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5.1. The role of immune response to virus and genetic predisposition
Direct viral cytopathic effects followed by an immune response
is the current theory of myocyte damage. The immune response to
virus is what is considered to cause increased tissue damage, or as
in the majority of the cases of asymptomatic disease or spontaneous
remission [97], to be what facilitates recovery. It is also
postulated that autoimmune disease is triggered by certain
viruses or that there is a hypersensitivity response due to cytokineregulated
activity [13].
Many different cell types play a role in the development of
myocarditis [98]. T lymphocytes are significant in the development
ofmyocarditis. Using CD4 and CD8 knockout mice to test the role of
specific lymphocyte function on virus-induced myocarditis was
shown to affect prognosis due to the absence and/or presence of
these cell types [64].
Natural killer cells and their role in cardiac inflammation has only
recently been described. A recent review article highlighting their
role in inflammatory myocarditis illustrates their potential to serve
as protectors of inflammation and as inhibitors to fibrosis formation
[99]. Interestingly, one study found that in murine models, natural
killer cells may have a protective effect in the progression of autoimmune
myocarditis by inhibiting eosinophilic infiltration Eosinophils have been found to drive the progression of autoimmune
myocarditis to DCM by producing IL-4 [101].
The expression of TNF a, a proinflammatory cytokine, may be
partly responsible for injury to the myocardium. Among TNF apositive
cases, the greater TNF a mRNAs, the more impaired the
cardiac function in a studied population of virus-positive myocarditis
patients [102]. Detection of heart reactive antibodies demonstrate
a possible immune-mediated pathway of tissue destruction,
as increased levels of IgG are found circulating in patients with
myocarditis as compared to controls [103]. A detailed summary of
serum cardiac autoantibodies can be found in the 2013 review
article ‘Current state of knowledge on aetiology, diagnosis, management,
and therapy of myocarditis: a position statement of the
European Society of Cardiology Working Group on Myocardial and
Pericardial Diseases’ [55].
Autoimmune myocarditis can be induced in murine models
using myocarditogenic peptide [100,104]. Cardiac myosin and
Troponin-I have been indicated as the antigen targets of autoantibodies,
and these arewell known to circulate in the blood following
cardiac injury [105]. The antibodies may contribute to further tissue
dysfunction as they are deposited in immune complexes in the
myocardium [106]. The present understanding of the four main
mechanisms of autoimmune myocarditis was recently summarized
by Root-Bernstein and Fairweather [107]. Why the myocardium is
targeted is not clear, although there are multiple theories that offer
some clues. One of which is that molecular antigenic mimicry may
be one of the mechanisms [108].
Additionally, genetic susceptibility may play a role in the
development of disease rather than or in addition to the pathogenicity
of the virus [11]. Families show evidence of inheritance
patterns, and the detection of anti-heart autoantibodies in the
serum of healthy relatives of patients with myocarditis and/orDCM
is correlative with increased risk of developing disease. Regardless
of viral presence, HLA DQ8 was found to be associated with the
development of auto immune myocarditis in a murine model. In
this population it was found that CD8 was the initiator of disease
progression and CD4 (via recruitment of macrophage) is specific to
the cardiac pathway [109]. This further indicates that HLA status
may have a role in the development of an autoimmune response to
antigens.
===The Heart in Toxoplasma gondii Myocarditis===
===The Heart in Toxoplasma gondii Myocarditis===


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==Overview==
The exact pathogenesis of [disease name] is not fully understood.


OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
==Pathophysiology==
===Physiology===
The normal physiology of [name of process] can be understood as follows:
===Pathogenesis===
*The exact pathogenesis of [disease name] is not completely understood.
OR
*It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*The progression to [disease name] usually involves the [molecular pathway].
*The pathophysiology of [disease/malignancy] depends on the histological subtype.
==Genetics==
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
*[Gene1]
*[Gene2]
*[Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
*[Mutation 1]
*[Mutation 2]
*[Mutation 3]
==Associated Conditions==
Conditions associated with [disease name] include:
*[Condition 1]
*[Condition 2]
*[Condition 3]
==Gross Pathology==
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
==Microscopic Pathology==
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].




==References==
==References==
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Latest revision as of 22:51, 29 July 2020

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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., 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

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

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The Heart in Coxsackie B2 Myocarditis

{{#ev:youtube|R_7AXF61QGg}}



References

  1. ↑ Liu PP, Mason JW (2001). "Advances in the understanding of myocarditis". Circulation. 104 (9): 1076–82. PMID 11524405.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ 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.
  5. ↑ Ginsberg F, Parrillo JE (2005). "Eosinophilic myocarditis". Heart Fail Clin. 1 (3): 419–29. doi:10.1016/j.hfc.2005.06.013. PMID 17386864.
  6. ↑ 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.
  7. ↑ Feldman AM, McNamara D (2000). "Myocarditis". N Engl J Med. 343 (19): 1388–98. doi:10.1056/NEJM200011093431908. PMID 11070105.

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