Myocarditis pathophysiology: Difference between revisions
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[[Cytokines]], which are produced in reaction to infection and [[cell death]], are 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]]. | [[Cytokines]], which are produced in reaction to infection and [[cell death]], are 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>. | [[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>. The pathogenesis of this [[hypersensitivity reaction]] include: | ||
====Immediate reaction==== | |||
Degranulation of [[mast cell]]s and [[basophil]]s mediated by [[IgE]]. | |||
====Delayed reaction==== | |||
Activation of [[helper T-cell]]s and [[interleukin-5]]. | |||
==References== | ==References== | ||
Revision as of 23:50, 4 September 2011
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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, get internalized in peripheral tissues and activate the immune system. A few of these viral genomes attach 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
The host immune system eliminates the viral genomes from the body and promote recovery. However, sometimes the immune system remains activated even after elimination of virus. This leads to the development of an autoimmune reaction where T-cells and cytokines target the host tissue such as the myocardium which causes further myocyte damage.
Phase III: Dilated cardiomyopathy
Cytokines, which are produced in reaction to infection and cell death, are 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]. The pathogenesis of this hypersensitivity reaction 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.