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| | __NOTOC__ |
| {{Myocarditis}} | | {{Myocarditis}} |
| {{CMG}}; '''Associate Editor-In-Chief:''' [[Varun Kumar]], M.B.B.S. | | {{CMG}} {{AE}} [[Varun Kumar]], M.B.B.S. {{Maliha}} {{Homa}} |
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| ==Overview== | | ==Overview== |
| '''Myocarditis''' is [[inflammation]] of the [[myocardium]]. It may present with [[chest pain]], [[ST segment elevation]], elevated biomarkers of [[myonecrosis]], [[heart failure]], and / or [[sudden death]].
| | 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]]. [[Myocarditis]] can be classified clinicopathologically into fulminant myocarditis, acute myocarditis, chronic active myocarditis, and chronic persistent myocarditis. During either an infection or a [[hypersensitivity reaction]], the inflammatory response may cause [[myonecrosis]] either directly or indirectly as part of an [[autoimmune]] reaction. 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. Myocarditis must be distinguished from [[pericarditis]] and the life threatening condition of [[ST elevation myocardial infarction]]. 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. 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. 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 [[sudden death]] and [[cardiac transplantation]]. 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]]. |
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| | ==Historical Perspective== |
| | Myocarditis was first discovered by Jean Baptiste Senac, a French [[physician]], in 1794. The term myocarditis was introduced by German [[physician]] Joseph Friedrich Sobernheim in 1837. In 1980s, the [[World Health Organization]] and the International Society and Federation of Cardiology were the first to [[differentiate]] between myocarditis and other [[cardiomyopathies]]. The [[Dallas criteria]] was published in 1986 as a [[Guideline (medical)|guideline]] for [[classification]] of myocarditis. |
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| | ==Classification== |
| | Myocarditis can be [[Classification|classified]] based on the [[Causes|causative]], [[histological]], and clinicopathological [[criteria]]. [[Causes|Causative]] [[criteria]] include three main groups, as well as [[infectious]], [[Immune-mediated disease|immune-mediated,]] and [[toxic]] myocarditis. Based on the type of [[Infiltration (medical)|infiltrating]] [[Cells (biology)|cells]] myocarditis divided in [[lymphocytic]], [[eosinophilic]], [[polymorphic]], [[giant cell]] myocarditis, and [[cardiac sarcoidosis]]. [[Acute]], [[fulminant]], [[chronic]] active, and [[Chronic (medicine)|chronic]] persistent are subtypes of clinicopathopogical [[classification]]. |
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| ==Pathophysiology== | | ==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. Myocarditis is a continuum of three phases of the disease processes with each one evolving into the next<ref name="pmid11524405">{{cite journal| author=Liu PP, Mason JW| title=Advances in the understanding of myocarditis. | journal=Circulation | year= 2001 | volume= 104 | issue= 9 | pages= 1076-82 | pmid=11524405 | doi= | pmc= | url= }} </ref>: | | During either an infection or a [[hypersensitivity reaction]], the inflammatory response may cause [[myonecrosis]] either directly or indirectly as part of an [[autoimmune]] reaction. |
| ===Phase I: Viral Infection and Replication===
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| Viruses such as [[coxsackie virus|coxsackie]] and [[enterovirus]], get internalized in peripheral tissues and activate the immune system. A few of these viral genomes attach to the immunologic cells which circulate throughout the body and lodge in other organs such as the heart where they further replicate and cause localized tissue destruction.
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| ===Phase II: Autoimmune Injury=== | | ==Causes== |
| After the host immune system eliminates the viral genomes from the body, the immune system may remains activated in patients who develop myocarditis. This leads to the development of an [[autoimmune reaction]] where [[T-cells]] and [[cytokines]] target the host tissue such as the [[myocardium]] which causes further [[myocyte]] damage.
| | Life-threatening causes of myocarditis include [[carbon monoxide poisoning]] and [[Dengue fever]]. Common causes of myocarditis include infections such as [[Lyme disease]] and medications. Idiopathic myocarditis is the most common type of myocarditis and is often suspected to be secondary to a [[viral]] infection. |
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| ===Phase III: Dilated Cardiomyopathy=== | | ==Differentiating Myocarditis from other Diseases== |
| [[Cytokines]], which are produced in reaction to infection and [[cell death]], are a leading cause of [[dilated cardiomyopathy]]. Matrix [[metalloproteinase]]s, such as [[gelatinase]], [[collagenase]]s, and [[elastase]]s may also be activated by [[cytokines]] during the [[autoimmune]] phase<ref name="pmid9679721">{{cite journal| author=Ono K, Matsumori A, Shioi T, Furukawa Y, Sasayama S| title=Cytokine gene expression after myocardial infarction in rat hearts: possible implication in left ventricular remodeling. | journal=Circulation | year= 1998 | volume= 98 | issue= 2 | pages= 149-56 | pmid=9679721 | doi= | pmc= | url= }} </ref><ref name="pmid9846575">{{cite journal| author=Lee JK, Zaidi SH, Liu P, Dawood F, Cheah AY, Wen WH et al.| title=A serine elastase inhibitor reduces inflammation and fibrosis and preserves cardiac function after experimentally-induced murine myocarditis. | journal=Nat Med | year= 1998 | volume= 4 | issue= 12 | pages= 1383-91 | pmid=9846575 | doi=10.1038/3973 | pmc= | url= }} </ref>. [[Protease]] produced by [[coxsackie virus]] can also modify the [[sarcoglycan complex]] in [[myocytes]]<ref name="pmid10086389">{{cite journal| author=Badorff C, Lee GH, Lamphear BJ, Martone ME, Campbell KP, Rhoads RE et al.| title=Enteroviral protease 2A cleaves dystrophin: evidence of cytoskeletal disruption in an acquired cardiomyopathy. | journal=Nat Med | year= 1999 | volume= 5 | issue= 3 | pages= 320-6 | pmid=10086389 | doi=10.1038/6543 | pmc= | url= }} </ref> leading to [[ventricular dilation]]. | | Myocarditis must be distinguished from [[pericarditis]] and the life threatening condition of [[ST elevation myocardial infarction]]. |
| | ==Risk factors== |
| | There are no established [[risk factors]] for myocarditis. |
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| [[Eosinophilic]] and [[hypersensitive]] myocarditis may occur secondary to [[parasitic infection]]s, drug [[hypersensitivity]] or [[hypereosinophilic syndrome]]. [[Eosinophilic]] infiltration in [[myocardium]] lead to release of [[eosinophilic]] proteins which increase cellular membrane permeability which in turn leads to [[cell death]]<ref name="pmid17386864">{{cite journal| author=Ginsberg F, Parrillo JE| title=Eosinophilic myocarditis. | journal=Heart Fail Clin | year= 2005 | volume= 1 | issue= 3 | pages= 419-29 | pmid=17386864 | doi=10.1016/j.hfc.2005.06.013 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17386864 }} </ref><ref name="pmid20181108">{{cite journal| author=Amini R, Nielsen C| title=Eosinophilic myocarditis mimicking acute coronary syndrome secondary to idiopathic hypereosinophilic syndrome: a case report. | journal=J Med Case Reports | year= 2010 | volume= 4 | issue= | pages= 40 | pmid=20181108 | doi=10.1186/1752-1947-4-40 | pmc=PMC2830978 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20181108 }} </ref>. | | ==Screening== |
| | There is insufficient [[evidence]] to recommend routine [[screening]] for myocarditis. |
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| ==Epidemiology and Demographics== | | ==Epidemiology and Demographics== |
| In developed countries, myocarditis is generally due to [[viral infections]] such as [[coxsackie B]], [[enterovirus]],[[adenovirus]], [[parvovirus B19]], [[hepatitis C]], and [[herpes virus]] 6. In developing countries, myocarditis is generally due to [[HIV]] and [[rheumatic heart disease]]. In routine [[autopsy|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. There is a male predominance.
