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==[[Myocarditis epidemiology|Epidemiology]]==
==[[Myocarditis epidemiology|Epidemiology]]==


==[[Myocarditis signs and symptoms|Signs and symptoms]]==
==[[Myocarditis diagnosis|Diagnosis]]==
[[Myocarditis signs and symptoms|Signs and symptoms]] | [[Myocarditis diagnosis#Electrocardiographic Findings|Electrocardiogram]] | [[Myocarditis diagnosis#Endomyocardial Biopsy|Endomyocardial Biopsy]] | [[Myocarditis diagnosis#Cardiac Magnetic Resonance Imaging|Cardiac MRI]] | [[Myocarditis differential diagnosis of underlying causes|Differential Diagnosis]]


== Diagnosis ==
==[[Myocarditis treatment|Treatment]]==


Myocardial inflammation can be suspected on the basis of [[electrocardiogram|electrocardiographic]] results (ECG), elevated [[C-reactive protein|CRP]] and/or [[Erythrocyte sedimentation rate|ESR]] and increased [[IgM]] ([[serology]]) against viruses known to affect the [[myocardium]]. Markers of myocardial damage ([[troponin]] or [[creatine kinase]] cardiac isoenzymes) are elevated.<ref name=Feldman/>
==[[Myocarditis pathologic findings|Pathologic Findings]]==
 
===Electrocardiographic Findings===
 
The [[electrocardiogram|ECG]] findings most commonly seen in myocarditis are [[sinus tachycardia]], diffuse [[T wave]] inversions; [[ST segment]] elevation may also be present (these are also seen in pericarditis).<ref name=Feldman/>
 
===Endomyocardial Biopsy===
 
The [[gold standard (test)|gold standard]] is still [[biopsy]] of the [[myocardium]], generally done in the setting of [[angiography]]. A small tissue sample of the [[endocardium]] and [[myocardium]] is taken, and investigated by a pathologist by and if necessary[[immunochemistry]] and special staining methods. Histopathological features are: myocardial interstitium with abundant edema and inflammatory infiltrate, rich in [[lymphocyte]]s and [[macrophage]]s. Focal destruction of myocytes explains the myocardial pump failure.<ref name=Feldman/>
 
===Cardiac Magnetic Resonance Imaging===
Recently, cardiac [[magnetic resonance imaging]] (cMRI or CMR) has been shown to be very useful in diagnosing myocarditis by visualizing markers for [[inflammation]] of the [[myocardium]].<ref>{{cite journal |author=Skouri HN, Dec GW, Friedrich MG, Cooper LT |title=Noninvasive imaging in myocarditis |journal=J. Am. Coll. Cardiol. |volume=48 |issue=10 |pages=2085-93 |year=2006 |pmid=17112998 |doi=10.1016/j.jacc.2006.08.017}}</ref>
 
== Differential Diagnosis of Underlying Causes ==
 
A large number of different causes have been identified as leading to myocarditis:<ref name=Feldman/>
 
===[[Infectious disease|Infectious]]===
 
*[[Virus|Viral]]
:*[[Enterovirus]]
:*[[Coxsackie virus]]
:*[[Rubella virus]]
:*[[Polio virus]]
:*[[Cytomegalovirus]]
:*[[Adenoviruses]]
:*[[Arboviruses]]
:*[[Coxsackie virus|Coxsackie virus A]]
:*[[Coxsackie virus|Coxsackie virus B1-B5]]
:*[[CMV]]
:*[[Echovirus]]
:*[[Epstein-Barr virus]]
:*[[Flavivirus]]
:*[[Hepatitis|Hepatitis virus]]
:*:*[[Hepatitis C]]
:*[[HIV]]
:*[[Influenza]]
:*[[Measles virus]]
:*[[Mumps|Mumps virus]]
:*[[Polio|Polio virus]]
:*[[Rabies|Rabies virus]]
:*[[Varicella Zoster Virus]]
* [[Bacterium|Bacterial]]
:*[[Actinomyces]]
:*[[Whipple's disease|Tropheryma whipplei]]
:*[[Vibrio cholerae]]
:*[[Group A streptococcal infection|Beta hemolytic Streptococci]]
:*[[Brucella]]
:*[[Corynebacterium diphtheriae]]
:*[[Enterococci]]
:*[[Gonococcus]]
:*[[Legionella]]
:*[[Meningococci]]
:*[[Pertussis]]
:*[[Psittacosis]]
:*[[Rickettsia]]
:*[[Salmonella]]
:*[[Syphilis|T. Pallidum]]
:*[[Staphylococci]]
:*[[Tetanus|Clostridium Tetani]]
:*[[Tuberculosis]]
:*[[Tularemia]]
:*[[Spirochete|Spirochetal]]
:*:*[[Borrelia burgdorferi]]
:*:*[[Leptospirosis]]
*[[Protozoa]]l
:*[[Toxoplasma gondii]]
:*[[Trypanosoma cruzi]]
* [[Fungus|Fungal]]
:*[[Aspergillus]]
* [[Parasite|Parasitic]]
:*[[Ascaris]]
:*[[Echinococcus granulosus]]
:*[[Paragonimus westermani]]
:*[[Schistosoma]]
:*[[Taenia solium]]
:*[[Trichinella spiralis]]
:*[[Visceral larva migrans]]
:*[[Wuchereria bancrofti]]
 
