Internal Diseases and Therapy · MU Sofia

19. Myocardial diseases: myocarditis

Covers the definition of myocarditis and its place in the inflammatory myopericardial spectrum, then the wide range of causes grouped by type, from viral and bacterial to toxic and drug-related. It goes on to pathogenesis, histological classification with the Dallas and immunohistochemical criteria, clinical presentations and special forms such as giant cell, sarcoid and checkpoint inhibitor myocarditis. Diagnosis covers ECG patterns, laboratory tests, imaging including Lake Louise criteria, and biopsy indications, followed by treatment, complications and prognostic factors.

Inside: 8 sections · 2 labelled pictures · 4 tables · 16 flashcards · 12 min

Topic 19 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 8 sections, about 1,312 words (12 min of reading), with 16 flashcards.

In this note

  1. Definition
  2. Etiology
  3. Pathogenesis
  4. Clinical features
  5. Diagnosis
  6. Treatment
  7. Complications
  8. Prognosis

Definition

Myocarditis is inflammation of the heart muscle with myocyte injury, proven by histology, immunohistochemistry or cardiac magnetic resonance (CMR), and not caused by ischaemia.

  • Inflammatory cardiomyopathy: myocarditis with ventricular dysfunction and remodelling (it can evolve into dilated cardiomyopathy).
  • Inflammatory myopericardial syndrome (European Society of Cardiology, ESC 2025): the spectrum from pure pericarditis through myopericarditis (mainly pericarditis, with myocardial involvement) and perimyocarditis (mainly myocarditis, with pericardial involvement) to pure myocarditis. Pericarditis is covered in topic 18.
  • Incidence about 10–20 per 100,000 per year, probably underestimated (many cases are mild). Mostly young adults, men about twice as often; an important cause of sudden cardiac death in young people and athletes.

Pathogenesis

Viral myocarditis is the model; three phases overlap:

  1. Acute phase (days): the virus enters the myocytes (enteroviruses and adenoviruses through the coxsackie–adenovirus receptor; parvovirus B19 infects endothelial cells) → direct cell damage and innate immune response (cytokines, natural killer cells, macrophages).
  2. Subacute phase (weeks): adaptive immune response with T cells and antibodies; autoimmunity against cardiac proteins (e.g. myosin) through molecular mimicry. In most patients the virus is cleared and inflammation settles.
  3. Chronic phase (months): in some, inflammation or viral genome persists → myocyte loss, fibrosis and remodelling → dilated cardiomyopathy.
  • Non-viral forms are driven by hypersensitivity (eosinophils), autoimmunity (giant cells, granulomas) or direct toxicity.

Histological classification

H&E micrograph of active lymphocytic myocarditis: a lymphocyte in the inflammatory infiltrate (white arrow) next to a necrotic, hypereosinophilic myocyte (black arrow).

Image: “Histopathology of lymphocytic myocarditis with myocyte necrosis, annotated” by Mikael Häggström , M.D. Author info - Reusing images - Conflicts of interest: None Mikael Häggström , M.D. Consent note , CC0, via Wikimedia Commons.

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