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| ==Natural History, Complications & Prognosis==
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| 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 <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> . The prognosis of fulminant myocarditis is better than that of either acute myocarditis or [[giant cell myocarditis]].
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| The presence of [[left bundle branch block]], [[q waves]], [[AV block]], [[syncope]] and a [[left ventricular ejection fraction]] < 40% are associated with [[sudden death]] and [[cardiac transplantation]]<ref name="pmid1194054">{{cite journal| author=Scartazzini R, Schneider P, Bickel H| title=[New beta-lactam antibiotics. Functionalisation of the cephem 3-position with sulfur or nitrogen bearing substituents (author's transl)]. | journal=Helv Chim Acta | year= 1975 | volume= 58 | issue= 8 | pages= 2437-50 | pmid=1194054 | doi=10.1002/hlca.19750580824 | pmc= | url= }} </ref>.
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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>==
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| *'''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>. On [[endomyocardial biopsy]], there are multiple focci of inflammation. Fulminant myocarditis is associated with a non-dilated [[hypocontractile left ventricle]] with thick [[interventricular septum]] while acute myocarditis (see below) is associated with a dilated [[hypocontractile left ventricle]] with normal [[interventricular septum]]<ref name="pmid10898439">{{cite journal| author=Felker GM, Boehmer JP, Hruban RH, Hutchins GM, Kasper EK, Baughman KL et al.| title=Echocardiographic findings in fulminant and acute myocarditis. | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 1 | pages= 227-32 | pmid=10898439 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10898439 }} </ref>.
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| *'''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]].
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| *'''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.
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| *'''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.
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| ==Symptoms==
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| 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. Symptoms may include:
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| *[[Palpitations]]
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| *[[Chest pain]]
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| *[[Fatigue]]
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| *[[Fever]] and other signs of infection including [[headache]], muscle aches, [[sore throat]], [[diarrhea]], or rashes
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| *Joint pain or swelling
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| *[[Pedal edema]]
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| *[[Shortness of breath]]
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| *[[Fainting]], often related to irregular heart rhythms
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| *[[Low urine output]]
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| ==Causes of Myocarditis==
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| ==Differential Diagnosis of the Underlying Causes of Myocarditis==
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| (By organ system)
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| {|style="width:70%; height:100px" border="1"
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| |style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
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| |style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | Acute [[rheumatic fever]], [[Dressler syndrome]]
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| |-bgcolor="LightSteelBlue"
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| | '''Chemical / poisoning'''
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| |bgcolor="Beige"| [[Arsenic]], [[Carbon monoxide]], [[Lead]]
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| |-bgcolor="LightSteelBlue"
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| | '''Dermatologic'''
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| |bgcolor="Beige"| [[Scleroderma]], [[Systemic lupus erythematosus]]
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| |-bgcolor="LightSteelBlue"
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| | '''Drug Side Effect'''
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| |bgcolor="Beige"| Drugs are known to cause hypersensitive myocarditis<ref name="pmid19189924">{{cite journal| author=Pursnani A, Yee H, Slater W, Sarswat N| title=Hypersensitivity myocarditis associated with azithromycin exposure. | journal=Ann Intern Med | year= 2009 | volume= 150 | issue= 3 | pages= 225-6 | pmid=19189924 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19189924 }} </ref><ref name="pmid4010343">{{cite journal| author=Taliercio CP, Olney BA, Lie JT| title=Myocarditis related to drug hypersensitivity. | journal=Mayo Clin Proc | year= 1985 | volume= 60 | issue= 7 | pages= 463-8 | pmid=4010343 | doi= | pmc= | url= }} </ref><ref name="pmid19440116">{{cite journal| author=Ben m'rad M, Leclerc-Mercier S, Blanche P, Franck N, Rozenberg F, Fulla Y et al.| title=Drug-induced hypersensitivity syndrome: clinical and biologic disease patterns in 24 patients. | journal=Medicine (Baltimore) | year= 2009 | volume= 88 | issue= 3 | pages= 131-40 | pmid=19440116 | doi=10.1097/MD.0b013e3181a4d1a1 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19440116 }} </ref>. Peripheral eosinophilia and eosinophilic myocardial infiltrates may be seen on myocardial biopsy. Some of the common drugs are: [[Amphetamines]], [[Benzodiazepines]], [[Carbamazepine]], [[Chloramphenicol]], [[Clozapine]]<ref name="pmid17194170">{{cite journal| author=Haas SJ, Hill R, Krum H, Liew D, Tonkin A, Demos L et al.| title=Clozapine-associated myocarditis: a review of 116 cases of suspected myocarditis associated with the use of clozapine in Australia during 1993-2003. | journal=Drug Saf |year= 2007 | volume= 30 | issue= 1 | pages= 47-57 | pmid=17194170 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17194170 }} </ref>, [[Cocaine]], [[Cyclophosphamide]], [[Dobutamine]]<ref name="pmid7578186">{{cite journal| author=Spear GS|title=Eosinophilic explant carditis with eosinophilia: ?Hypersensitivity to dobutamine infusion. | journal=J Heart Lung Transplant | year= 1995 | volume= 14 | issue= 4 | pages= 755-60 | pmid=7578186 | doi= | pmc= | url= }} </ref><ref name="pmid15090985">{{cite journal| author=Johnson MR| title=Eosinophilic myocarditis in the explanted hearts of cardiac transplant recipients: Interesting pathologic finding or pathophysiologic entity of clinical significance? | journal=Crit Care Med | year= 2004 | volume= 32 | issue= 3 | pages= 888-90 | pmid=15090985 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15090985 }} </ref>, [[Methyldopa]], [[Penicillin]], [[Phenytoin]], [[Spironolactone]], [[Streptomycin]], [[Sulfonamides]], [[Tricyclic antidepressants]].
