Myocarditis overview: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
During an infection or hypersensitive reaction, immune system produces special cells that release chemicals to fight off the disease. The disease-fighting cells enter the heart | During an infection or hypersensitive reaction, the immune system produces special cells that release chemicals to fight off the disease. The disease-fighting cells enter the heart where the infection affects the heart. However, the chemicals produced by an immune response can damage the heart muscle. As a result, the heart can become thick, swollen, and weak. This may further lead to symptoms of [[heart failure]]. | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
Revision as of 20:19, 4 September 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.
Pathophysiology
During an infection or hypersensitive reaction, the immune system produces special cells that release chemicals to fight off the disease. The disease-fighting cells enter the heart where the infection affects the heart. However, the chemicals produced by an immune response can damage the heart muscle. As a result, the heart can become thick, swollen, and weak. This may further lead to symptoms of heart failure.
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:
- Palpitations
- Chest pain
- Fatigue
- Fever and other signs of infection including headache, muscle aches, sore throat, diarrhea, or rashes
- Joint pain or swelling
- Pedal edema
- Shortness of breath
- Fainting, often related to irregular heart rhythms
- Low urine output
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]
Echocardiography
Echocardiography in patients with myocarditis help in assessing the pump function of heart, monitoring the progress and in differentiating acute from fulminant myocarditis[4].
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]
Coronary Angiography
Coronary angiography may be helpful in assessing the coronaries and excluding myocardial ischemia or infarction as the cause for abnormal findings on lab tests.
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.[5]. Cardiac MRI is useful in identifying myocarditis by detecting myocardial inflammations which appear as high intensity signals and delayed gadolinium enhancement. Using two of the three MRI sequences provide high diagnostic accuracy[6].
Lab Findings
Myocardial inflammation can be suspected on the basis of elevated C-reactive protein, ESR and antibodies against viruses known to affect the myocardium. Markers of myocardial damage such as troponin or creatine kinase are often elevated.[3]. Other auto antibodies such as ANA and rheumatoid factor may also be detected.
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. diuretics and/or inotropes for ventricular failure. ACE inhibitor therapy may aid in left ventricular remodeling after the inflammation has begun to resolve.
According to 2010 HFSA guidelines[7], routine use of immunosuppressive therapies in management of myocarditis is not recommended (Strength of Evidence A). Immunotherapy is beneficial in giant cell myocarditis. Other alternative therapy in severe myocarditis is cardiac transplantation.
References
- ↑ 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.
- ↑ 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.
- ↑ 3.0 3.1 3.2 Feldman AM, McNamara D (2000). "Myocarditis". N Engl J Med. 343 (19): 1388–98. doi:10.1056/NEJM200011093431908. PMID 11070105.
- ↑ Felker GM, Boehmer JP, Hruban RH, Hutchins GM, Kasper EK, Baughman KL; et al. (2000). "Echocardiographic findings in fulminant and acute myocarditis". J Am Coll Cardiol. 36 (1): 227–32. PMID 10898439.
- ↑ 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.
- ↑ Abdel-Aty H, Boyé P, Zagrosek A, Wassmuth R, Kumar A, Messroghli D; et al. (2005). "Diagnostic performance of cardiovascular magnetic resonance in patients with suspected acute myocarditis: comparison of different approaches". J Am Coll Cardiol. 45 (11): 1815–22. doi:10.1016/j.jacc.2004.11.069. PMID 15936612.
- ↑ Heart Failure Society of America. Lindenfeld J, Albert NM, Boehmer JP, Collins SP, Ezekowitz JA; et al. (2010). "HFSA 2010 Comprehensive Heart Failure Practice Guideline". J Card Fail. 16 (6): e1–194. doi:10.1016/j.cardfail.2010.04.004. PMID 20610207.