===[[Immunology|Immunological]]===
* [[Allergy|Allergic]]
:*[[Acetazolamide]]
:*[[Amitriptyline]]
* [[heart transplant|Rejection after a heart transplant]]
* [[Autoimmune disorder|Autoantigens]]
:*[[Vasculitis|systemic vasculitis]]
:*[[Churg-Strauss syndrome]]
:*[[Wegener's granulomatosis]]
 
===[[Toxicology|Toxic]]===
*[[Medication|Drugs]]
:*[[Anthracycline]]s
:*[[Chemotherapy]]
:*[[Ethanol]]
:*[[Antipsychotic]]s
:*:*[[Clozapine]]
:*[[Remicade]]
* [[Toxin]]s
:*[[Arsenic]]
:*[[Carbon monoxide]]
:*[[Snake venom]]
* [[Heavy metals]]
:*[[Copper]]
:*[[Iron]]
 
===Physical agents===
* [[Electric shock]]
* [[Fever|Hyperpyrexia]]
* [[Radiation]]
 
Bacterial myocarditis is rare in patients without [[immunodeficiency]].
 
===The Heart in Toxoplasma Gondii Myocarditis===
 
<youtube v=2s9OuW9XlUw/>
 
===The Heart in Coxsackie B2 Myocarditis===
 
<youtube v=R_7AXF61QGg/>
 
==Treatment==
Bacterial infections are treated with [[antibiotic]]s, dependent on the nature of the pathogen and its sensitivity to antibiotics. As most viral infections cannot be treated with directed therapy, symptomatic treatment is the only form of therapy for those forms of myocarditis, e.g. [[NSAID]]s for the inflammatory component and [[diuretic]]s and/or [[inotrope]]s for ventricular failure. [[ACE inhibitor]] therapy may aid in left ventricular remodeling after the inflammation has begun to resolve.
 
==Pathologic Findings==
 
===Autopsy Study===
 
===Clinical Summary===
 
A 21-year-old male with [[sickle cell anemia]] had recurrent attacks of [[acute rheumatic fever]] beginning at age 14.
 
[[Mitral insufficiency]] and [[mitral stenosis|stenosis]] were present by age 16.
 
On prophylactic antibiotics, the patient had no evidence of recurrence until three weeks before his final admission, when an upper respiratory infection developed. A few weeks later he developed acute migratory polyarthritis. This was associated with rapid deterioration of cardiac function and death.
 
===Autopsy Findings===
 
At autopsy, the heart was enlarged (weighing 675 grams) especially the [[left atrium]]. Both the [[aortic valve|aortic]] and [[mitral valve]]s showed fibrosis as well as the fresh, tiny verrucae characteristic of [[acute rheumatic fever]].
 
===Images===
 
[http://www.peir.net Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
 
<div align="left">
<gallery heights="225" widths="225">
Image:Acute rheumatic myocarditis case 1.jpg|This is a gross photograph of mitral valve demonstrating marked thickening and fibrosis of the valve leaflet. There are also numerous foci of fibrinoid necrosis within the cusps and friable vegetations (verrucae) along the lines of closure (arrows). These irregular, warty projections are found at sites of erosion on the inflamed endocardial surface. The verrucae probably result from the precipitation of fibrin where the leaflets impinge on each other.
Image:Acute rheumatic myocarditis case 2.jpg|This is a low-power photomicrograph of heart tissue. Little can be seen at this magnification, except that the tissue looks relatively normal.
</gallery>
</div>
 
 
<div align="left">
<gallery heights="225" widths="225">
Image:Acute rheumatic myocarditis case 3.jpg|This is a higher-power photomicrograph of myocardium showing cellular accumulations--Aschoff bodies (arrows)--within the interstitium of the myocardium. These are found especially around blood vessels.
Image:Acute rheumatic myocarditis case 4.jpeg|This is a higher-power photomicrograph of myocardium containing Aschoff bodies (arrows) within the interstitium.
</gallery>
</div>
 
 
<div align="left">
<gallery heights="225" widths="225">
Image:Acute rheumatic myocarditis case 5.jpeg|This high-power photomicrograph of myocardium shows the cellular detail of an Aschoff body. Aschoff bodies are foci of fibrinoid necrosis surrounded by lymphocytes, macrophages, an occasional plasma cell, and plump “activated” histiocytes called Anitschkow cells or Aschoff cells (arrows). These distinctive cells have abundant amphophilic cytoplasm and central round-to-ovoid nuclei in which the chromatin is disposed in a central, slender, wavy ribbon resembling a caterpillar (hence the designation “caterpillar cells”).
Image:Acute rheumatic myocarditis case 6.jpeg|This high-power photomicrograph of myocardium shows the cellular detail of another Aschoff body. In this case there appears to be a multinucleated Aschoff giant cell (arrow).
</gallery>
</div>


==References==
==References==

Revision as of 19:30, 17 June 2011

Myocarditis
Histopathological image of viral myocarditis at autopsy in a patient with acute onset of congestive heart failure. Viral etiology, however, failed to be determined in postmortem serological study.
ICD-10 I09.0, I51.4
ICD-9 391.2, 422, 429.0
DiseasesDB 8716
MedlinePlus 000149
eMedicine med/1569  emerg/326
MeSH D009205

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Overview

Epidemiology

Diagnosis

Signs and symptoms | Electrocardiogram | Endomyocardial Biopsy | Cardiac MRI | Differential Diagnosis

Treatment

Pathologic Findings

References

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