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| | '''Ear Nose Throat'''
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| |bgcolor="Beige"| No underlying causes
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| |-bgcolor="LightSteelBlue"
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| | '''Endocrine'''
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| |bgcolor="Beige"| [[Thyrotoxicosis]]
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| | '''Environmental'''
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| |bgcolor="Beige"| [[Heatstroke]], Scorpion stings, snake bites, bites from black widow spider, wasp venom, tick paralysis
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| |-bgcolor="LightSteelBlue"
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| | '''Gastroenterologic'''
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| |bgcolor="Beige"| [[Celiac disease]]<ref name="pmid12045166">{{cite journal| author=Frustaci A, Cuoco L, Chimenti C, Pieroni M, Fioravanti G, Gentiloni N et al.| title=Celiac disease associated with autoimmune myocarditis. | journal=Circulation | year= 2002 | volume= 105 | issue= 22 | pages= 2611-8 | pmid=12045166 | doi= | pmc= | url= }} </ref>, [[Crohn disease]], [[Ulcerative colitis]]
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| |-bgcolor="LightSteelBlue"
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| | '''Genetic'''
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| |bgcolor="Beige"| [[Haemochromatosis]], [[Friedreich ataxia]]
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| |-bgcolor="LightSteelBlue"
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| | '''Hematologic'''
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| |bgcolor="Beige"| No underlying causes
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| |-bgcolor="LightSteelBlue"
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| | '''Iatrogenic'''
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| |bgcolor="Beige"| Inflammatory myocarditis may be seen in post transplant rejection.
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| |-bgcolor="LightSteelBlue"
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| | '''Infectious Disease'''
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| |bgcolor="Beige"|
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| '''Viral:''' The idiopathic myocarditis is the most common type of myocarditis and is often suspected to be secondary to viral infection<ref name="pmid15699250">{{cite journal| author=Kühl U, Pauschinger M, Noutsias M, Seeberg B, Bock T, Lassner D et al.| title=High prevalence of viral genomes and multiple viral infections in the myocardium of adults with "idiopathic" left ventricular dysfunction. | journal=Circulation | year= 2005 | volume= 111 | issue= 7 | pages= 887-93 | pmid=15699250 | doi=10.1161/01.CIR.0000155616.07901.35 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15699250 }} </ref>. Common virus associated with myocarditis are- [[Adenovirus]]<ref name="pmid12906974">{{cite journal| author=Bowles NE, Ni J, Kearney DL, Pauschinger M, Schultheiss HP, McCarthy R et al.| title=Detection of viruses in myocardial tissues by polymerase chain reaction. evidence of adenovirus as a common cause of myocarditis in children and adults. | journal=J Am Coll Cardiol | year= 2003 | volume= 42 | issue= 3 | pages= 466-72 | pmid=12906974 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12906974 }} </ref><ref name="pmid16172268">{{cite journal| author=Kühl U, Pauschinger M, Seeberg B, Lassner D, Noutsias M, Poller W et al.| title=Viral persistence in the myocardium is associated with progressive cardiac dysfunction. | journal=Circulation | year= 2005 | volume= 112 | issue= 13 | pages= 1965-70 | pmid=16172268 | doi=10.1161/CIRCULATIONAHA.105.548156 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16172268 }} </ref>, [[Arbovirus]], [[Coxsackie B]]<ref name="pmid1558005">{{cite journal|author=Rose NR, Neumann DA, Herskowitz A| title=Coxsackievirus myocarditis. | journal=Adv Intern Med | year= 1992 | volume= 37 | issue= | pages= 411-29 | pmid=1558005 | doi= | pmc=| url= }} </ref><ref name="pmid4887187">{{cite journal| author=Grist NR, Bell EJ| title=Coxsackie viruses and the heart. | journal=Am Heart J | year= 1969 | volume= 77 | issue= 3 |pages= 295-300 | pmid=4887187 | doi= | pmc= | url= }} </ref>, [[Cytomegalovirus]]<ref name="pmid12906974">{{cite journal| author=Bowles NE, Ni J, Kearney DL, Pauschinger M, Schultheiss HP, McCarthy R et al.| title=Detection of viruses in myocardial tissues by polymerase chain reaction. evidence of adenovirus as a common cause of myocarditis in children and adults. | journal=J Am Coll Cardiol | year= 2003 | volume= 42 | issue= 3 | pages= 466-72 | pmid=12906974 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12906974 }} </ref><ref name="pmid2983175">{{cite journal|author=Cohen JI, Corey GR| title=Cytomegalovirus infection in the normal host. | journal=Medicine (Baltimore) | year= 1985 | volume= 64 | issue= 2 | pages= 100-14 | pmid=2983175 |doi= | pmc= | url= }} </ref>, [[Echovirus]], [[Enterovirus]], [[Epstein-Barr virus]]<ref name="pmid12906974">{{cite journal| author=Bowles NE, Ni J, Kearney DL, Pauschinger M, Schultheiss HP, McCarthy R et al.|title=Detection of viruses in myocardial tissues by polymerase chain reaction. evidence of adenovirus as a common cause of myocarditis in children and adults. | journal=J Am Coll Cardiol | year= 2003 | volume= 42 | issue= 3 | pages= 466-72 | pmid=12906974 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12906974 }} </ref><ref name="pmid15557377">{{cite journal| author=Chimenti C, Russo A, Pieroni M, Calabrese F, Verardo R, Thiene G et al.| title=Intramyocyte detection of Epstein-Barr virus genome by laser capture microdissection in patients with inflammatory cardiomyopathy. |journal=Circulation | year= 2004 | volume= 110 | issue= 23 | pages= 3534-9 | pmid=15557377 | doi=10.1161/01.CIR.0000148823.08092.0E | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15557377 }} </ref>, [[Herpes simplex virus]], [[Hepatitis B]], [[Hepatitis C]]<ref name="pmid10908160">{{cite journal| author=Matsumori A, Yutani C, Ikeda Y, Kawai S, Sasayama S| title=Hepatitis C virus from the hearts of patients with myocarditis and cardiomyopathy. | journal=Lab Invest | year= 2000 | volume= 80 | issue= 7 | pages= 1137-42 | pmid=10908160 | doi= | pmc= | url= }} </ref>, [[HIV-1]], [[Influenza]]<ref name="pmid12906974">{{cite journal| author=Bowles NE, Ni J, Kearney DL, Pauschinger M, Schultheiss HP, McCarthy R et al.