Etiology
- Acute inflam of the myocardium
- Coxsackie or adenoviral infection – MCC
- Streptococcus, diphtheria, CMV, lyme disease, Polio, toxoplasmosis
- HIV
- Chagas disease due Trypanosoma cruzi – edemic in South America
- Drugs that cause hypersensitivity reaction – methyldopa, penicillin
- Autoimmune
Pathogenesis
- Acute phase – heart is flabby with focal haemorrhages
- Chronic phase – heart is enlarged and hypertrophied
- Histology – inflammatory infiltrate
- Lymphocytes – in viral etiology
- PMNLs – in bacterial Etiology (neutrophils)
- Eosinophils – in allergic/HSR etiologies
Clinical features
- Fulminant Myocarditis – follows viral/flu-like prodrome. Results in severe HF or cardiogenic shock
- Acute MC – presents over a longer period with HF. It can lead to dilated cardiomyopathy
- Chronic active MC – rare. Associated with chronic myocardial inflam
- Chronic persistent MC – characterised by focal myocardial infiltrates. Causes chest pain and arrhythmia
- cardiomyopathy
Signs
- prominent S3
- tachycardia
- pericardial friction rub
Diagnosis
- CXR – heart enlargement
- ECG – ST + T wave abnormalities. Arrhythmias. Heart block (diphtheria)
- Elevated troponins (cardiac muscle damage) – diagnostic if no signs of myocardial infarction
- Endomyocardial biopsy – to confirm diagnosis
Treatment
- In most pts it is self-limiting with good prognosis
- Treat underlying cause – antibiotics (broad spec)
- Bed rest and avoidance of physical activities
- Treat HF – diuretics, ACEi/ARBs, BB, spironolactone
- Treat arrhythmias
- NSAIDs contraindicated in acute phase
Giant cell Myocarditis
- Severe form of Myocarditis
- Characterised by present of multinucleated giant cells within myocardium
- Cause is unknown
- May be associated with sarcoidosis, thymomas and autoimmune disease
- Rapidly progressive with poor prognosis