Eosinophilic myocarditis is inflammation in the heart muscle that is caused by the infiltration and destructive activity of a type of white blood cell, the eosinophil. Typically, the disorder is associated with hypereosinophilia, i.e. an eosinophil blood cell count greater than 1,500 per microliter (normal 100 to 400 per microliter). It is distinguished from non-eosinophilic myocarditis, which is heart inflammation caused by other types of white blood cells, i.e. lymphocytes and monocytes, as well as the respective descendants of these cells, NK cells and macrophages. This distinction is important because the eosinophil-based disorder is due to a particular set of underlying diseases and its preferred treatments differ from those for non-eosinophilic myocarditis.[1][2]
Eosinophilic myocarditis is often viewed as a disorder that has three progressive stages. The first stage of eosinophilic myocarditis involves acute inflammation and cardiac cell necrosis (i.e. areas of dead cells); it is dominated by symptoms characterized as the acute coronary syndrome such as angina, heart attack and/or congestive heart failure. The second stage is a thrombotic stage wherein the endocardium (i.e. interior wall) of the diseased heart forms blood clots which break off, travel in, and block blood through systemic or pulmonary arteries; this stage may dominate the initial presentation in some individuals. The third stage is a fibrotic stage wherein scarring replaces damaged heart muscle tissue to cause a clinical presentation dominated by a poorly contracting heart and cardiac valve disease.[3][4][5] Perhaps less commonly, eosinophilic myocarditis, eosinophilic thrombotic myocarditis, and eosinophilic fibrotic myocarditis are viewed as three separate but sequentially linked disorders in a spectrum of disorders termed eosinophilic cardiac diseases.[1] The focus here is on eosinophilic myocarditis as a distinct disorder separate from its thrombotic and fibrotic sequelae.
Eosinophilic myocarditis is a rare disorder. It is usually associated with, and considered secondary to, an underlying cause for the pathological behavior of the eosinophils such a toxic reaction to a drug (one of its more common causes in developed nations), the consequence of certain types of parasite and protozoan infections (a more common cause of the disorder in areas with these infestations), or the result of excessively high levels of activated blood eosinophils due to a wide range of other causes.[6] The specific treatment (i.e. treatment other than measures to support the cardiovascular system) of eosinophilic myocarditis differs from the specific treatment of other forms of myocarditis in that it is focused on relieving the underlying reason for the excessively high numbers and hyperactivity of eosinophils as well as on inhibiting the pathological actions of these cells.[6][7][8]
^Rose NR (2016). "Viral myocarditis". Current Opinion in Rheumatology. 28 (4): 383–9. doi:10.1097/BOR.0000000000000303. PMC 4948180. PMID 27166925.
^Diny NL, Rose NR, Čiháková D (2017). "Eosinophils in Autoimmune Diseases". Frontiers in Immunology. 8: 484. doi:10.3389/fimmu.2017.00484. PMC 5406413. PMID 28496445.
^Cheung CC, Constantine M, Ahmadi A, Shiau C, Chen LY (2017). "Eosinophilic Myocarditis". The American Journal of the Medical Sciences. 354 (5): 486–492. doi:10.1016/j.amjms.2017.04.002. PMID 29173361. S2CID 205476783.
^Li H, Dai Z, Wang B, Huang W (2015). "A case report of eosinophilic myocarditis and a review of the relevant literature". BMC Cardiovascular Disorders. 15: 15. doi:10.1186/s12872-015-0003-7. PMC 4359588. PMID 25887327.
^ abSohn KH, Song WJ, Kim BK, Kang MK, Lee SY, Suh JW, Yoon YE, Kim SH, Youn TJ, Cho SH, Chang YS (2015). "Eosinophilic myocarditis: case series and literature review". Asia Pacific Allergy. 5 (2): 123–7. doi:10.5415/apallergy.2015.5.2.123. PMC 4415178. PMID 25938077.
^Kuchynka P, Palecek T, Masek M, Cerny V, Lambert L, Vitkova I, Linhart A (2016). "Current Diagnostic and Therapeutic Aspects of Eosinophilic Myocarditis". BioMed Research International. 2016: 1–6. doi:10.1155/2016/2829583. PMC 4738989. PMID 26885504.
^Grimaldi A, Mocumbi AO, Freers J, Lachaud M, Mirabel M, Ferreira B, Narayanan K, Celermajer DS, Sidi D, Jouven X, Marijon E (2016). "Tropical Endomyocardial Fibrosis: Natural History, Challenges, and Perspectives". Circulation. 133 (24): 2503–15. doi:10.1161/CIRCULATIONAHA.115.021178. PMID 27297343. S2CID 29931.
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