Prof. of Cardiology
Layers of the Heart Muscle
Inflammatory Disorders of the Heart
Myocarditis is an inflammatory
disease of the myocardium
caused by different infectious and
Acute Viral Myocarditis
Viruses That Have Been Shown to
• Less Common
Herpes simplex virus type 1
Respiratory syncytial virus
Endomyocardial biopsy in acute myocarditis:
Arrow shows a collection of lymphocytes infiltrating the cardiac
muscle in response to a viral infection.
The arrowhead shows an area of cardiac muscle damage induced by
the virus directly or to the cytotoxic immune response to the viral infection.
New England Journal of Medicine 343:1391 2000
Pathophysiology of myocarditis
The domino effect
Inflammation and Injury
Decreased Myocardial Contractility
Heart Enlarges: LVEDV
Myocarditis represents a clinically and
pathogenetically highly variable disease entity.
Myocarditis is a challenging diagnosis due to
the heterogeneity of clinical presentations.
Myocarditis presents in many different ways, ranging from
mild symptoms of chest pain and palpitations associated
with transient ECG changes to life-threatening cardiogenic
shock and ventricular arrhythmia
Signs and symptoms
• Chest pain (often described as "stabbing" in character).
• CHF(leading to edema,breathlessness and hepatic congestion).
• Palpitations (due to arrhythmias).
• Sudden death (in young adults, myocarditis causes up to 20% of all
cases of sudden death).
• Fever (especially when infectious)
• Since myocarditis is often due to a viral illness, many patients give a
history of symptoms consistent with a recent viral
infection, including fever, diarrhea, joint pains, and easy
• Myocarditis is often associated with pericarditis, and many patients
present with signs and symptoms that suggest concurrent
ECG- Non-specific T-wave abnormalities
CK-MB and Troponin may be elevated
Chest X-Ray- Variable (Normal to Cardiomegaly)
Cardiovascular Magnetic Resonance
A safe and sensitive noninvasive diagnostic test to confirm the
diagnosis is not available
• Endomyocardial biopsy- there are risks and not used for every
case but is definitive for myocarditis
ESR and CRP levels are often raised in myocarditis, but they do not
confirm the diagnosis and are often increased in acute pericarditis
While cardiac troponins are more sensitive of myocyte
injury in patients with clinically suspected myocarditis than
creatine kinase levels, they are non-specific and when
normal do not exclude myocarditis.
ECG in Myocarditis
ECG changes can be variable and include
•QRS / QT prolongation
•Diffuse T wave inversion
•AV conduction defects
•With inflammation of the adjacent pericardium, ECG
features of pericarditis can also been seen
NB. The most common abnormality seen in myocarditis is
sinus tachycardia with non-specific ST segment and T wave
Myocarditis mimicking acute
Occasionally, a pseudo infarct pattern
and ischemic changes are seen.
ST segment elevation is commonly
seen, but ST segment depression,T
wave inversion, poor R wave
progression,and Q waves have also
•Echocardiography helps to rule out non-inflammatory
cardiac disease such as valve disease and to monitor
changes in cardiac chamber size, wall thickness, ventricular
function, and pericardial effusions.
• Global ventricular dysfunction, regional wall motion
abnormalities,and diastolic dysfunction with preserved EF
may occur in myocarditis.
• Histologically proven myocarditis may resemble dilated,
hypertrophic, and restrictive cardiomyopathy and can
mimic ischaemic heart disease.
markedly dilated heart
with ejection fraction
of 15 %, mural
thrombus was present
Echocardiographic Findings in
Fulminant and Acute Myocarditis
Fulminant myocarditis often presents with a non-dilated, thickened,
and hypocontractile left ventricle as the intense inflammatory response
results in interstitial oedema and loss of ventricular contractility
Fulminant myocarditis is characterized by more
extensive and diffuse lympocytic infiltration and
myocyte necrosis than acute myocarditis
The diagnosis of myocarditis made based
on clinical , laboratory , ECG , and echo
findings is not always easy.
The gold standard in
myocarditis is still the
RV - EMB : The technique (jugular approach)
Histological Dallas criteria defined as follows:
histological evidence of inflammatory infiltrates within
the myocardium associated with myocyte degeneration
and necrosis of nonischaemic origin
Endomyocardial biopsy is limited today
cases with conduction disturbances and
malignant arrhythmias to rule out giant cell
cases unresponsive to standard anti-failure
MRI is emerging as an important
tool for the diagnosis and followup of patients with acute
Cine images are shown in diastole and systole and
suggest absence of any wall motion abnormality
T2-weighted edema images
demonstrate the presence of
patchy focal edema in the
subepicardium of the
T1-weighted LGE images
distributed LGE which
is typical for acute
MRI can also play a role in discriminating myocarditis from
myocardial infarction, which can help in the evaluation of acute
In myocarditis the infiltrates are characteristically located in the
mid-wall and tend to spare the sub-endocardium,whereas in
infarction, the sub-endocardium is involved first.
When is a heart attack
not a heart attack?
Viral myocarditis may have various
clinical presentations, sometimes
mimicking acute myocardial
infarction or ischaemia.
Disproportionate thickening, increased
echogenicity, and dyskinesis of the
inferolateral wall relative to the septum;
findings are consistent with tissue edema.
Diffuse ST-segment elevation in precordial
and limb leads. Hyperacute T waves are seen
in leads V2 and V3
(A) asymmetric thickening
consistent with extensive
myocardial oedema in the
inferior and inferolateral
segments of the left ventricle.
(B) extensive enhancement of
mid-wall and epicardium with
sparing of the
Acute myocarditis resolves in about 50% of cases in the
first 2–4 weeks, but about 25% will develop persistent
cardiac dysfunction and 12–25% may acutely deteriorate
and either die or progress to end-stage DCM with a need
for heart transplantation.
The core principles of treatment in myocarditis are
optimal care of arrhythmia and of heart failure
* Patients with LV dysfunction or symptomatic HF
should follow current HF therapy
guidelines, including diuretics and ACE inhibitors
*Beta-blockers can be used cautiously in the acute
*Digoxin should be avoided in patients suffering
from acute HF induced by viral myocarditis
Diet and Lifestyle
• Restrict salt intake to 2-3g of sodium per day
• Exercise especially during the acute phase of
virus myocarditis enhances viral replication
rate, enhances immune mechanisms and
increases inflammatory lesions and necrosis.
Resumption of physical activity can take place
within 2 months of the acute disease.
Investigational treatment options.
Because mechanism-based therapy of myocarditis is not
proven, different approaches have been investigated in
clinical studies in recent years.
More than 20 treatment trials have been reported,
using immunosuppressive, immunomodulating, or
antiinflammatory agents as well as immunoadsorption
Acute myocarditis presents multiple
challenges in diagnosis and treatment.
Clinical Presentation of Myocarditis
Acute Viral Myocarditis
Have a high clinical suspicion, if we don’t think of it, we won’t dx