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PH-CV16

Myocarditis

How viruses, toxins, parasites, medicines and the immune system inflame and kill heart muscle cells, why troponin rises and the ECG changes, and how myocarditis heals, kills suddenly or leaves a dilated, failing heart.

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  • 5 steps · 9 questions
  • 3D normal anatomy

By the end, you can

  • Explain how viruses such as coxsackie B reach and enter heart muscle cells, and how the immune response both clears them and injures the muscle.
  • Describe the infiltrate with muscle cell necrosis that defines myocarditis (the Dallas criteria) and contrast lymphocytic, giant cell and eosinophilic myocarditis.
  • Explain how diphtheria toxin, Trypanosoma cruzi, immune checkpoint inhibitors and mRNA vaccines can each cause myocarditis.
  • Relate muscle cell injury and inflammation to chest pain, troponin release, ECG changes, arrhythmias and heart failure, and explain how myocarditis can lead to dilated cardiomyopathy.
  • Recognise the exam detail of myocarditis, including MRI and biopsy findings, and explain how each main treatment acts on the mechanism.

What it is

Myocarditis is inflammation of the heart muscle with injury to its muscle cells that is not caused by ischaemia. Viruses are the commonest recognised cause; bacterial toxins, parasites, medicines, vaccines and autoimmune disease cause the rest. It ranges from a silent illness to sudden death, and it can heal completely or leave a dilated, weak heart (post-myocarditic or inflammatory dilated cardiomyopathy).

5 types to tell apart
Lymphocytic (usually viral)
T lymphocytes and macrophages beside dying muscle cells; the commonest pattern.
Giant cell myocarditis
Rare, autoimmune and rapidly progressive: widespread necrosis with multinucleated giant cells and no granulomas.
Eosinophilic myocarditis
Eosinophils damage the muscle and endocardium: drug hypersensitivity, hypereosinophilic syndromes, eosinophilic granulomatosis with polyangiitis, parasites.
Toxin- and parasite-related
Diphtheria toxin stops protein synthesis in heart cells; Trypanosoma cruzi causes acute and, years later, chronic Chagas heart disease.
By course
Fulminant (sudden shock), acute, or chronic (inflammation that persists for months).

US spelling: ischaemia → ischemia, fibres → fibers.

Normal function

Heart muscle that cannot be replaced

The is the thick muscular layer of the heart wall, covered on the outside by the and lined on the inside by the . Its muscle cells are joined into a network that contracts as one, and beneath the endocardium the spread each impulse through the ventricles. Branches of the coronary arteries feed a dense capillary network between the cells.

Heart muscle cells work continuously, cannot divide and have no reserve of spare cells. Those that die are replaced by scar, so injury shows quickly as weaker contraction or a disturbed rhythm, and lost muscle does not grow back.

The cells are packed with contractile proteins, including cardiac troponins T and I, forms found only in heart muscle. Troponin stays inside healthy cells; when a cell membrane is damaged it leaks into the blood, which makes it a sensitive marker of heart muscle injury from any cause.

Point to it on the model