Myocarditis overview: Difference between revisions
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==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
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In young adults, up to 20% of all cases of [[sudden death]] are due to myocarditis. Myocarditis is slightly more frequent among males than females.<ref name="pmid15527830">{{cite journal| author=Schwartz J, Sartini D, Huber S| title=Myocarditis susceptibility in female mice depends upon ovarian cycle phase at infection. | journal=Virology | year= 2004 | volume= 330 | issue= 1 | pages= 16-23 | pmid=15527830 | doi=10.1016/j.virol.2004.06.051 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15527830 }} </ref> | |||
==Natural History, Complications and Prognosis== | ==Natural History, Complications and Prognosis== | ||
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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 defined as inflammation of the myocardium. It may present with chest pain, ST segment elevation, elevated biomarkers of myonecrosis, heart failure, and/ or sudden death.
Classification
Myocarditis can be classified clinicopathologically into fulminant myocarditis, acute myocarditis, chronic active myocarditis, and chronic persistent myocarditis.
Pathophysiology
During either an infection or a hypersensitivity reaction, the inflammatory response may cause myonecrosis either directly or indirectly as part of an autoimmune reaction.
Causes
Life-threatening causes of myocarditis include carbon monoxide poisoning and Dengue fever. Common causes of myocarditis include infections, Lyme disease, and medications. Idiopathic myocarditis is the most common type of myocarditis and is often suspected to be secondary to a viral infection.[1]
Differentiating Myocarditis from other Diseases
Myocarditis must be distinguished from pericarditis and the life threatening condition of ST elevation myocardial infarction.
Epidemiology and Demographics
In young adults, up to 20% of all cases of sudden death are due to myocarditis. Myocarditis is slightly more frequent among males than females.[2]
Natural History, Complications and 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, myocarditis may be associated with sudden death. Patients with fulminant myocarditis have a good long term prognosis if they survive the acute phase of the disease.[3] The prognosis of fulminant myocarditis is better than that of either acute myocarditis or giant cell myocarditis. The presence of left bundle branch block, q waves, AV block, syncope and a left ventricular ejection fraction < 40% are associated with cardiac transplantation and sudden death.[4]
Diagnosis
History and Symptoms
The symptoms and the intensity of symptoms associated with myocarditis are variable. Myocarditis may be associated with no symptoms. If symptoms are present, they may be similar to the flu. Patients may present with chest pain as a result of the inflammatory process involving the myocardium or with symptoms of congestive heart failure. Patients may complain of palpitations, a racing heart or syncope. In fulminant myocarditis, patients present with the abrupt onset of flu-like symptoms and the abrupt onset of heart failure symptoms. In chronic and acute myocarditis, the onset of symptoms may be more insidious.
Physical Examination
The physical examination in patients with myocarditis may reveal tachycardia, a cardiac gallop, mitral regurgitation due to left ventricular dilation and pedal edema suggestive of cardiac failure. A pericardial friction rub may be noted in presence of concomitant pericarditis, a condition sometimes referred to as myopericarditis.
Laboratory 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 elevated, particularly early on in the course of the disease[5]. Other auto antibodies such as ANA and rheumatoid factor may also be detected.
Electrocardiogram
The presence of ST segment elevation in patients with myocarditis can mimic pericarditis and myocardial infarction. Arrhythmias and heart block may also be observed in myocarditis patients. Myocarditis can be distinguished from pericarditis by the presence of PR depression in the patient with pericarditis.
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 using immunochemistry and special staining techniques as necessary. 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 results in left ventricular dysfunction.[5] Endomyocardial biopsy is recommended when the results would identify an underlying disease that is amenable to therapy. Routine performance of endomyocardial biopsy is not recommended in all patients with myocarditis.
Chest X Ray
Chest x-ray in myocarditis may demonstrate pulmonary congestion in acute cases secondary to cardiac dysfunction. Cardiomegaly may be noted in patients with dilated ventricles.
