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  1. 1. MYOCARDITIS Magdy El-Masry Prof. of Cardiology Tanta University
  2. 2. Layers of the Heart Muscle
  3. 3. Inflammatory Disorders of the Heart • Endocarditis • Pericarditis • Myocarditis
  4. 4. Myocarditis is an inflammatory disease of the myocardium caused by different infectious and noninfectious triggers
  5. 5. Acute Viral Myocarditis
  6. 6. 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
  7. 7. 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.
  8. 8. New England Journal of Medicine 343:1391 2000
  9. 9. 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
  10. 10. Myocarditis represents a clinically and pathogenetically highly variable disease entity.
  11. 11. 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
  12. 12. 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
  13. 13. 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
  14. 14. 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.
  15. 15. 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
  16. 16. 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
  17. 17. Chest Radiograph
  18. 18. 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.
  19. 19. Echocardiogram Echocardiogram markedly dilated heart with ejection fraction of 15 %, mural thrombus was present
  20. 20. 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
  21. 21. Fulminant myocarditis Acute myocarditis Fulminant myocarditis is characterized by more extensive and diffuse lympocytic infiltration and myocyte necrosis than acute myocarditis
  22. 22. 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.
  23. 23. RV - EMB : The technique (jugular approach)
  24. 24. 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
  25. 25. 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
  26. 26. MRI is emerging as an important tool for the diagnosis and followup of patients with acute myocarditis
  27. 27. Cine images are shown in diastole and systole and suggest absence of any wall motion abnormality
  28. 28. 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.
  29. 29. 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.
  30. 30. When is a heart attack not a heart attack? Viral myocarditis may have various clinical presentations, sometimes mimicking acute myocardial infarction or ischaemia.
  31. 31. 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.
  32. 32. 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
  33. 33. 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
  34. 34. 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.
  35. 35. 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
  36. 36. Conclusions Acute myocarditis presents multiple challenges in diagnosis and treatment.
  37. 37. 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
  38. 38. Time course of viral myocarditis in 3 phases