Myocarditis pathophysiology: Difference between revisions
Jump to navigation
Jump to search
m Bot: Removing from Primary care |
|||
| (28 intermediate revisions by 9 users not shown) | |||
| Line 1: | Line 1: | ||
__NOTOC__ | |||
{{Myocarditis}} | {{Myocarditis}} | ||
{{CMG}} | {{CMG}} {{AE}} [[Varun Kumar|Varun Kumar, M.B.B.S.]], {{Maliha}}{{Homa}} | ||
==Overview== | ==Overview== | ||
During either an infection or a [[hypersensitivity reaction]], the inflammatory response may cause [[myonecrosis]] either directly or indirectly as part of an [[autoimmune]] reaction. | During either an infection or a [[hypersensitivity reaction]], the inflammatory response may cause [[myonecrosis]] either directly or indirectly as part of an [[autoimmune]] reaction. Histopathological features include abundant [[edema]] in the myocardial [[interstitium]] and an inflammatory infiltrate which is rich in [[lymphocyte]]s and [[macrophage]]s. Focal destruction of [[myocytes]] as a result of the inflammatory process results in [[left ventricular dysfunction]]. | ||
== | ==Pathogenesis== | ||
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> | 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]], 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 lodge in other organs such as the heart where they further replicate and cause localized tissue destruction. | Viruses such as [[coxsackie virus|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 lodge in other organs such as the heart where they further replicate and cause localized tissue destruction. | ||
===Phase II: Autoimmune Injury=== | ===Phase II: Autoimmune Injury=== | ||
After the host immune system eliminates the viral genomes from the body, the immune system may remains activated in patients who develop myocarditis. 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. | After the host [[immune system]] eliminates the viral genomes from the body, the [[immune system]] may remains activated in patients who develop myocarditis. 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=== | ===Phase III: Dilated Cardiomyopathy=== | ||
[[Cytokines]], which are produced in reaction to infection and [[cell death]], are a leading cause of [[dilated cardiomyopathy]]. Matrix [[metalloproteinase]]s, such as [[gelatinase]], [[collagenase]]s, and [[elastase]]s may also 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> | *[[Cytokines]], which are produced in reaction to infection and [[cell death]], are a leading cause of [[dilated cardiomyopathy]]. | ||
*Matrix [[metalloproteinase]]s, such as [[gelatinase]], [[collagenase]]s, and [[elastase]]s may also 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 modify the [[sarcoglycan complex]] in [[myocytes]] leading to [[ventricular dilation]].<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> | |||
[[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 either an immediate reaction which involves the degranulation of [[mast cell]]s and [[basophil]]s mediated by [[IgE]], or a delayed reaction involving the activation of [[helper T-cell]]s and [[interleukin-5]]. | ||
== | ==Microscopic Pathology== | ||
Histopathological features include abundant [[edema]] in the myocardial [[interstitium]] and an inflammatory infiltrate which is rich in [[lymphocyte]]s and [[macrophage]]s. Focal destruction of [[myocytes]] as a result of the inflammatory process results in [[left ventricular dysfunction]].<ref name="pmid11070105">{{cite journal| author=Feldman AM, McNamara D| title=Myocarditis. | journal=N Engl J Med | year= 2000 | volume= 343 | issue= 19 | pages= 1388-98 | pmid=11070105 | doi=10.1056/NEJM200011093431908 | pmc= | url= }} </ref> | |||
===The Heart in Toxoplasma gondii Myocarditis=== | |||
{{#ev:youtube|2s9OuW9XlUw}} | |||
===The Heart in Coxsackie B2 Myocarditis=== | ===The Heart in Coxsackie B2 Myocarditis=== | ||
{{#ev:youtube|R_7AXF61QGg}} | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
{{WS}} | {{WS}} | ||
{{WH}} | {{WH}} | ||
[[Category:Medicine]] | |||
[[Category:Cardiology]] | [[Category:Cardiology]] | ||
[[Category:Up-To-Date]] | [[Category:Up-To-Date]] | ||
[[Category: | [[Category:Emergency medicine]] | ||
[[Category:Intensive care medicine]] | |||
Latest revision as of 22:51, 29 July 2020
|
Myocarditis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Myocarditis pathophysiology On the Web |
|
American Roentgen Ray Society Images of Myocarditis pathophysiology |
|
Risk calculators and risk factors for Myocarditis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S., Maliha Shakil, M.D. [2] Homa Najafi, M.D.[3]
Overview
During either an infection or a hypersensitivity reaction, the inflammatory response may cause myonecrosis either directly or indirectly as part of an autoimmune reaction. Histopathological features include abundant edema in the myocardial interstitium and an inflammatory infiltrate which is rich in lymphocytes and macrophages. Focal destruction of myocytes as a result of the inflammatory process results in left ventricular dysfunction.
Pathogenesis
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 lodge in other organs such as the heart where they further replicate and cause localized tissue destruction.
Phase II: Autoimmune Injury
After the host immune system eliminates the viral genomes from the body, the immune system may remains activated in patients who develop myocarditis. 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 a leading cause of dilated cardiomyopathy.
- Matrix metalloproteinases, such as gelatinase, collagenases, and elastases may also be activated by cytokines during the autoimmune phase.[2][3]
- Protease produced by coxsackie virus can modify the sarcoglycan complex in myocytes leading to ventricular dilation.[4]
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 either an immediate reaction which involves the degranulation of mast cells and basophils mediated by IgE, or a delayed reaction involving the activation of helper T-cells and interleukin-5.
Microscopic Pathology
Histopathological features include abundant edema in the myocardial interstitium and an inflammatory infiltrate which is rich in lymphocytes and macrophages. Focal destruction of myocytes as a result of the inflammatory process results in left ventricular dysfunction.[7]
The Heart in Toxoplasma gondii Myocarditis
{{#ev:youtube|2s9OuW9XlUw}}
The Heart in Coxsackie B2 Myocarditis
{{#ev:youtube|R_7AXF61QGg}}
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.
- ↑ Feldman AM, McNamara D (2000). "Myocarditis". N Engl J Med. 343 (19): 1388–98. doi:10.1056/NEJM200011093431908. PMID 11070105.