MRI
Cardiac MRI findings associated with myocarditis include myocardial inflammation, myocardial edema, capillary leak, and reduced left ventricular function. While the cMRI pattern of gadolinium hyperenhancement in ST segment elevation myocardial infarction is transmural and extends from the endocardium to the epicardium, the patchy, non-segmental hyperenhancement pattern in myocarditis in contrast involves the epicardium and spares the subendocardium[6][7].
Echocardiography
Echocardiography in patients with myocarditis allows for serial assessment of left ventricular dysfunction[8], and can be used to distinguish fulminant (non-dilated hypocontractile left ventricle with thick interventricular septum) from acute myocarditis (dilated hypocontractile left ventricle with normal interventricular septum)[8].
Other Imaging Findings
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.
Treatment
Medical Therapy
Insofar as most viral infections cannot be treated with directed therapy, symptomatic treatment is the mainstay of therapy for patients with viral myocarditis. Supportive therapy includes diuretics and inotropes for left ventricular failure. ACE inhibitor therapy may aid in left ventricular remodeling after the inflammation has begun to resolve. In patients with fulminant myocarditis, placement of an intra-aortic balloon pump or a left ventricular assist device may be necessary as bridge to recovery.
According to 2010 HFSA guidelines[9], routine use of immunosuppressive therapies in management of myocarditis is not recommended (Strength of Evidence A). Immunotherapy is beneficial in giant cell myocarditis. Finally, cardiac transplantation can be performed in patients with severe myocarditis who fail to recover.
Bacterial infections are treated with antibiotics the selection of which is based upon the nature of the pathogen and its sensitivity to antibiotics.
Cardiac Transplantation
Cardiac transplantation is sometimes required to treat refractory giant cell myocarditis. However, the condition can recur in post-transplant patients. Recurrence of biopsy proven giant cell myocarditis between 3 weeks to 9 years was observed in 9 of 34 cardiac transplant patients [10].
References
- ↑ Kühl U, Pauschinger M, Noutsias M, Seeberg B, Bock T, Lassner D; et al. (2005). "High prevalence of viral genomes and multiple viral infections in the myocardium of adults with "idiopathic" left ventricular dysfunction". Circulation. 111 (7): 887–93. doi:10.1161/01.CIR.0000155616.07901.35. PMID 15699250. Unknown parameter
|http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=ignored (help) - ↑ Schwartz J, Sartini D, Huber S (2004). "Myocarditis susceptibility in female mice depends upon ovarian cycle phase at infection". Virology. 330 (1): 16–23. doi:10.1016/j.virol.2004.06.051. PMID 15527830.
- ↑ 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.
- ↑ Scartazzini R, Schneider P, Bickel H (1975). "[New beta-lactam antibiotics. Functionalisation of the cephem 3-position with sulfur or nitrogen bearing substituents (author's transl)]". Helv Chim Acta. 58 (8): 2437–50. doi:10.1002/hlca.19750580824. PMID 1194054.
- ↑ 5.0 5.1 Feldman AM, McNamara D (2000). "Myocarditis". N Engl J Med. 343 (19): 1388–98. doi:10.1056/NEJM200011093431908. PMID 11070105.
- ↑ 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.
- ↑ Friedrich MG, Sechtem U, Schulz-Menger J, Holmvang G, Alakija P, Cooper LT; et al. (2009). "Cardiovascular magnetic resonance in myocarditis: A JACC White Paper". J Am Coll Cardiol. 53 (17): 1475–87. doi:10.1016/j.jacc.2009.02.007. PMC 2743893. PMID 19389557.
- ↑ 8.0 8.1 Felker GM, Boehmer JP, Hruban RH, Hutchins GM, Kasper EK, Baughman KL; et al. (2000). ; "Echocardiographic findings in fulminant and acute myocarditis" Check
|url=value (help). J Am Coll Cardiol. 36 (1): 227–32. PMID 10898439. - ↑ 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.
- ↑ Cooper LT, Berry GJ, Shabetai R (1997). "Idiopathic giant-cell myocarditis--natural history and treatment. Multicenter Giant Cell Myocarditis Study Group Investigators". N Engl J Med. 336 (26): 1860–6. doi:10.1056/NEJM199706263362603. PMID 9197214.
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