What are the causes of myocarditis?

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Last updated: October 19, 2026 • View editorial policy

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Causes of Myocarditis

Myocarditis results from myocardial infection and/or autoimmunity causing active inflammatory destruction of myocytes, with a wide spectrum of infectious agents (viruses, bacteria, chlamydia, rickettsia, fungi, protozoans) and non-infectious triggers (toxic exposures, hypersensitivity reactions, autoimmune processes) as etiologic factors 1.

Infectious Causes

Viral Etiologies (Most Common in Western Countries)

In North America and Western Europe, viral infections are the most commonly identified causes of myocarditis 2.

  • Most frequent viral pathogens in Western Europe:

    • Parvovirus B19
    • Human herpes virus 6
    • Enteroviruses (Coxsackie B) - particularly important in acute and fulminant myocarditis
    • Adenoviruses 1, 2

  • Other viral causes:

    • HIV - causes myocarditis through multiple mechanisms: cardiotoxicity with cellular apoptosis induced by viral glycoprotein 120, opportunistic infections, autoimmune response, drug-related cardiac toxicity, and nutritional deficiencies 1
    • SARS-CoV-2 (COVID-19) 3
    • Approximately 2 dozen viruses have been linked to myocarditis overall 2

Important clinical note: Coinfection with ≥2 viruses occurs in a substantial minority of cases 2.

Bacterial and Other Infectious Agents

  • Bacteria - including Borrelia burgdorferi (Lyme carditis, affecting 0.3-8% of infected patients) 4
  • Fungi
  • Protozoa - notably Trypanosoma cruzi (Chagas disease, common in Central and South America) 4
  • Metazoa
  • Spirochetes
  • Rickettsia 1, 4, 1, 4

Regional Variations in Infectious Causes

Geographic location significantly influences etiology 2:

  • Chagas disease - important cause in Central and South America
  • Poststreptococcal rheumatic heart disease - specific world regions
  • Diphtheria - case series from Afghanistan and India
  • Typhoid fever, rubella, scorpion bite - reported from regions of Asia

Clinical pearl: A careful travel and exposure history is essential for evaluating unexplained cardiomyopathy 2.

Non-Infectious Causes

Toxic Exposures

Drugs and chemicals causing myocarditis:

  • Cardiotoxic medications: Adriamycin, cyclophosphamide
  • Drugs of abuse: Heroin, cocaine, amphetamines, alcohol
  • Other toxins: Sulfonamides, lead, arsenic, cobalt, phosphorus, ethylene glycol 5
  • Radiation exposure 4

Hypersensitivity Reactions

Drug-induced hypersensitivity myocarditis is increasingly recognized, particularly with:

  • Immune checkpoint inhibitor therapies - emerging as important causes 6
  • Various medications triggering allergic/hypersensitivity responses 1

Autoimmune and Inflammatory Disorders

Collagen vascular diseases:

  • Systemic lupus erythematosus
  • Rheumatoid arthritis
  • Systemic sclerosis
  • Polyarteritis nodosa
  • Hypersensitivity vasculitis
  • Takayasu syndrome
  • Polymyositis
  • Reiter's syndrome 5

Specific autoimmune entities:

  • Giant cell myocarditis - aggressive, noninfectious autoimmune disorder that is rapidly fatal without advanced heart failure treatment and multidrug immunosuppression 2
  • Cardiac sarcoidosis - often affects the heart without clinical evidence of extracardiac disease 2
  • Kawasaki disease 2

Metabolic and Endocrine Disorders

  • Nutritional deficiencies: Protein, thiamine, selenium, L-carnitine
  • Electrolyte disorders: Hypocalcemia, hypophosphatemia, hyponatremia, hypokalemia
  • Endocrine diseases: Diabetes, thyroid disease (both hypo- and hyperthyroidism), hypoparathyroidism with hypocalcemia, pheochromocytoma, acromegaly 5

Other Causes

  • Tachycardia-induced: Incessant supraventricular tachyarrhythmias or atrial fibrillation with rapid ventricular rates
  • Peripartum cardiomyopathy
  • Hypereosinophilic syndrome
  • Sleep apnea syndrome
  • Whipple's disease 5

Pathophysiologic Mechanisms

The pathogenesis involves complex interplay between:

  1. Direct viral invasion - though SARS-CoV-2 mRNA is found largely in pericytes and subendothelium, not cardiac myocytes 3
  2. Host inflammatory/immune responses - maladaptive immune response with excessive innate immune pathway activation, proinflammatory cytokine surge, deregulated thromboinflammation 3
  3. Autoimmune processes - molecular mimicry, pathogenic autoantibodies, genetic susceptibility 6, 7
  4. Microvascular angiopathy - thrombotic microangiopathy, endothelial dysfunction 3

Critical distinction: Most viral myocarditis does NOT show diffuse lymphocytic infiltration or confluent myocyte necrosis typical of classic viral myocarditis; instead, it demonstrates increased CD68+ macrophage/monocytic infiltration, endothelialitis, microvascular dysfunction, and individual cell necrosis 3.

Clinical Implications

Risk factors for myocardial injury vary by etiology:

  • COVID-19 myocardial injury: Advanced age, male sex, underlying cardiovascular disease, obesity, diabetes mellitus, hypertension, immunosuppression, severe systemic disease 3
  • Classic viral myocarditis: Male predominance (68% in SARS-CoV-2 series), younger age 3

Prognostic consideration: Viral persistence after acute disease can be detected from heart biopsy samples in chronic dilated cardiomyopathy settings, though clinical trials are ongoing to determine if antiviral treatment impacts outcomes 2.

References

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