| title=Detection of viruses in myocardial tissues by polymerase chain reaction. evidence of adenovirus as a common cause of myocarditis in children and adults. | journal=J Am Coll Cardiol | year= 2003 | volume= 42 | issue= 3 | pages= 466-72 | pmid=12906974 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12906974 }} </ref>, [[Mumps]], [[Parvovirus B19]]<ref name="pmid12906974">{{cite journal|author=Bowles NE, Ni J, Kearney DL, Pauschinger M, Schultheiss HP, McCarthy R et al.| title=Detection of viruses in myocardial tissues by polymerase chain reaction. evidence of adenovirus as a common cause of myocarditis in children and adults. | journal=J Am Coll Cardiol | year= 2003 | volume= 42 | issue= 3 | pages= 466-72 | pmid=12906974 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12906974 }} </ref><ref name="pmid20456978">{{cite journal|author=Breinholt JP, Moulik M, Dreyer WJ, Denfield SW, Kim JJ, Jefferies JL et al.| title=Viral epidemiologic shift in inflammatory heart disease: the increasing involvement of parvovirus B19 in the myocardium of pediatric cardiac transplant patients. | journal=J Heart Lung Transplant | year= 2010 | volume= 29 | issue= 7 | pages= 739-46 | pmid=20456978 |doi=10.1016/j.healun.2010.03.003 | pmc=PMC2902647 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20456978 }} </ref><ref name="pmid12792925">{{cite journal| author=Pankuweit S, Moll R, Baandrup U, Portig I, Hufnagel G, Maisch B| title=Prevalence of the parvovirus B19 genome in endomyocardial biopsy specimens. | journal=Hum Pathol | year= 2003 | volume= 34 | issue= 5 | pages= 497-503 | pmid=12792925 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12792925 }} </ref>, [[Poliomyelitis]], [[Rabies]], [[Respiratory syncytial virus]], [[Rubeola]], [[Varicella]], [[Variola]]/vaccinia<ref name="pmid15120802">{{cite journal| author=Cassimatis DC, Atwood JE, Engler RM, Linz PE, Grabenstein JD, Vernalis MN|title=Smallpox vaccination and myopericarditis: a clinical review. | journal=J Am Coll Cardiol | year= 2004 | volume= 43 | issue= 9 | pages= 1503-10 | pmid=15120802 |doi=10.1016/j.jacc.2003.11.053 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15120802 }} </ref>, [[Viral hepatitis]], [[Yellow fever virus]]
| |
|
| |
| '''Bacterial:''' [[Borrelia burgdorferi]], [[Brucellosis]], [[Clostridia]], [[Diphtheria]], [[Melioidosis]], [[Meningococci]], [[Mycoplasma pneumoniae]], [[Psittacosis]], [[Salmonella typhi]], [[Staphylococci]], [[Streptococci]], [[Tuberculosis]]
| |
|
| |
| '''Fungal:''' [[Actinomycosis]], [[Aspergillosis]], [[Blastomycosis]], [[Candidiasis]], [[Coccidioidomycosis]], [[Cryptococcosis]], [[Histoplasmosis]], [[Mucormycosis]]
| |
|
| |
| '''Parasitic:''' [[Balantidiasis]], [[Chagas disease]], [[Cysticercosis]], [[Echinococcosis]], [[Filariasis]], Heterophyiasis, [[Leishmaniasis]], [[Malaria]], Sarcosporidiosis, [[Schistosomiasis]], [[Toxoplasmosis]], [[Trichinosis]], [[Trypanosomiasis]], [[Visceral larva migrans]]
| |
|
| |
|
| '''Rickettsial:''' [[Q fever]], [[Rocky mountain spotted fever]], [[Scrub typhus]], [[Typhus fever]]
| | The [[incidence]] of myocarditis is approximately 10 to 20 per 100,000 [[patients]] worldwide. It commonly affects younger individuals. Yong [[males]] are slightly more commonly affected by myocarditis than [[females]]. There is no [[racial]] predilection to myocarditis. [[Viral infections]] especially [[coxsackie B]] and [[enterovirus]] are the most common cause of myocarditis in [[Developed country|developed countries]]. While, In South America, [[Chagas' disease]] (caused by ''[[Trypanosoma cruzi]]'') is the main cause of myocarditis. |
|
| |
|
| '''Spirochetal:''' [[leptospirosis]]/Weil disease, [[Lyme disease]], [[relapsing fever]]/[[Borrelia]], [[Syphilis]]
| | ==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]] [[Rare|rarely]] [[Development|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]]. The [[prognosis]] of fulminant myocarditis is better than that of either [[acute]] myocarditis or [[giant cell myocarditis]]. The presence of [[syncope]], [[pulmonary hypertension]], [[Ventricular dysfunction|biventricular dysfunction]], [[left bundle branch block]], [[q waves]], [[AV block]], and a [[left ventricular ejection fraction]] < 40% are associated with [[sudden death]] and [[cardiac transplantation]]. [[Complications]] of myocarditis include [[chronic]] [[dilated cardiomyopathy]], [[heart block]], [[congestive heart failure]], [[pericarditis]], [[ventricular dysfunction]], [[arrythmia]]s, and [[sudden cardiac death]]. |
| |-bgcolor="LightSteelBlue"
| |
| | '''Musculoskeletal / Ortho'''
| |
| |bgcolor="Beige"| [[Rheumatoid arthritis]]
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Neurologic'''
| |
| |bgcolor="Beige"| [[Friedreich ataxia]]
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Nutritional / Metabolic'''
| |
| |bgcolor="Beige"| [[Amyloidosis]], [[Haemochromatosis]]
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Obstetric/Gynecologic'''
| |
| |bgcolor="Beige"| [[Peripartum cardiomyopathy]]
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Oncologic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Opthalmologic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Overdose / Toxicity'''
| |
| |bgcolor="Beige"| [[Doxorubicin]], Radiation exposure
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Psychiatric'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Pulmonary'''
| |
| |bgcolor="Beige"| [[Aspergillosis]], [[Sarcoidosis]]
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Renal / Electrolyte'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Rheum / Immune / Allergy'''
| |
| |bgcolor="Beige"| [[Crohn disease]], [[Dressler syndrome]], [[Giant cell myocarditis]]<ref name="pmid19026310">{{cite journal| author=Cooper LT, Hare JM, Tazelaar HD, Edwards WD, Starling RC, Deng MC et al.| title=Usefulness of immunosuppression for giant cell myocarditis. | journal=Am J Cardiol | year= 2008 | volume= 102 | issue= 11 | pages= 1535-9 | pmid=19026310 | doi=10.1016/j.amjcard.2008.07.041 | pmc=PMC2613862 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19026310 }} </ref>, [[Kawasaki disease]], [[Rheumatoid arthritis]], [[Sarcoidosis]], [[Scleroderma]], [[Systemic lupus erythematosus]], [[Thyrotoxicosis]], [[Ulcerative colitis]], [[Wegener granulomatosis]]
