myocarditis

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MYOCARDITIS Magdy El-Masry Prof. of Cardiology Tanta University

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Page 1: Myocarditis

MYOCARDITIS

Magdy El-MasryProf. of Cardiology

Tanta University

Page 2: Myocarditis

Layers of the Heart Muscle

Page 4: Myocarditis

Myocarditis is an inflammatory disease of the myocardium

caused by different infectious and noninfectious triggers

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Acute Viral Myocarditis

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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

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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.

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New England Journal of Medicine 343:1391 2000

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PATHOPHYSIOLOGY OF MYOCARDITISTHE DOMINO EFFECT

Viral Infection

Inflammation and Injury

Decreased Myocardial Contractility

Heart Enlarges: LVEDV

Cardiac Output

Sympathetic Tone

CHF

LAP

Pulm.edema

Scarring

Dysrhythmias

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Myocarditis represents a clinically and pathogenetically highly variable disease entity.

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Diagnosis Myocarditis is a challenging diagnosis due to

the heterogeneity of clinical presentations.

Clinical presentationMyocarditis 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

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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.

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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

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Inflammatory markersESR 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

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ECG in MyocarditisECG 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. 

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Myocarditis mimicking acutemyocardial 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

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Chest Radiograph

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•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

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Echocardiogram

Echocardiogram markedly dilated heart with ejection fraction

of 15 %, mural thrombus was present

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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

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Fulminant myocarditis

Acute myocarditis

Fulminant myocarditis is characterized by moreextensive and diffuse lympocytic infiltration and myocyte necrosis than acute myocarditis

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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.

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Endomyocardial Biopsy

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

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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

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Endomyocardial biopsy is limited today

to fulminant cases,

to cases with conduction disturbances andmalignant arrhythmias to rule out giant cell myocarditis, and

to cases unresponsive to standard anti-failure therapy

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

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

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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

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When is a heart attack not a heart attack ?

Viral myocarditis may have various clinical presentations, sometimes mimicking acute myocardial infarction or ischaemia.

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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 extensivemyocardial oedema in the inferior and inferolateral segments of the left ventricle. (B) extensive enhancement of mid-wall and epicardium with sparing of the subendocardium.

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MRI can also play a role in discriminating myocarditis frommyocardial 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.

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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

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* 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

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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.

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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 .

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Acute myocarditis presents multiple challenges in diagnosis and treatment.

Conclusions

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Acute Viral Myocarditis

Heart Failure

Complete Recovery

No Symptoms

Chronic DilatedCardiomyopathy

Dysrhythmias/ConductionDisorders

Sudden Death

Clinical Presentation of Myocarditis

Have a high clinical suspicion, if we don’t think of it, we won’t dx it

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Time course of viral myocarditis in 3 phases