MYOCARDITIS
Magdy El-Masry
Prof. of Cardiology
Tanta University
Layers of the Heart Muscle
Inflammatory Disorders of the Heart
• Endocarditis
• Pericarditis
• Myocarditis
Myocarditis is an inflammatory
disease of the myocardium
caused by different infectious and
noninfectious triggers
Acute Viral Myocarditis
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
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
Viral Infection
Inflammation and Injury
Decreased Myocardial Contractility
Heart Enlarges:  LVEDV
 Cardiac Output
 Sympathetic Tone
CHF
 LAP
Pulm.
edema
Scarring
Dysrhythmias
Myocarditis represents a clinically and
pathogenetically highly variable disease entity.
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
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.
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
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.
Biomarkers
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
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
Chest Radiograph
•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.
Echocardiography
Echocardiogram
Echocardiogram
markedly dilated heart
with ejection fraction
of 15 %, mural
thrombus was present
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
Fulminant myocarditis
Acute myocarditis
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.
Endomyocardial biopsy
The gold standard in diagnosis of
myocarditis is still the EMB.
Endomyocardial Biopsy
RV - EMB : THE TECHNIQUE (jugular approach)
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
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
MRI is emerging as an important tool
for the diagnosis and follow-up of
patients with acute myocarditis
cine-SSFP images are shown in diastole and systole
and suggest absence of any wall motion abnormality
T1-weighted LGE images
demonstrate presence of
subepicardially distributed
LGE which is typical for
acute myocarditis.
T2-weighted edema images
demonstrate the presence of
patchy focal edema in the
subepicardium of the
inferolateral wall
When is a heart attack
not a heart attack?
Viral myocarditis may have various
clinical presentations, sometimes
mimicking acute myocardial
infarction or ischaemia.
Diffuse ST-segment elevation in precordial and
limb leads. Hyperacute T waves are seen
in leads V2 and V3
Disproportionate thickening, increased
echogenicity, and dyskinesis of the
inferolateral wall relative to the septum;
findings are consistent with tissue edema.
(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.
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.
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
* 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
Treatment
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.
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
Investigational treatment options.
Acute myocarditis presents multiple
challenges in diagnosis and treatment.
Conclusions
Acute Viral Myocarditis
Heart Failure
Complete Recovery
No Symptoms
Chronic Dilated
Cardiomyopathy
Dysrhythmias/
Conduction
Disorders
Sudden Death
Clinical Presentation of Myocarditis
Have a high clinical suspicion, if we don’t think of it, we won’t dx
Time course of viral myocarditis in 3 phases

Myocarditis

  • 1.
    MYOCARDITIS Magdy El-Masry Prof. ofCardiology Tanta University
  • 2.
    Layers of theHeart Muscle
  • 3.
    Inflammatory Disorders ofthe Heart • Endocarditis • Pericarditis • Myocarditis
  • 4.
    Myocarditis is aninflammatory disease of the myocardium caused by different infectious and noninfectious triggers
  • 6.
  • 7.
    Viruses That HaveBeen 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 inacute 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 Journalof Medicine 343:1391 2000
  • 10.
    PATHOPHYSIOLOGY OF MYOCARDITIS THEDOMINO EFFECT Viral Infection Inflammation and Injury Decreased Myocardial Contractility Heart Enlarges:  LVEDV  Cardiac Output  Sympathetic Tone CHF  LAP Pulm. edema Scarring Dysrhythmias
  • 11.
    Myocarditis represents aclinically and pathogenetically highly variable disease entity.
  • 12.
    Diagnosis Myocarditis is achallenging 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.
    Inflammatory markers ESR andCRP 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. Biomarkers
  • 16.
    ECG in Myocarditis ECGchanges 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 myocardialinfarction: 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.
  • 19.
    •Echocardiography helps torule 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. Echocardiography
  • 20.
    Echocardiogram Echocardiogram markedly dilated heart withejection fraction of 15 %, mural thrombus was present
  • 21.
    Echocardiographic Findings in Fulminantand 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 Fulminantmyocarditis is characterized by more extensive and diffuse lympocytic infiltration and myocyte necrosis than acute myocarditis
  • 23.
    The diagnosis ofmyocarditis 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.
  • 25.
    RV - EMB: THE TECHNIQUE (jugular approach)
  • 26.
    Viral myocarditis: *N.B. establishedhistological 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 islimited 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 emergingas an important tool for the diagnosis and follow-up of patients with acute myocarditis
  • 29.
    cine-SSFP images areshown in diastole and systole and suggest absence of any wall motion abnormality
  • 30.
    T1-weighted LGE images demonstratepresence of subepicardially distributed LGE which is typical for acute myocarditis. T2-weighted edema images demonstrate the presence of patchy focal edema in the subepicardium of the inferolateral wall
  • 32.
    When is aheart attack not a heart attack? Viral myocarditis may have various clinical presentations, sometimes mimicking acute myocardial infarction or ischaemia.
  • 33.
    Diffuse ST-segment elevationin precordial and limb leads. Hyperacute T waves are seen in leads V2 and V3 Disproportionate thickening, increased echogenicity, and dyskinesis of the inferolateral wall relative to the septum; findings are consistent with tissue edema. (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 alsoplay 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 resolvesin 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.
    * Patients withLV 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 Treatment
  • 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.
    Because mechanism-based therapyof 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 Investigational treatment options.
  • 39.
    Acute myocarditis presentsmultiple challenges in diagnosis and treatment. Conclusions
  • 40.
    Acute Viral Myocarditis HeartFailure Complete Recovery No Symptoms Chronic Dilated Cardiomyopathy Dysrhythmias/ Conduction Disorders Sudden Death Clinical Presentation of Myocarditis Have a high clinical suspicion, if we don’t think of it, we won’t dx
  • 42.
    Time course ofviral myocarditis in 3 phases