Myocarditis overview: Difference between revisions
(/* Clinicopathological classification{{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= 1) |
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==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>== | ||
*'''Fulminant myocarditis''' - Fulminant myocarditis occurs following a viral prodrome. Fulminant myocarditis | *'''Fulminant myocarditis''' - Fulminant myocarditis occurs following a viral prodrome. Fulminant myocarditis presents as acute severe cardiovascular compromise with ventricular dysfunction. The prognosis is good if the patient survives the acute illness<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>. | ||
*'''Acute myocarditis''' - Acute myocarditis presents with a less distinct onset of the illness | *'''Acute myocarditis''' - Acute myocarditis presents with a less distinct onset of the illness. When the patient does present, there is already a decline in left ventricular dysfunction. Acute myocarditis may progress to [[dilated cardiomyopathy]]. | ||
*'''Chronic active myocarditis''' Chronic active myocarditis has a less distinct onset of the illness. There are clinical and histologic relapses and the development of ventricular dysfunction. Histologically, chronic inflammatory changes with mild to moderate fibrosis may be present. | *'''Chronic active myocarditis''' Chronic active myocarditis has a less distinct onset of the illness. There are clinical and histologic relapses and the development of ventricular dysfunction. Histologically, chronic inflammatory changes with mild to moderate fibrosis may be present. | ||
Revision as of 21:27, 4 September 2011
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: 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
Developed Countries
Myocarditis is generally due to viral infections such as adenovirus, parvovirus B19, hepatitis C, and herpes virus 6 in developed countries.
Developing Countries
Myocarditis is generally due to HIV and rheumatic heart disease in developing countries.
Natural History, Complications & Prognosis
Myocarditis is usually self limiting and is associated with a good prognosis especially if it is secondary to a viral infection. Patients rarely 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 [1] . The prognosis of fulminant myocarditis is better than that of either acute myocarditis or giant cell myocarditis.
Serological markers such as Fas, Fas ligand, interleukin-10 or antimyosin autoantibodies are of prognostic value in myocarditis.
Clinicopathological classification[2]
- Fulminant myocarditis - Fulminant myocarditis occurs following a viral prodrome. Fulminant myocarditis presents as acute severe cardiovascular compromise with ventricular dysfunction. The prognosis is good if the patient survives the acute illness[1].
- Acute myocarditis - Acute myocarditis presents with a less distinct onset of the illness. When the patient does present, there is already a decline in left ventricular dysfunction. Acute myocarditis may progress to dilated cardiomyopathy.
- Chronic active myocarditis Chronic active myocarditis has a less distinct onset of the illness. There are clinical and histologic relapses and the development of ventricular dysfunction. Histologically, chronic inflammatory changes with mild to moderate fibrosis may be present.
- Chronic persistent myocarditis - Chronic persistent myocarditis has a less distinct onset ff the illness. Histologically it is characterized by persistent infiltration and myocyte necrosis. Despite the presence of symptoms, ventricular dysfunction is absent.
Symptoms
Myocarditis may be associated with no symptoms. If symptoms are present,they may be similar to the flu. Symptoms 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, a cardiac gallop, mitral regurgitation and edema suggestive of cardiac failure. A friction rub may be noted in presence of concomitant pericarditis, a condition sometimes referred to as myopericarditis.
Electrocardiographic Findings
Common ECG findings in myocarditis include[3]:
- Sinus tachycardia
- Diffuse T wave inversions
- ST segment elevation may also be present
ST segment elevation may also be seen in pericarditis. PR depression is also present, however, in patients with pericarditis.
Echocardiography
Echocardiography in patients with myocarditis allows for serial assessment of left ventricular dysfunction. Echocardiography is helpful in differentiating acute from fulminant myocarditis[4].
Endomyocardial Biopsy
Endomyocardial biopsy remains the gold standard test to evaluate for the presence of and to subclassify the type of myocarditis. A small tissue sample of the endocardium and myocardium is obtained via right sided cardiac catheterization. The sample is then evaluated by a pathologist and if necessary using immunochemistry and special staining techniques. Histopathological features include abundant edema in the myocardial interstitium and an inflammatory infiltrate which is rich in lymphocytes and macrophages. Focal destruction of myocytes as a result of the inflammatory process explains the myocardial pump failure.[3]
Coronary Angiography
Coronary angiography may be helpful in excluding either myocardial ischemia or infarction as the cause of ST segment elevation, elevated cardiac biomarkers, or left ventricular dysfunction.
Cardiac Magnetic Resonance Imaging
Cardiac magnetic resonance imaging (cMRI or CMR) demonstrates a patchy pattern of inflammation in the myocardium.[5]. Myocardial inflammation appears as high intensity signal and with delayed gadolinium enhancement on cardiac MRI. Using two of the three MRI sequences provides a 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.