiazide, methyldopa, and
sulfonamide drugs.
Numerous medications has been associated with
myocarditis.eg, lithium, doxorubicin, cocaine, numerous
catecholamines, acetaminophen) may exert a direct
cytotoxic effect on the heart. Zidovudine (AZT)
Environmental toxins include arsenic, and carbon
monoxide. Cases have been attributed to Chinese sumac.
Wasp, scorpion, and spider stings
Radiation therapy may cause a myocarditis with the
development of a dilated cardiomyopathy.
 Causes (4)
Immunologic etiologies
Connective tissue disorders such as
systemic lupus erythematosus (SLE),
rheumatoid arthritis, scleroderma, and
dermatomyositis

Idiopathic inflammatory and infiltrative

disorders such as Kawasaki disease,
sarcoidosis, and giant cell arteritis
 Lab Studies
Cardiac enzyme levels
These levels are only elevated in a minority of patients.
Normally, a characteristic pattern of slow elevation
and fall over a period of days occurs; however, a more
abrupt rise is observed in patients with acute
myocardial infarction.
Cardiac troponin I may be more sensitive
because it is present for longer periods after
myocardial damage from any cause.2
Erythrocyte sedimentation rate (ESR) is elevated
in 60% of patients with acute myocarditis.
Leukocytosis is present in 25% of cases.
 Imaging Studies (1)
Chest radiography
A chest radiograph often reveals a
normal cardiac silhouette, but
pericarditis or overt clinical CHF is
associated with cardiomegaly.
Vascular redistribution

Interstitial and alveolar edema

Pleural effusion
Myocarditis Infectious/Inflammatory
 Other Test (2)
Electrocardiography
Sinus tachycardia is the most frequent finding.
ST-segment elevation without reciprocal depression,
particularly when diffuse, is helpful in differentiating
myocarditis from acute myocardial infarction.
Decreased QRS amplitude and transitory Q-wave
development is very suggestive of myocarditis.
As many as 20% of patients will have a conduction
delay, including Mobitz I, Mobitz II, or complete
heart block.
Left or right bundle-branch block is observed in
approximately 20% of abnormal ECG findings and
may persist for months.
 Imaging Studies (2)
Echocardiography
Impairment of left ventricular systolic and
diastolic function
Segmental wall motion abnormalities

Impaired ejection fraction

A pericardial effusion may be present,

although findings of tamponade are rare.

Ventricular thrombus has been identified in

15% of patients studied with

echocardiography.
 Imaging Studies (3)
MRI is capable of showing abnormal signal
intensity in the affected myocardium.
Cardiac MRI is an emerging field in general, and
contrast-enhanced T1- weighted MRI has been
shown to have sensitivities and specificities
approaching 100% for diagnosis.3
MRI can demonstrate nodular and patchy areas of
inflammation, often seen first in the lateral and
inferior wall and can be used to guide later biopsy.
MRI is also one of the modalities used in the
evaluation of young patients with apparently
idiopathic dysrhythmias, and this imaging study
can differentiate focal and diffuse inflammation
from the rare electrically significant myocardial
tumor.
 Other Test (4)
Viral isolation from other body sites may be
supportive of the diagnosis.
Polymerase chain reaction (PCR) identification of
a viral infection from myocardial tissue,
pericardial fluid, or other body fluid sites can be
helpful. Persistent viral genome, as detected by
PCR, has been identified as one marker of
increased incidence of dilated cardiomyopathy
and mortality.
If a systemic disorder (eg, SLE) is suspected,
antinuclear antibody (ANA) and other collagen
vascular disorder laboratory investigations may be
useful.
 Medication
Medical therapy for myocarditis is an
area of avid research interest but with
little success in human trials.

Treatment primarily involves

managing the complications of
myocarditis

thromboembolism, dysrhythmia, and

CHF
 Drug Category
Angiotensin converting enzyme
inhibitors. Ex : Captopril.
Calcium channel blockers. Ex. :
Amlodipine
Loop diuretics. Ex. : Furosemide
(Lasix).
Cardiac glycosides. Ex. : Digoxin
Beta-adrenergic blockers. Ex. :
Carvedilol
 Complications
Congestive heart failure
Pulmonary edema
Cardiogenic shock

Cardiac failure

Dilated cardiomyopathy
Dysrhythmias
Recurrent myositis
 Prognosis (1)
Most cases are believed to be
clinically silent and resolve
spontaneously without sequelae
Patients who present with CHF
experience morbidity and mortality
based on the degree of left ventricular
dysfunction.
Of patients who present with
cardiogenic shock, elderly patients
and patients with giant cell arteritis
have a poor prognosis.
 Prognosis (2)
Patients with HIV and persistent viral
genome expression from myocytes have
dismal outcomes.
Patients who require transplantation have
an increased risk of recurrent myocarditis
and graft rejection.
 Clinical Manifestations
Many patients present with a nonspecific illness
characterized by fatigue, mild dyspnea, and myalgias. A few
patients present acutely with fulminant congestive heart
failure (CHF)

Small and focal areas of inflammation in electrically sensitive

areas may be the etiology in patients whose initial
presentation is sudden death.

Most cases of myocarditis are subclinical; therefore, the

patient rarely seeks medical attention during acute illness.
These subclinical cases may have transient ECG
abnormalities.

The appearance of cardiac-specific symptoms occurs

primarily in the subacute virus-clearing phase; therefore,
patients commonly present 2 weeks after the acute viremia.