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Sexual'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Trauma'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Urologic'''
| |
| |bgcolor="Beige"| No underlying causes
| |
| |-
| |
| |-bgcolor="LightSteelBlue"
| |
| | '''Miscellaneous'''
| |
| |bgcolor="Beige"| [[Amyloidosis]], [[Heatstroke]], [[Hyperthermia]], Radiation exposure
| |
| |-
| |
| |}
| |
|
| |
|
| ==Diagnosis== | | ==Diagnosis== |
| ===Physical examination=== | | ===History and Symptoms=== |
| | Myocarditis should be suspected in a [[patient]] with [[acute]] [[decompensation]] of [[Cardiac function curve|cardiac function]] who is at low risk of [[ischemic heart disease]]. A [[History and Physical examination|history]] of a recent (within the preceding 2-4 weeks) [[viral]] [[illness]] is often elicited in a large [[number]] of [[patients]] with myocarditis. [[Cardiac]] specific [[symptoms]] may become apparent usually in the [[subacute]] [[virus]]-clearing [[Phase (matter)|phase]]. In myocarditis due to [[drug hypersensitivity]], [[patients]] may give a [[History and Physical examination|history]] of ingesting an offending [[drug]]. 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. Common [[symptoms]] of myocarditis include [[chest pain]], [[pedal edema]], [[palpitation]]s, [[fever]], and [[joint pain]]s. |
|
| |
|
| Physical examination in patients with myocarditis may reveal [[tachycardia]], a [[cardiac gallop]], [[mitral regurgitation]] and [[pulmonary edema]] suggestive of [[cardiac failure]]. A [[pericardial friction rub]] may be noted in presence of concomitant [[pericarditis]], a condition sometimes referred to as [[myopericarditis]]. | | ===Physical Examination=== |
| | There are no specific findings for myocarditis. [[Patients]] with myocarditis usually show [[signs]] of [[cardiac dysfunction]] and underlying [[diseases]]. 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]]. |
|
| |
|
| ===Electrocardiographic Findings=== | | ===Laboratory Findings=== |
| | [[Laboratory|Laboratory findings]] consistent with the [[diagnosis]] of myocarditis include [[Elevation|elevated]] [[Marker|markers]] of [[myonecrosis]], [[inflammatory]] [[Marker|markers]], and other [[biomarkers]]. [[Marker|Markers]] of [[myonecrosis]] include [[creatine kinase]] ([[CK-MB]]), [[Troponin|cardiac troponin]] I ([[cTnI]]) or T ([[cTnT]]), [[lactate dehydrogenase]] ([[LDH]]), [[alanine transaminase]] ([[ALT]]), and [[aspartate transaminase]] ([[AST]]). [[Elevation|Elevated]] levels of [[C-reactive protein]] and [[erythrocyte sedimentation rate]] ([[ESR]]), and [[leukocytosis]] are suggestive of myocarditis. [[Serologic]] [[Marker|markers]] such as [[Fas]], [[Fas ligand]], [[interleukin-10]] or antimyosin [[autoantibodies]] are of [[prognostic]] value in myocarditis. Other [[Autoantibodies|auto-antibodies]] such as [[ANA]] and [[rheumatoid factor]] may also be detected. |
|
| |
|
| Common [[electrocardiogram|ECG]] findings in myocarditis include<ref name="pmid11070105">{{cite journal| author=Feldman AM, McNamara D| title=Myocarditis. | journal=N Engl J Med | year= 2000 | volume= 343 | issue= 19 | pages= 1388-98 | pmid=11070105 | doi=10.1056/NEJM200011093431908 | pmc= | url= }} </ref>:
| | ===Electrocardiogram=== |
| * [[Sinus tachycardia]]
| | 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]]. |
| * 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]]. | | ===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 [[lymphocyte]]s and [[macrophage]]s. Focal destruction of [[myocytes]] as a result of the inflammatory process results in [[left ventricular dysfunction]]. [[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=== |
| | Findings on [[Chest X-ray|chest x-ray]] suggestive of myocarditis include [[cardiomegaly]], [[Cephalization on chest x-ray|cephalization]] of the [[pulmonary vessels]] and, [[Kerley B lines|Kerley B-lines]] in presence of [[heart failure]] [[pericardial]] thickening in presence of [[pericarditis]], [[pulmonary edema]], and [[pleural effusion]]. |
|
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| ===Echocardiography=== | | ===Echocardiography=== |
| [[Echocardiography]] in patients with [[myocarditis]] allows for serial assessment of left ventricular dysfunction<ref name="pmid10898439">{{cite journal| author=Felker GM, Boehmer JP, Hruban RH, Hutchins GM, Kasper EK, Baughman KL et al.| title=Echocardiographic findings in fulminant and acute myocarditis. | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 1 | pages= 227-32 | pmid=10898439 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10898439 ; }} </ref>, 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]])<ref name="pmid10898439">{{cite journal| author=Felker GM, Boehmer JP, Hruban RH, Hutchins GM, Kasper EK, Baughman KL et al.| title=Echocardiographic findings in fulminant and acute myocarditis. | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 1 | pages= 227-32 | pmid=10898439 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10898439 }} </ref>. | | [[Echocardiography]] in patients with [[myocarditis]] allows for serial assessment of left ventricular dysfunction 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]]). Echocardiography may be helpful in the diagnosis of myocarditis. Findings on an echocardiography suggestive of myocarditis include wall [[Motion (physics)|motion]] [[abnormalities]], [[Systolic dysfunction|systolic]] and [[diastolic dysfunction]], changes in [[image]] texture, [[pericardial effusion]], and functional [[regurgitation]] through the [[Atrioventricular valves|AV valves]]. |
| | |
| Echocardiographic findings in myocardits include:
| |
| *Wall motion abnormalities<ref name="pmid3400607">{{cite journal| author=Pinamonti B, Alberti E, Cigalotto A, Dreas L, Salvi A, Silvestri F et al.| title=Echocardiographic findings in myocarditis. | journal=Am J Cardiol | year= 1988 | volume= 62 | issue= 4 | pages= 285-91 | pmid=3400607 | doi= | pmc= | url= }} </ref>.
