1. MYOCARDITIS
Magdy El-Masry
Prof. of Cardiology
Tanta University

2. Layers of the Heart Muscle

3. Inflammatory Disorders of the Heart
• Endocarditis
• Pericarditis
• Myocarditis

4. Myocarditis is an inflammatory
disease of the myocardium
caused by different infectious and
noninfectious triggers

6. Acute Viral Myocarditis

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. 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.

9. New England Journal of Medicine 343:1391 2000

10. PATHOPHYSIOLOGY OF MYOCARDITIS
THE DOMINO EFFECT
Viral Infection
Inflammation and Injury
Decreased Myocardial Contractility
Scarring
Heart Enlarges:  LVEDV
 LAP
 Cardiac Output
Dysrhythmias

Sympathetic Tone
CHF
Pulm.
edema

11. Myocarditis represents a clinically and
pathogenetically highly variable disease entity.

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
myocarditis and pericarditis.

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 Resonace
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 nonspecific 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

18. Chest Radiograph

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.

20. Echocardiogram
Echocardiogram
markedly dilated heart
with ejection fraction
of 15 %, mural
thrombus was present

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

22. Fulminant myocarditis
Acute myocarditis
Fulminant myocarditis is characterized by more
extensive and diffuse lympocytic infiltration and
myocyte necrosis than acute myocarditis

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.

24. Endomyocardial Biopsy

25. RV - EMB : THE TECHNIQUE (jugular approach)

26. Viral myocarditis:
*N.B. established histological Dallas
criteria defined as
follows:histological evidence of inflammatory infiltrates within the
myocardium associated with myocyte degeneration and necrosis of
nonischaemic origin

27. Endomyocardial biopsy is limited today
to fulminant cases,
to cases with conduction disturbances and
malignant arrhythmias to rule out giant cell
myocarditis, and
to cases unresponsive to standard anti-failure
therapy

28. MRI is emerging as an important tool
for the diagnosis and follow-up of
patients with acute myocarditis

29. cine-SSFP images are shown in diastole and systole
and suggest absence of any wall motion abnormality

30. 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.

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. 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.

35. 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

36. 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

37. 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.

38. 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. Conclusions
Acute myocarditis presents multiple
challenges in diagnosis and treatment.

40. 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

42. Time course of viral myocarditis in 3 phases