Clinical Pathology · MU Sofia

55. Myocarditis: classification, pathomorphology.

Covers inflammation of the heart muscle, opening with its typical symptoms such as breathlessness, stabbing chest pain and arrhythmias. It then sets out infectious and non-infectious causes, with the non-infectious forms split into hypersensitivity and giant cell types, and Chagas myocarditis noted as infectious. The pathomorphology section describes gross and microscopic changes by stage, with a labelled H&E micrograph and a short list linking each infiltrate pattern to its cause. It ends with diagnostic markers and treatment options.

Inside: 1 section · 1 labelled picture · 15 flashcards · 2 min

Topic 55 of 138 in the MU Sofia syllabus for Clinical Pathology (Medicine, Year 4). The free AceMed note covers it in 1 section, about 386 words (2 min of reading), with 15 flashcards.

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  1. Myocarditis: classification, pathomorphology

Myocarditis: classification, pathomorphology

Also known as inflammatory cardiomyopathy, it is inflammation of the heart muscle. Symptoms include shortness of breath, chest pain (stabbing in nature), decreased exercise tolerance, and arrhythmias. In infectious causes fever is also common.

Etiology and Classification

Most commonly caused by viral infections (adenovirus, parvovirus, coxsackie virus, rubella, Epstein-Barr, HIV), but other causes include bacteria (Brucella, corynebacterium diphtheria, haemophilus influenzae), protozoan (Trypanosoma cruzi) and Fungal (Aspergillus). Non infectious causes include drugs (alcohol, clozapine), and autoantigens.

These two etiologies, give it its classification, infectious and non-infectious. Non-infectious myocarditis can be further broken down to hypersensitivity myocarditis and Giant cell myocarditis (Chagas myocarditis is infectious).

Pathomorphology

The mechanism sees the infiltration of the heart tissue by pro-inflammatory blood cells, causing an inflammatory response in the myocardium. Morphologically the heart may appear normal or dilated in the acute stages, in advanced stages the myocardium appears flabby and mottled with pale and hemorrhagic areas.

Microscopically, the myocarditis can be seen to be edematous, with inflammatory cell infiltrates. After resolution, if the patient survives, the myocardium can survive without significant dysfunction.

H&E, lymphocytic (viral-type) myocarditis: interstitial lymphocytes (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.

In non-infectious cases of myocarditis, the cellular infiltrates are dominated by lymphocytes, macrophages and a high proportion of eosinophils (giant cell myocarditis has many multinucleated giant cells).

Remember: the infiltrate points to the cause:

  • Viral (classically Coxsackie B): lymphocytes with focal myocyte necrosis
  • Hypersensitivity (drugs): perivascular lymphocytes, macrophages and many eosinophils
  • Giant cell myocarditis: multinucleated giant cells and widespread necrosis, poor prognosis
  • Chagas disease: T. cruzi parasites inside myocytes with mixed inflammation

Diagnosis and Treatment

Diagnosis is based on ECG and/or C-reactive protein and/or erythrocyte sedimentation rate and/or biopsy and/or MRI showing increased (late) uptake of contrast in inflamed or scarred areas. Markers of myocardial damage are also elevated (troponin, CK). Basically, looking for evidence of inflammation AND myocardial damage.

Treatment is supportive in viral form. Digoxin and diuretics may help in acute stage (reduce heart work), ACE inhibitors may also be used. Systemic corticosteroids may or may not be beneficial. Where drugs do not work, surgery is indicated.

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