| |
| *[[Systolic dysfunction]]<ref name="pmid3400607">{{cite journal| author=Pinamonti B, Alberti E, Cigalotto A, Dreas L, Salvi A, Silvestri F et al.| title=Echocardiographic findings in myocarditis. | journal=Am J Cardiol | year= 1988 | volume= 62 | issue= 4 | pages= 285-91 | pmid=3400607 | doi= | pmc= | url= }} </ref><ref name="pmid6711435">{{cite journal| author=Nieminen MS, Heikkilä J, Karjalainen J| title=Echocardiography in acute infectious myocarditis: relation to clinical and electrocardiographic findings. | journal=Am J Cardiol | year= 1984 | volume= 53 | issue= 9 | pages= 1331-7 | pmid=6711435 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6711435 }} </ref>.
| |
| *[[Diastolic dysfunction]]<ref name="pmid8296760">{{cite journal| author=James KB, Lee K, Thomas JD, Hobbs RE, Rincon G, Bott-Silverman C et al.| title=Left ventricular diastolic dysfunction in lymphocytic myocarditis as assessed by Doppler echocardiography. | journal=Am J Cardiol | year= 1994 | volume= 73 | issue= 4 | pages= 282-5 | pmid=8296760 | doi= | pmc= | url= }} </ref>.
| |
| *Changes in image texture on echocardiogram, i.e. increase in brightness, heterogeneity, and contrast<ref name="pmid8682119">{{cite journal| author=Lieback E, Hardouin I, Meyer R, Bellach J, Hetzer R| title=Clinical value of echocardiographic tissue characterization in the diagnosis of myocarditis. | journal=Eur Heart J | year= 1996 | volume= 17 | issue= 1 | pages= 135-42 | pmid=8682119 | doi= | pmc= | url= }} </ref>.
| |
| *[[Pericardial effusion]]
| |
| *Functional regurgitation through the AV valves may be noted due to [[ventricular dilation]].
| |
|
| |
|
| In general, [[left ventricular function]] improves in fulminant myocarditis over a course of approximately 6 months<ref name="pmid10898439">{{cite journal| author=Felker GM, Boehmer JP, Hruban RH, Hutchins GM, Kasper EK, Baughman KL et al.| title=Echocardiographic findings in fulminant and acute myocarditis. | journal=J Am Coll Cardiol | year= 2000 | volume= 36 | issue= 1 | pages= 227-32 | pmid=10898439 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10898439 }} </ref>.
| | ===CT scan=== |
| | [[Cardiac]] [[CT scan]] may be helpful in the [[diagnosis]] of myocarditis. [[Cardiac]] [[CT scan]] can be used in [[diagnosis]] of [[acute myocarditis]] ( [[Epicardium|subepicardial]] late [[iodine]] enhancement), [[Exclusion criteria|exclusion]] of [[Acute coronary syndromes|acute coronary syndrome]] by [[CT angiography]], and alternative [[diagnostic]] tool in [[patients]] with [[CMR]] [[contraindications]]. |
|
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|
| ===Endomyocardial Biopsy=== | | ===MRI=== |
| | [[Cardiac]] [[MRI]] is indicated in [[patients]] with new or persisting [[symptoms]] of [[chest pain]] and [[congestive heart failure]], who have [[evidence]] of [[significant]] [[myocardial injury]], in the absence of or in whom there is a low suspicion of coronary [[Atherosclerosis|atherosclerosis.]] [[Cardiac MRI]] findings associated with [[myocarditis]] include [[myocardial inflammation]], [[myocardial edema]], [[capillary leak]], and [[reduced left ventricular function]]. While the [[CMR]] 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 [[Endocardium|subendocardium]]. [[CMR]] has a [[sensitivity]] of 76%, [[specificity]] of 95.5%, and overall [[diagnostic]] [[accuracy]] of 85% when any-two of the following three sequences are used, focal and global T2 signal [[intensity]], [[myocardial]] global relative enhancement, and delayed [[gadolinium]] enhancement. |
|
| |
|
| 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 [[lymphocyte]]s and [[macrophage]]s. Focal destruction of [[myocytes]] as a result of the inflammatory process explains the myocardial [[pump failure]].<ref name="pmid11070105">{{cite journal| author=Feldman AM, McNamara D| title=Myocarditis. | journal=N Engl J Med | year= 2000 | volume= 343 | issue= 19 | pages= 1388-98 | pmid=11070105 | doi=10.1056/NEJM200011093431908 | pmc= | url= }} </ref>
| | ===Other Imaging Findings=== |
| | [[Coronary angiography]] may be helpful in excluding either [[myocardial ischemia]] or [[MI|infarction]] as the cause of [[ST segment elevation]], elevated [[cardiac biomarkers]], or [[left ventricular dysfunction]]. [[Nuclear]] [[imaging]] may be useful in [[diagnosis]] of [[cardiac sarcoidosis]]. |
|
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| ===Coronary Angiography=== | | ===Other Diagnostic Findings=== |
| [[Coronary angiography]] may be helpful in excluding either [[myocardial ischemia]] or [[MI|infarction]] as the cause of [[ST segment elevation]], elevated [[cardiac biomarkers]], or [[left ventricular dysfunction]].
| |
|
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|
| ===Cardiac Magnetic Resonance Imaging=== | | ==Treatment== |
| Myocardial inflammation associated with myocarditis appears as a high intensity signal with delayed gadolinium hyperenhancement on cardiac MRI (cMRI). <ref name="pmid15936612">{{cite journal| author=Abdel-Aty H, Boyé P, Zagrosek A, Wassmuth R, Kumar A, Messroghli D et al.| title=Diagnostic performance of cardiovascular magnetic resonance in patients with suspected acute myocarditis: comparison of different approaches. | journal=J Am Coll Cardiol | year= 2005 | volume= 45 | issue= 11 | pages= 1815-22 | pmid=15936612 | doi=10.1016/j.jacc.2004.11.069 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15936612 }} </ref>. 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<ref>{{cite journal |author=Skouri HN, Dec GW, Friedrich MG, Cooper LT |title=Noninvasive imaging in myocarditis |journal=J. Am. Coll. Cardiol. |volume=48 |issue=10 |pages=2085-93 |year=2006 |pmid=17112998 |doi=10.1016/j.jacc.2006.08.017}}</ref>.
