Myocarditis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S.
Pathophysiology of Myocarditis
Myocarditis is inflammation of myocardium resulting in cardiac dysfunction and arrhythmais. Using animal models, Liu PP and Mason JW explained that myocarditis is a continuum of 3 distinct disease processes with one evolving into the other[1]:
- Phase I: Viral infection and replication
- Viruses such as coxsackie and enterovirus, gets internalized in peripheral tissues and initiate immune system activation. Few of these viral genomes harbor on to the immunologic cells which circulate throughout the body and are thus seeded to other target organs such as heart where they further replicate and cause tissue destruction.
- Phase II: Autoimmune injury
- Host immune system eliminates the viral genomes from the body and promote recovery. However, sometimes immune system remain active even after elimination of virus. This leads to development of autoimmune reaction where the T-cells and the cytokines targets the host tissue which causes further myocyte damages.
- Phase III: Dilated cardiomyopathy
- Cytokines which are produced in reaction to infection and cell death, is the leading cause of dilated cardiomyopathy. Matrix metalloproteinases, such as gelatinase, collagenases, and elastases may be activated by cytokines during the autoimmune phase[2][3]. Protease produced by coxsackie virus can also modify the sarcoglycan complex in myocytes[4] leading to ventricular dilation.
References
- ↑ Liu PP, Mason JW (2001). "Advances in the understanding of myocarditis". Circulation. 104 (9): 1076–82. PMID 11524405.
- ↑ Ono K, Matsumori A, Shioi T, Furukawa Y, Sasayama S (1998). "Cytokine gene expression after myocardial infarction in rat hearts: possible implication in left ventricular remodeling". Circulation. 98 (2): 149–56. PMID 9679721.
- ↑ Lee JK, Zaidi SH, Liu P, Dawood F, Cheah AY, Wen WH; et al. (1998). "A serine elastase inhibitor reduces inflammation and fibrosis and preserves cardiac function after experimentally-induced murine myocarditis". Nat Med. 4 (12): 1383–91. doi:10.1038/3973. PMID 9846575.
- ↑ Badorff C, Lee GH, Lamphear BJ, Martone ME, Campbell KP, Rhoads RE; et al. (1999). "Enteroviral protease 2A cleaves dystrophin: evidence of cytoskeletal disruption in an acquired cardiomyopathy". Nat Med. 5 (3): 320–6. doi:10.1038/6543. PMID 10086389.