Eosinophilic myocarditis

Eosinophilic myocarditis is

• Clonal hypereosinophilia.^{[1][4][7][10]}
• Chronic eosinophilic leukemia.^{[1][4][7][10]}
• The idiopathic hypereosinophilic syndrome.^[4][7][10]

Secondary conditions that may lead to eosinophilic myocarditis are:

• Infections agents:^{[4][6][8][11][12][13][14][15][16]}
  • Parasitic worms: various Ascaris, Strongyloides, Schistosoma, filaria, Trematoda, and Nematode species. Parasitic infestations often cause significant heart valve disease along with myocarditis and the disorder in this setting is sometimes termed Tropical endomyocardial fibrosis. While commonly considered to be due to the cited parasites, this particular form of eosinophilic myocarditis may more often develop in individuals with other disorders, e.g. malnutrition
    , dietary toxins, and genetic predisposition, in addition to or in place of round worm infestation.
  • Infections by protozoa: various Toxoplasma gondii, Trypanosoma cruzi, trichinella spiralis, Entamoeba, and Echinococcus species.
  • Viruses: While some viral infections (e.g. HIV
    ) have been considered causes of eosinophilic endocarditis, a study of 20 patients concluded that viral myocarditis lacks the characteristic of eosinophil-induced damage in hearts taken during cardiac transplantation.
• Allergic and autoimmune diseases such as severe
  transplanted hearts.^[4][7]
• Malignancies and/or premalignant hematologic conditions not due to a primary disorder in eosinophils such as
  myelofibrosis, chronic myelomonocytic leukemia, and T-lymphoblastic leukemia/lymphoma-associated or myelodysplastic–myeloproliferative syndrome-associated eosinophilias; IgG4-related disease and Angiolymphoid hyperplasia with eosinophilia as well as non-hematologic cancers such as solid tumors of the lung, gastrointestinal tract, and genitourinary tract.^[7]
• Hypersensitivity reactions to agents include:^{[7][11][17][18][19]}
  • Antibiotics/anti-viral agents: various
    4-aminosalicylic acid), linezolid, amphotericin B, chloramphenicol, streptomycin, dapsone, nitrofurantoin, metronidazole, nevirapine, efavirenz, abacavir, nevirapine
    .
  • valproic acid, carbamazepine, desipramine, fluoxetine, amitriptyline, olanzapine
    .
  • indomethacin, phenylbutazone, oxyphenbutazone, acetazolamide, piroxicam, diclofenac
    .
  • Diuretics: hydrochlorothiazide, spironolactone, chlortalidone
    .
  • ACE inhibitors: captopril, enalapril
    .
  • Other drugs: digoxin, ranitidine, lenalidomide, methyldopa, interleukin 2, dobutamine, acetazolamide.
  • Contaminants: Unidentified contaminants in
    L-tryptophan, cause the eosinophilia–myalgia syndrome
    .
  • Tetanus toxoid, smallpox, and diphtheria/pertussis/tetanus
    vaccinations.

• Infectious agents: specific drug treatment of helminth and protozoan infections typically takes precedence over non-specific immunosuppressive therapy, which, if used without specific treatment, could worsen the infection. In moderate-to-severe cases, non-specific immunosuppression is used in combination with specific drug treatment.
• Toxic reactions to ingested agents: discontinuance of the ingested agent plus corticosteroids or other non-specific immunosuppressive regimens.
• Clonal eosinophilia caused by mutations in genes that are highly susceptible to
  bone marrow transplantation
  , may be useful for treating the FGFR1 mutations.
• Clonal hypereosinophilia due to mutations in other genes or primary malignancies: specific treatment regimens used for these pre-malignant or malignant diseases may be more useful and necessary than non-specific immunosuppression.
• Allergic and autoimmune diseases: non-specific treatment regimens used for these diseases may be useful in place of a simple corticosteroid regimen. For example, eosinophilic granulomatosis with polyangiitis can be successfully treated with mepolizumab.
• Idiopathic hypereosinphilic syndrome and lymphocyte-variant hypereosinophilia: corticosteroids; for individuals with these hypereosinophilias that are refractory to or break through corticosteroid therapy and individuals requiring corticosteroid-sparing therapy, recommended alternative drug therapies include
  tyrosine kinase inhibitors
  viz., imatinib and mepolizumab).

Prognosis

The prognosis of eosinophilic myocarditis is anywhere from rapidly fatal to extremely chronic or non-fatal. Progression at a moderate rate over many months to years is the most common prognosis.^[1][9] In addition to the speed of inflammation-based heart muscle injury, the prognosis of eosinophilc myocarditis may be dominated by that of its underlying cause. For example, an underlying malignant cause for the eosinophilia may be survival-limiting.^[6][9]

History

In 1936, the famed Swiss physician