| | ===Medical Therapy=== |
| | | [[Symptomatic]] [[Therapy|treatment]] is the mainstay of [[therapy]] for [[patients]] with [[viral myocarditis]]. Supportive [[therapy]] includes [[diuretic]]s and [[inotrope]]s for [[left ventricular failure]]. [[ACE inhibitor]] [[therapy]] may aid in left [[ventricular remodeling]]. Among patients with [[fulminant myocarditis]], placement of either an [[intra-aortic balloon pump]] or a [[left ventricular assist device]] may be necessary as bridge to [[recovery]]. Administration of [[antimicrobial]] [[therapy]] is recommended for [[bacterial myocarditis]]. [[Immunosuppressive therapy]] may be effective in the management of [[giant cell myocarditis]], [[autoimmune myocarditis]], and [[eosinophilic myocarditis]]. In [[patients]] with [[arrythmias]], [[Therapy|treatment]] should be initiated only if [[arrhythmias]] are [[symptomatic]] or sustained. [[Myocarditis]] [[patients]] presenting with [[Electrical conduction system of the heart|conduction]] abnormalities, particularly [[Mobitz II|Mobitz type II]] and [[complete heart block]] require temporary [[pacemaker]] usually during the [[acute]] phase. |
| ===Laboratory Findings===
| |
| Myocardial inflammation can be suspected on the basis of the clinical history along with elevations of<ref name="pmid11070105">{{cite journal| author=Feldman AM, McNamara D| title=Myocarditis. | journal=N Engl J Med | year= 2000 | volume= 343 | issue= 19 | pages= 1388-98 | pmid=11070105 | doi=10.1056/NEJM200011093431908 | pmc= | url= }} </ref>:
| |
| *Biomarkers of myocardial damage such as [[troponin]] or [[creatine kinase]]
| |
| *Antibodies against viruses known to affect the [[myocardium]] and cause myocarditis
| |
| *[[Erythrocyte sedimentation rate|ESR]]
| |
| *[[C-reactive protein]]
| |
| *Auto antibodies such as [[ANA]] and [[rheumatoid factor]]
| |
| | |
| ==Differentiating Myocarditis from Pericarditis and Myocardial Infarction==
| |
| Myocarditis presents with [[chest pain]] and [[ST segment elevation]]. Myocarditis must be distinguished from [[pericarditis]] and the life threatening condition of [[ST elevation myocardial infarction]].
| |
| | |
| ===Differentiating Myocarditis from ST Segment Elevation Myocardial Infarction===
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| Both diseases present with [[chest pain]], elevated [[cardiac biomarkers]], and focal [[left ventricular dysfunction]]. There are two studies that can be used to distinguish the two syndromes:
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| ====Coronary Angiography====
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| [[Coronary angiography]] can be performed to distinguish myocarditis from [[ST segment elevation myocardial infarction]]. [[ST segment elevation myocardial infarction]] is associated with either complete or subtotal occlusion of an epicardial [[coronary artery]] on coronary angiography. | |
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| ====Cardiac Magnetic Resonance Imaging====
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| [[Cardiac magnetic resonance imaging]] is also useful in distinguishing between the two syndromes as well. On cardiac [[MRI]], myocarditis is associated with patchy, non-sentimental, hyperenhancement which is confined to the epicardial layer of the myocardium. In contrast, in [[ST segment elevation myocardial infarction]] there is confluent hyperenhancement extending from the [[endocardium]] in a distribution that mimics the distribution of the epicardial coronary arteries. | |
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| ===Differentiating Myocarditis from Pericarditis===
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| Both diseases present with [[chest pain]] and [[ST segment elevation]]. The two conditions can be distinguished by the following studies:
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| ====Electrocardiogram====
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| While both disorders are associated with [[ST segment elevation]], [[pericarditis]] is also associated with [[PR segment]] depression.
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| ====Cardiac Biomarkers====
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| Myocarditis is associated with elevations of the [[CK-MB]] and the [[troponin]], while pericarditis is not. If [[pericarditis]] is associated with underlying inflammation of the [[myocardium]], then this is called [[myopericarditis]]. If there is concomitant involvement of both the [[pericardium]] and [[myocardium]] in [[myopericarditis]], then there are elevations of the [[cardiac biomarkers]].
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| ====Echocardiography====
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| In patients with myocarditis there will be a focal wall motion abnormalities, while these will be absent in the patient with pericarditis. There may be a [[pericardial effusion]] in the patient with [[pericarditis]], while myocarditis is not associated with a [[pericardial effusion]].
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| ==Treatment== | | ===Surgery=== |
| 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 [[diuretic]]s and [[inotrope]]s 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.
| | [[Cardiac transplantation]] is sometimes required to [[Therapy|treat]] [[refractory]] [[giant cell myocarditis]]. However, the [[condition]] can recur in post-[[transplant]] [[patients]]. |
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| According to 2010 HFSA guidelines<ref name="pmid20610207">{{cite journal| author=Heart Failure Society of America. Lindenfeld J, Albert NM, Boehmer JP, Collins SP, Ezekowitz JA et al.| title=HFSA 2010 Comprehensive Heart Failure Practice Guideline. | journal=J Card Fail | year= 2010 | volume= 16 | issue= 6 | pages= e1-194 | pmid=20610207 | doi=10.1016/j.cardfail.2010.04.004 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20610207 }} </ref>, 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.
| | ===Primary prevention=== |
| | There are no established measures for the [[primary prevention]] of all types of myocarditis. [[Vaccination]] against [[measles]], [[rubella]], [[mumps]], [[poliomyelitis]], and [[influenza]] could [[Prevention|prevent]] myocarditis [[secondary]] to these [[diseases]]. |
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| [[Bacterial infection]]s are treated with [[antibiotic]]s the selection of which is based upon the nature of the pathogen and its sensitivity to antibiotics. | | ===Secondary prevention=== |
| | Effective measures for the [[secondary prevention]] of myocarditis include, [[clinical]] evaluation, [[ECG]], and [[echocardiography]]. [[CMR]], [[cardiac]] [[CT scan]], [[Nuclear|nuclear assessment]] in [[patients]] that [[echocardiography]] is undiagnostic. [[Patients]] should udergo [[Cardiac function curve|cardiac function]] assessment at one and six months and yearly after that. |
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| ==References== | | ==References== |
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| [[Category:Cardiology]] | | [[Category:Cardiology]] |
| | [[Category:Cardiovascular diseases]] |
| | [[Category:Inflammations]] |
| | [[Category:Infectious diseases]] |
| | [[Category:Emergency medicine]] |
| [[Category:Disease]] | | [[Category:Disease]] |
| [[Category:Up-To-Date]] | | [[Category:Up-To-Date]] |
| [[Category:Up-To-Date cardiology]] | | [[Category:Up-To-Date cardiology]] |
| [[Category:Overview complete]] | | [[Category:Best pages]] |
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| {{WH}} | | {{WH}} |
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| {{WS}} | | {{WS}} |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. Maliha Shakil, M.D. [2] Homa Najafi, M.D.[3]
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. Myocarditis can be classified clinicopathologically into fulminant myocarditis, acute myocarditis, chronic active myocarditis, and chronic persistent myocarditis. During either an infection or a hypersensitivity reaction, the inflammatory response may cause myonecrosis either directly or indirectly as part of an autoimmune reaction. 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. Myocarditis must be distinguished from pericarditis and the life threatening condition of ST elevation myocardial infarction. 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. 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. 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 sudden death and cardiac transplantation. 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.
