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==References==
==References==
{{reflist}}
{{reflist}}

== External links ==/people/roddonald
== External links ==
* [http://www.greens.org.nzRod Donald biography] (Green Party website
* [http://www.greens.org.nz/people/roddonald Rod Donald biography] (Green Party website)


{{Circulatory system pathology}}
{{Circulatory system pathology}}

Revision as of 02:34, 13 February 2009

Tobyhanna

In medicine (cardiology), myocarditis is inflammation of the myocardium, the muscular part of the heart. It is generally due to infection (viral or bacterial). It may cause chest pain, rapid signs of heart failure, or sudden death.

Signs and symptoms

The signs and symptoms associated with myocarditis 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)
  • Symptoms in infants and toddlers tend to be more non-specific with generalized malaise, poor appetite, abdominal pain, chronic cough. Later stages of the illness will present with respiratory symptoms with increased work of breathing and is often mistaken for asthma.

Since myocarditis is often due to a viral illness, many patients give a history of symptoms consistent with a recent viral infection, including fever, rash, 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

Endomyocardial biopsy specimen. Extensive eosinophilic infiltrate involving the endocardium and myocardium (hematoxylin and eosin stain).

In myocarditis, the process of inflammation is the cause of the injury, and not the response to it. As a result, inflammation of the myocardium by itself is not enough to be diagnostic for myocarditis[3].

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]

The ECG findings most commonly seen in myocarditis are diffuse T wave inversions; saddle-shaped ST-segment elevations may be present (these are also seen in pericarditis).[1]

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 light microscopy and—if necessary—immunochemistry 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]

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]

Causes

A large number of different causes have been identified as leading to myocarditis:[1]

Bacterial myocarditis is rare in patients without immunodeficiency.

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.[1]

In South America, Chagas' disease (caused by Trypanosoma cruzi) is the main cause of myocarditis.

Therapy

As most viral infections cannot be treated with directed therapy, symptomatic treatment is the only form of therapy for those forms of myocarditis. In the acute phase, supportive therapy including bed rest is indicated. For symptomatic patients, digoxin and diuretics provide clinical improvement. For patients with moderate to severe dysfunction, cardiac function can be supported by use of inotropes such as Milrinone in acute phase followed by oral therapy with ACE inhibitors ( Captopril, Lisinopril) when tolerated. Patients who do not respond to conventional therapy are candidates for bridge therapy with left ventricular assist devices (LVADs). Heart transplantation is reserved for patients who fail to improve with conventional therapy.

Famous deaths

References

  1. ^ a b c d e f Feldman AM, McNamara D (2000). "Myocarditis". N. Engl. J. Med. 343 (19): 1388–98. doi:10.1056/NEJM200011093431908. PMID 11070105. {{cite journal}}: Unknown parameter |month= ignored (help)
  2. ^ Eckart RE, Scoville SL, Campbell CL; et al. (2004). "Sudden death in young adults: a 25-year review of autopsies in military recruits". Ann. Intern. Med. 141 (11): 829–34. PMID 15583223. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  3. ^ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 414-416 ISBN 978-1-4160-2973-1
  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.{{cite journal}}: CS1 maint: multiple names: authors list (link)

External links