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 present with chest pain, rapid signs of
heart failure, or sudden death.
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]
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]
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.[3]
Causes
A large number of different causes have been identified as leading to myocarditis:[1]
- Infectious:
- Viral (e.g. enterovirus, Coxsackie virus, rubella virus, polio
virus, cytomegalovirus, possibly hepatitis
C)
- Bacterial (e.g. brucella, Corynebacterium diphtheriae, gonococcus,
Haemophilus influenzae, Actinomyces, Tropheryma whipplei, and
Vibrio cholerae).
- Spirochetal (Borrelia burgdorferi
and leptospirosis)
- Protozoal (Toxoplasma gondii and
Trypanosoma cruzi)
- Fungal (e.g. aspergillus)
- Parasitic: ascaris, Echinococcus granulosus, Paragonimus
westermani, schistosoma, Taenia
solium, Trichinella spiralis, visceral larva migrans, and Wuchereria
bancrofti
- Rickettsial
- Immunological:
- Toxic:
- Physical agents (electric shock, hyperpyrexia, and
radiation)
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.
In South America, Chagas' disease (caused by
Trypanosoma cruzi) is the main cause of myocarditis.
Therapy
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 the healing process.
Famous deaths
References
- ^ a b c d e 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.
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