7. Viruses That Have Been Shown to
Cause Myocarditis
• Common
–
–
–
–
Coxsackievirus A
Coxsackievirus B
Echovirus
Human immunodeficiency
virus
– Influenza
• Less Common
–
–
–
–
–
–
–
–
–
Adenovirus family
Arbovirus
Epstein-Barr virus
Herpes simplex virus type 1
Human cytomegalovirus
Measles virus
Respiratory syncytial virus
Rubella virus
Varicella-zoster virus
8. EMB
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.
12. Diagnosis
Myocarditis is a challenging diagnosis due to
the heterogeneity of clinical presentations.
Clinical presentation
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
13. 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
fatigueability.
• Myocarditis is often associated with pericarditis, and many patients
present with signs and symptoms that suggest concurrent
14. Diagnostic Tests
•
•
•
•
•
•
ECG- Non-specific T-wave abnormalities
CK-MB and Troponin may be elevated
Chest X-Ray- Variable (Normal to Cardiomegaly)
Echocardiogram
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
15. Biomarkers
Inflammatory markers
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.
16. ECG in Myocarditis
ECG changes can be variable and include
•Sinus tachycardia
•QRS / QT prolongation
•Diffuse T wave inversion
•Ventricular arrhythmias
•AV conduction defects
•With inflammation of the adjacent pericardium, ECG
features of pericarditis can also been seen
( myopericarditis
NB. The most common abnormality seen in myocarditis is
sinus tachycardia with non-specific ST segment and T wave
changes
17. Myocarditis mimicking acute
myocardial infarction:
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
been described
19. Echocardiography
•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.
21. Echocardiographic Findings in
Fulminant and Acute Myocarditis
Fulminant myocarditis
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
23. The diagnosis of myocarditis made based
on clinical , laboratory , ECG , and echo
findings is not always easy.
Endomyocardial biopsy
The gold standard in
diagnosis of
myocarditis is still the
EMB.
25. Viral myocarditis:
Histological Dallas criteria defined as follows:
histological evidence of inflammatory infiltrates within
the myocardium associated with myocyte degeneration
and necrosis of nonischaemic origin
26. Endomyocardial biopsy is limited today
to
fulminant cases
cases with conduction disturbances and
malignant arrhythmias to rule out giant cell
myocarditis
cases unresponsive to standard anti-failure
therapy
27. MRI is emerging as an important
tool for the diagnosis and followup of patients with acute
myocarditis
28. Cine images are shown in diastole and systole and
suggest absence of any wall motion abnormality
29. T2-weighted edema images
demonstrate the presence of
patchy focal edema in the
subepicardium of the
inferolateral wall
T1-weighted LGE images
demonstrate presence
of subepicardially
distributed LGE which
is typical for acute
myocarditis.
30. MRI can also play a role in discriminating myocarditis from
myocardial infarction, which can help in the evaluation of acute
chest pain.
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.
31.
32. When is a heart attack
not a heart attack?
Viral myocarditis may have various
clinical presentations, sometimes
mimicking acute myocardial
infarction or ischaemia.
33. 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
subendocardium.
34. Treatment
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
35. Treatment
* Patients with LV dysfunction or symptomatic HF
should follow current HF therapy
guidelines, including diuretics and ACE inhibitors
or ARBs
*Beta-blockers can be used cautiously in the acute
setting.
*Digoxin should be avoided in patients suffering
from acute HF induced by viral myocarditis
36. 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.
37. 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
therapy
39. Clinical Presentation of Myocarditis
Acute Viral Myocarditis
No Symptoms
Chronic Dilated
Cardiomyopathy
Heart Failure
Dysrhythmias/
Conduction
Disorders
Complete Recovery
Sudden Death
Have a high clinical suspicion, if we don’t think of it, we won’t dx
