Myocarditis pathophysiology: Difference between revisions
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==Pathophysiology of Myocarditis== | ==Pathophysiology of Myocarditis== | ||
Myocarditis is a continuum of three phases of the disease processes with each one evolving into the next<ref name="pmid11524405">{{cite journal| author=Liu PP, Mason JW| title=Advances in the understanding of myocarditis. | journal=Circulation | year= 2001 | volume= 104 | issue= 9 | pages= 1076-82 | pmid=11524405 | doi= | pmc= | url= }} </ref>: | |||
===Phase I: Viral infection and replication=== | ===Phase I: Viral infection and replication=== | ||
Viruses such as [[coxsackie virus|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=== | ===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=== | ===Phase III: Dilated cardiomyopathy=== | ||
Cytokines which are produced in reaction to infection and cell death, is the leading cause of [[dilated cardiomyopathy]]. Matrix [[metalloproteinase]]s, such as gelatinase, [[collagenase]]s, and [[elastase]]s may be activated by [[cytokines]] during the autoimmune phase<ref name="pmid9679721">{{cite journal| author=Ono K, Matsumori A, Shioi T, Furukawa Y, Sasayama S| title=Cytokine gene expression after myocardial infarction in rat hearts: possible implication in left ventricular remodeling. | journal=Circulation | year= 1998 | volume= 98 | issue= 2 | pages= 149-56 | pmid=9679721 | doi= | pmc= | url= }} </ref><ref name="pmid9846575">{{cite journal| author=Lee JK, Zaidi SH, Liu P, Dawood F, Cheah AY, Wen WH et al.| title=A serine elastase inhibitor reduces inflammation and fibrosis and preserves cardiac function after experimentally-induced murine myocarditis. | journal=Nat Med | year= 1998 | volume= 4 | issue= 12 | pages= 1383-91 | pmid=9846575 | doi=10.1038/3973 | pmc= | url= }} </ref>. [[Protease]] produced by [[coxsackie virus]] can also modify the sarcoglycan complex in myocytes<ref name="pmid10086389">{{cite journal| author=Badorff C, Lee GH, Lamphear BJ, Martone ME, Campbell KP, Rhoads RE et al.| title=Enteroviral protease 2A cleaves dystrophin: evidence of cytoskeletal disruption in an acquired cardiomyopathy. | journal=Nat Med | year= 1999 | volume= 5 | issue= 3 | pages= 320-6 | pmid=10086389 | doi=10.1038/6543 | pmc= | url= }} </ref> leading to ventricular dilation. | |||
Eosinophilic and hypersensitive myocarditis may occur secondary to [[parasitic infection]]s, drug [[hypersensitivity]] or [[hypereosinophilic syndrome]]. Eosinophilic infiltration in myocardium lead to release of eosinophilic proteins which increase cellular membrane permeability which in turn leads to [[cell death]<ref name="pmid17386864">{{cite journal| author=Ginsberg F, Parrillo JE| title=Eosinophilic myocarditis. | journal=Heart Fail Clin | year= 2005 | volume= 1 | issue= 3 | pages= 419-29 | pmid=17386864 | doi=10.1016/j.hfc.2005.06.013 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17386864 }} </ref><ref name="pmid20181108">{{cite journal| author=Amini R, Nielsen C| title=Eosinophilic myocarditis mimicking acute coronary syndrome secondary to idiopathic hypereosinophilic syndrome: a case report. | journal=J Med Case Reports | year= 2010 | volume= 4 | issue= | pages= 40 | pmid=20181108 | doi=10.1186/1752-1947-4-40 | pmc=PMC2830978 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20181108 }} </ref>. Pathogenesis include: | Eosinophilic and hypersensitive myocarditis may occur secondary to [[parasitic infection]]s, drug [[hypersensitivity]] or [[hypereosinophilic syndrome]]. Eosinophilic infiltration in myocardium lead to release of eosinophilic proteins which increase cellular membrane permeability which in turn leads to [[cell death]<ref name="pmid17386864">{{cite journal| author=Ginsberg F, Parrillo JE| title=Eosinophilic myocarditis. | journal=Heart Fail Clin | year= 2005 | volume= 1 | issue= 3 | pages= 419-29 | pmid=17386864 | doi=10.1016/j.hfc.2005.06.013 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17386864 }} </ref><ref name="pmid20181108">{{cite journal| author=Amini R, Nielsen C| title=Eosinophilic myocarditis mimicking acute coronary syndrome secondary to idiopathic hypereosinophilic syndrome: a case report. | journal=J Med Case Reports | year= 2010 | volume= 4 | issue= | pages= 40 | pmid=20181108 | doi=10.1186/1752-1947-4-40 | pmc=PMC2830978 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20181108 }} </ref>. Pathogenesis include: | ||
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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.
Overview
During an infection or hypersensitive reaction, the immune system produces special cells that release chemicals to fight off the disease. The disease-fighting cells enter the heart where the infection affects the heart. However, the chemicals produced by an immune response can damage the heart muscle. As a result, the heart can become thick, swollen, and weak. This may further lead to symptoms of heart failure.
Pathophysiology of Myocarditis
Myocarditis is a continuum of three phases of the disease processes with each one evolving into the next[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.
Eosinophilic and hypersensitive myocarditis may occur secondary to parasitic infections, drug hypersensitivity or hypereosinophilic syndrome. Eosinophilic infiltration in myocardium lead to release of eosinophilic proteins which increase cellular membrane permeability which in turn leads to [[cell death][5][6]. Pathogenesis include:
- Immediate reaction: Degranulation of mast cells and basophils mediated by IgE.
- Delayed reaction: Activation of helper T-cells and interleukin-5.
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.
- ↑ Ginsberg F, Parrillo JE (2005). "Eosinophilic myocarditis". Heart Fail Clin. 1 (3): 419–29. doi:10.1016/j.hfc.2005.06.013. PMID 17386864.
- ↑ Amini R, Nielsen C (2010). "Eosinophilic myocarditis mimicking acute coronary syndrome secondary to idiopathic hypereosinophilic syndrome: a case report". J Med Case Reports. 4: 40. doi:10.1186/1752-1947-4-40. PMC 2830978. PMID 20181108.