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{{Myocarditis}}
{{Myocarditis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}}; [[Varun Kumar]], M.B.B.S.
{{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}}; [[Varun Kumar]], M.B.B.S.


==Overview==
==Overview==
'''Myocarditis''' is [[inflammation]] of the [[myocardium]], the muscular part of the [[heart]]. It may present with [[chest pain]], rapid signs of [[heart failure]], or [[sudden death]].
'''Myocarditis''' is [[inflammation]] of the [[myocardium]], the muscular part of the [[heart]]. It may present with [[chest pain]], rapid signs of [[heart failure]], or [[sudden death]].


==Epidemiology and Demographics==
==Epidemiology and Demographics==
It is generally due to [[viral infections]] such as [[adenovirus]], [[parvovirus B19]], [[hepatitis C]], and [[herpes virus 6]] in developed countries and [[HIV]], [[rheumatic disease]] in developing countries.
It is generally due to [[viral infections]] such as [[adenovirus]], [[parvovirus B19]], [[hepatitis C]], and [[herpes virus 6]] in developed countries and [[HIV]], [[rheumatic disease]] in developing countries.
==Natural History, Complications & Prognosis==
Myocarditis is usually self limiting and has good prognosis especially if it is secondary to [[viral infection]]. Rarely patients may deteriorate and develop [[cardiac failure]], [[pulmonary edema]], [[arrhythmias]] or [[cardiogenic shock]]. In some instances may even lead to sudden death. Patients with fulminant myocarditis have a good long term prognosis if they survive the acute phase of the disease in comparison to acute myocarditis<ref name="pmid10706898">{{cite journal| author=McCarthy RE, Boehmer JP, Hruban RH, Hutchins GM, Kasper EK, Hare JM et al.| title=Long-term outcome of fulminant myocarditis as compared with acute (nonfulminant) myocarditis. | journal=N Engl J Med | year= 2000 | volume= 342 | issue= 10 | pages= 690-5 | pmid=10706898 | doi=10.1056/NEJM200003093421003 | pmc= | url= }} </ref> or [[giant cell myocarditis]]. Serological markers such as [[Fas]], [[Fas ligand]], [[interleukin-10]] or antimyosin autoantibodies are also of prognostic value in myocarditis


==Clinicopathological classification<ref name="pmid1960305">{{cite journal| author=Lieberman EB, Hutchins GM, Herskowitz A, Rose NR, Baughman KL| title=Clinicopathologic description of myocarditis. | journal=J Am Coll Cardiol | year= 1991 | volume= 18 | issue= 7 | pages= 1617-26 | pmid=1960305 | doi= | pmc= | url= }} </ref>==
==Clinicopathological classification<ref name="pmid1960305">{{cite journal| author=Lieberman EB, Hutchins GM, Herskowitz A, Rose NR, Baughman KL| title=Clinicopathologic description of myocarditis. | journal=J Am Coll Cardiol | year= 1991 | volume= 18 | issue= 7 | pages= 1617-26 | pmid=1960305 | doi= | pmc= | url= }} </ref>==

Revision as of 21:02, 19 August 2011

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S.

Overview

Myocarditis is inflammation of the myocardium, the muscular part of the heart. It may present with chest pain, rapid signs of heart failure, or sudden death.

Epidemiology and Demographics

It is generally due to viral infections such as adenovirus, parvovirus B19, hepatitis C, and herpes virus 6 in developed countries and HIV, rheumatic disease in developing countries.

Natural History, Complications & Prognosis

Myocarditis is usually self limiting and has good prognosis especially if it is secondary to viral infection. Rarely patients may deteriorate and develop cardiac failure, pulmonary edema, arrhythmias or cardiogenic shock. In some instances may even lead to sudden death. Patients with fulminant myocarditis have a good long term prognosis if they survive the acute phase of the disease in comparison to acute myocarditis[1] or giant cell myocarditis. Serological markers such as Fas, Fas ligand, interleukin-10 or antimyosin autoantibodies are also of prognostic value in myocarditis

Clinicopathological classification[2]

  • Fulminant myocarditis - Occurs after a viral prodrome. May present as acute severe cardiovascular compromise with ventricular dysfunction. The prognosis is good if the patients survive acute illness[1].
  • Acute myocarditis - Presents with less distinct onset of illness with ventricular dysfunction. They may progress to dilated cardiomyopathy.
  • Chronic active myocarditis - Has a less distinct onset of illness, with clinical and histologic relapses and development of ventricular dysfunction. Histologically, chronic inflammatory changes with mild to moderate fibrosis may be noted.
  • Chronic persistent myocarditis - It is of less distinct onset. It is characterized with persistent histologic infiltration and myocyte necrosis without ventricular dysfunction despite the presence of symptoms.

Symptoms

There may be no symptoms. Symptoms may be similar to the flu. If symptoms occur, they may include:

Diagnosis

Physical examination

Physical examination in patients with myocarditis may reveal tachycardia, cardiac gallop, mitral regurgitation and edema suggestive of cardiac failure. A friction rub too may be noted in presence of concomitant pericarditis.

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).[3]

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.[3]

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.[4]

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.

References

  1. 1.0 1.1 McCarthy RE, Boehmer JP, Hruban RH, Hutchins GM, Kasper EK, Hare JM; et al. (2000). "Long-term outcome of fulminant myocarditis as compared with acute (nonfulminant) myocarditis". N Engl J Med. 342 (10): 690–5. doi:10.1056/NEJM200003093421003. PMID 10706898.
  2. Lieberman EB, Hutchins GM, Herskowitz A, Rose NR, Baughman KL (1991). "Clinicopathologic description of myocarditis". J Am Coll Cardiol. 18 (7): 1617–26. PMID 1960305.
  3. 3.0 3.1 Feldman AM, McNamara D (2000). "Myocarditis". N Engl J Med. 343 (19): 1388–98. doi:10.1056/NEJM200011093431908. PMID 11070105.
  4. 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.

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