Historical Perspective
Myocarditis was first discovered by Jean Baptiste Senac, a French physician, in 1794. The term myocarditis was introduced by German physician Joseph Friedrich Sobernheim in 1837. In 1980s, the World Health Organization and the International Society and Federation of Cardiology were the first to differentiate between myocarditis and other cardiomyopathies. The Dallas criteria was published in 1986 as a guideline for classification of myocarditis.
Classification
Myocarditis can be classified based on the causative, histological, and clinicopathological criteria. Causative criteria include three main groups, as well as infectious, immune-mediated, and toxic myocarditis. Based on the type of infiltrating cells myocarditis divided in lymphocytic, eosinophilic, polymorphic, giant cell myocarditis, and cardiac sarcoidosis. Acute, fulminant, chronic active, and chronic persistent are subtypes of clinicopathopogical classification.
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 such as Lyme disease and medications. Idiopathic myocarditis is the most common type of myocarditis and is often suspected to be secondary to a viral infection.
Differentiating Myocarditis from other Diseases
Myocarditis must be distinguished from pericarditis and the life threatening condition of ST elevation myocardial infarction.
Risk factors
There are no established risk factors for myocarditis.
Screening
There is insufficient evidence to recommend routine screening for myocarditis.
Epidemiology and Demographics
The incidence of myocarditis is approximately 10 to 20 per 100,000 patients worldwide. It commonly affects younger individuals. Yong males are slightly more commonly affected by myocarditis than females. There is no racial predilection to myocarditis. Viral infections especially coxsackie B and enterovirus are the most common cause of myocarditis in developed countries. While, In South America, Chagas' disease (caused by Trypanosoma cruzi) is the main cause of myocarditis.
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. The prognosis of fulminant myocarditis is better than that of either acute myocarditis or giant cell myocarditis. The presence of syncope, pulmonary hypertension, biventricular dysfunction, left bundle branch block, q waves, AV block, and a left ventricular ejection fraction < 40% are associated with sudden death and cardiac transplantation. Complications of myocarditis include chronic dilated cardiomyopathy, heart block, congestive heart failure, pericarditis, ventricular dysfunction, arrythmias, and sudden cardiac death.
Diagnosis
History and Symptoms
Myocarditis should be suspected in a patient with acute decompensation of cardiac function who is at low risk of ischemic heart disease. A history of a recent (within the preceding 2-4 weeks) viral illness is often elicited in a large number of patients with myocarditis. Cardiac specific symptoms may become apparent usually in the subacute virus-clearing phase. In myocarditis due to drug hypersensitivity, patients may give a history of ingesting an offending drug. 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. Common symptoms of myocarditis include chest pain, pedal edema, palpitations, fever, and joint pains.
Physical Examination
There are no specific findings for myocarditis. Patients with myocarditis usually show signs of cardiac dysfunction and underlying diseases. 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
Laboratory findings consistent with the diagnosis of myocarditis include elevated markers of myonecrosis, inflammatory markers, and other biomarkers. Markers of myonecrosis include creatine kinase (CK-MB), cardiac troponin I (cTnI) or T (cTnT), lactate dehydrogenase (LDH), alanine transaminase (ALT), and aspartate transaminase (AST). Elevated levels of C-reactive protein and erythrocyte sedimentation rate (ESR), and leukocytosis are suggestive of myocarditis. Serologic markers such as Fas, Fas ligand, interleukin-10 or antimyosin autoantibodies are of prognostic value in myocarditis. 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. 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
Findings on chest x-ray suggestive of myocarditis include cardiomegaly, cephalization of the pulmonary vessels and, Kerley B-lines in presence of heart failure pericardial thickening in presence of pericarditis, pulmonary edema, and pleural effusion.
Echocardiography
Echocardiography in patients with myocarditis allows for serial assessment of left ventricular dysfunction 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). Echocardiography may be helpful in the diagnosis of myocarditis. Findings on an echocardiography suggestive of myocarditis include wall motion abnormalities, systolic and diastolic dysfunction, changes in image texture, pericardial effusion, and functional regurgitation through the AV valves.
CT scan
Cardiac CT scan may be helpful in the diagnosis of myocarditis. Cardiac CT scan can be used in diagnosis of acute myocarditis ( subepicardial late iodine enhancement), exclusion of acute coronary syndrome by CT angiography, and alternative diagnostic tool in patients with CMR contraindications.
MRI
Cardiac MRI is indicated in patients with new or persisting symptoms of chest pain and congestive heart failure, who have evidence of significant myocardial injury, in the absence of or in whom there is a low suspicion of coronary atherosclerosis. Cardiac MRI findings associated with myocarditis include myocardial inflammation, myocardial edema, capillary leak, and reduced left ventricular function. While the CMR 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. CMR has a sensitivity of 76%, specificity of 95.5%, and overall diagnostic accuracy of 85% when any-two of the following three sequences are used, focal and global T2 signal intensity, myocardial global relative enhancement, and delayed gadolinium enhancement.
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. Nuclear imaging may be useful in diagnosis of cardiac sarcoidosis.
Other Diagnostic Findings
Treatment
Medical 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. Among patients with fulminant myocarditis, placement of either an intra-aortic balloon pump or a left ventricular assist device may be necessary as bridge to recovery. Administration of antimicrobial therapy is recommended for bacterial myocarditis. Immunosuppressive therapy may be effective in the management of giant cell myocarditis, autoimmune myocarditis, and eosinophilic myocarditis. In patients with arrythmias, treatment should be initiated only if arrhythmias are symptomatic or sustained. Myocarditis patients presenting with conduction abnormalities, particularly Mobitz type II and complete heart block require temporary pacemaker usually during the acute phase.
Surgery
Cardiac transplantation is sometimes required to treat refractory giant cell myocarditis. However, the condition can recur in post-transplant patients.
Primary prevention
There are no established measures for the primary prevention of all types of myocarditis. Vaccination against measles, rubella, mumps, poliomyelitis, and influenza could prevent myocarditis secondary to these diseases.
Secondary prevention
Effective measures for the secondary prevention of myocarditis include, clinical evaluation, ECG, and echocardiography. CMR, cardiac CT scan, nuclear assessment in patients that echocardiography is undiagnostic. Patients should udergo cardiac function assessment at one and six months and yearly after that.
References
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