Myocarditis
| Myocarditis | |
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| 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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Editors-In-Chief: Josh Hare, M.D.; C. Michael Gibson, M.S., M.D. [1]
Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
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Myocarditis is inflammation of the myocardium, the muscular part of the heart. It is generally due to infection (viral or bacterial). It may present with chest pain, rapid signs of heart failure, or sudden death.
Epidemiology
The exact incidence of myocarditis is unknown. However, in series of routine autopsies, 1–9% of all patients had evidence of myocardial inflammation. In young adults, up to 20% of all cases of sudden death are due to myocarditis.
In South America, Chagas' disease (caused by Trypanosoma cruzi) is the main cause of myocarditis.
Signs and symptoms
The signs and symptoms associated with myocardits are varied, and relate either to the actual inflammation of the myocardium, or the weakness of the heart muscle that is secondary to the inflammation. Signs and symptoms of myocarditis include:[1]
- Chest pain (often described as "stabbing" in character)
- Congestive heart failure (leading to edema, breathlessness and hepatic congestion)
- Palpitations (due to arrhythmias)
- Sudden death (in young adults, myocarditis causes up to 20% of all cases of sudden death)[2]
- Fever (especially when infectious, e.g. in rheumatic fever)
Since myocarditis is often due to a viral illness, many patients give a history of symptoms consistent with a recent viral infection, including fever, diarrhea, joint pains, and easy fatigueability.
Myocarditis is often associated with pericarditis, and many patients present with signs and symptoms that suggest concurrent myocarditis and pericarditis.
Diagnosis
Myocardial inflammation can be suspected on the basis of electrocardiographic results (ECG), elevated CRP and/or ESR and increased IgM (serology) against viruses known to affect the myocardium. Markers of myocardial damage (troponin or creatine kinase cardiac isoenzymes) are elevated.[1]
Electrocardiographic Findings
The 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).[1]
Endomyocardial Biopsy
The 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 necessaryimmunochemistry and special staining methods. Histopathological features are: myocardial interstitium with abundant edema and inflammatory infiltrate, rich in lymphocytes and macrophages. Focal destruction of myocytes explains the myocardial pump failure.[1]
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.[3]
Differential Diagnosis of Underlying Causes
A large number of different causes have been identified as leading to myocarditis:[1]
Infectious
Immunological
Toxic
Physical agents
Bacterial myocarditis is rare in patients without immunodeficiency.
The Heart in Toxoplasma Gondii Myocarditis
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The Heart in Coxsackie B2 Myocarditis
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Treatment
Bacterial infections are treated with antibiotics, 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. NSAIDs for the inflammatory component and diuretics and/or inotropes 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 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 and mitral valves showed fibrosis as well as the fresh, tiny verrucae characteristic of acute rheumatic fever.
Images
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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. -
This is a low-power photomicrograph of heart tissue. Little can be seen at this magnification, except that the tissue looks relatively normal.
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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. -
This is a higher-power photomicrograph of myocardium containing Aschoff bodies (arrows) within the interstitium.
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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”). -
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).
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Feldman AM, McNamara D. Myocarditis. N Engl J Med 2000;343:1388-98. PMID 11070105.
- ↑ Eckart RE, Scoville SL, Campbell CL, Shry EA, Stajduhar KC, Potter RN, Pearse LA, Virmani R. Sudden death in young adults: a 25-year review of autopsies in military recruits. Ann Intern Med 2004;141:829-34. PMID 15583223.
- ↑ Skouri HN, Dec GW, Friedrich MG, Cooper LT (2006). "Noninvasive imaging in myocarditis". J. Am. Coll. Cardiol. 48 (10): 2085–93. doi:10.1016/j.jacc.2006.08.017. PMID 17112998.
External links
de:Myokarditis it:Miocardite fi:Sydänlihastulehdus sv:Hjärtmuskelinflammation