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{{Myocarditis}}
{{Myocarditis}}
{{CMG}} '''Associate Editor(s)-In-Chief:''' [[Varun Kumar|Varun Kumar, M.B.B.S.]]
{{CMG}} {{AE}} [[Varun Kumar|Varun Kumar, M.B.B.S.]], {{Maliha}}{{Homa}}


==Overview==
==Overview==
Myocardial inflammation can be suspected on the basis of elevated [[C-reactive protein]], [[Erythrocyte sedimentation rate|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<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 auto antibodies such as [[ANA]] and [[rheumatoid factor]] may also be detected.
[[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.


==Markers of Myonecrosis==
==Laboratory Findings==
The following markers of myonecrosis are often elevated in myocarditis, particularly early on in the course of the disease:
===Markers of Myonecrosis===
*'''[[Creatine Kinase]] (CK-MB)'''
The following [[Marker|markers]] of [[myonecrosis]] are often [[Elevation|elevated]] in myocarditis, particularly early on in the [[Course (medicine)|course]] of the [[disease]]:<ref name="pmid8994432">{{cite journal| author=Smith SC, Ladenson JH, Mason JW, Jaffe AS| title=Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates. | journal=Circulation | year= 1997 | volume= 95 | issue= 1 | pages= 163-8 | pmid=8994432 | doi= | pmc= | url= }} </ref><ref name="pmid9350939">{{cite journal| author=Lauer B, Niederau C, Kühl U, Schannwell M, Pauschinger M, Strauer BE et al.| title=Cardiac troponin T in patients with clinically suspected myocarditis. | journal=J Am Coll Cardiol | year= 1997 | volume= 30 | issue= 5 | pages= 1354-9 | pmid=9350939 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9350939  }} </ref><ref name="pmid12211203">{{cite journal| author=Soongswang J, Durongpisitkul K, Ratanarapee S, Leowattana W, Nana A, Laohaprasitiporn D et al.| title=Cardiac troponin T: its role in the diagnosis of clinically suspected acute myocarditis and chronic dilated cardiomyopathy in children. | journal=Pediatr Cardiol | year= 2002 | volume= 23 | issue= 5 | pages= 531-5 | pmid=12211203 | doi= | pmc= | url= }} </ref><ref name="pmid18055677">{{cite journal| author=Freedman SB, Haladyn JK, Floh A, Kirsh JA, Taylor G, Thull-Freedman J| title=Pediatric myocarditis: emergency department clinical findings and diagnostic evaluation. | journal=Pediatrics | year= 2007 | volume= 120 | issue= 6 | pages= 1278-85 | pmid=18055677 | doi=10.1542/peds.2007-1073 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18055677  }} </ref><ref name="pmid18381554">{{cite journal| author=Lippi G, Salvagno GL, Guidi GC| title=Cardiac troponins in pediatric myocarditis. | journal=Pediatrics | year= 2008 | volume= 121 | issue= 4 | pages= 864; author reply 864-5 | pmid=18381554 | doi=10.1542/peds.2008-0031 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18381554  }} </ref>
*'''[[troponin|Cardiac troponin]] I (cTnI) or T (cTnT)''' are elevated more frequently than CK-MB (34-53% versus 2-6 %) as reported in two series<ref name="pmid8994432">{{cite journal| author=Smith SC, Ladenson JH, Mason JW, Jaffe AS| title=Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates. | journal=Circulation | year= 1997 | volume= 95 | issue= 1 | pages= 163-8 | pmid=8994432 | doi= | pmc= | url= }} </ref><ref name="pmid9350939">{{cite journal| author=Lauer B, Niederau C, Kühl U, Schannwell M, Pauschinger M, Strauer BE et al.| title=Cardiac troponin T in patients with clinically suspected myocarditis. | journal=J Am Coll Cardiol | year= 1997 | volume= 30 | issue= 5 | pages= 1354-9 | pmid=9350939 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9350939  }} </ref>. cTnI is elevated early in the course and is suggestive of acute myocarditis<ref name="pmid8994432">{{cite journal| author=Smith SC, Ladenson JH, Mason JW, Jaffe AS| title=Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates. | journal=Circulation | year= 1997 | volume= 95 | issue= 1 | pages= 163-8 | pmid=8994432 | doi= | pmc= | url= }} </ref>. Persistently elevated cTnT or CK-MB is suggestive of ongoing [[myonecrosis]]. Cardiac enzymes may also be useful in differentiating myocarditis from [[dilated cardiomyopathy]] as [[CK-MB]] and [[cTnT]] levels are higher in [[myocarditis]] than [[dilated cardiomyopathy]]<ref name="pmid12211203">{{cite journal| author=Soongswang J, Durongpisitkul K, Ratanarapee S, Leowattana W, Nana A, Laohaprasitiporn D et al.| title=Cardiac troponin T: its role in the diagnosis of clinically suspected acute myocarditis and chronic dilated cardiomyopathy in children. | journal=Pediatr Cardiol | year= 2002 | volume= 23 | issue= 5 | pages= 531-5 | pmid=12211203 | doi= | pmc= | url= }} </ref>.
*[[Creatine kinase]] ([[CK-MB]])
*[[troponin|Cardiac troponin]] I ([[cTnI]]) or T ([[cTnT]]) are [[Elevation|elevated]] more frequently than [[CK-MB]] (34-53% versus 2-6 %) as reported in two series. [[troponin|Cardiac troponin]] I is [[Elevation|elevated]] early in the [[Course (medicine)|course]] and is suggestive of [[acute]] myocarditis. Persistently [[Elevation|elevated]] [[cTnT]] or [[CK-MB]] is suggestive of ongoing [[myonecrosis]]. [[Cardiac enzymes]] may also be useful in [[Differentiate|differentiating]] myocarditis from [[dilated cardiomyopathy]] as [[CK-MB]] and [[cTnT]] levels are higher in [[myocarditis]] than [[dilated cardiomyopathy]].


*'''[[Lactate Dehydrogenase]] (LDH)'''
*[[Lactate dehydrogenase]] ([[LDH]])
*'''[[Alanine Transaminase]] (ALT)'''
*[[Alanine transaminase]] ([[ALT]])
*'''[[Aspartate transaminase|Aspartate Transaminase]] (AST)'''
*[[Aspartate transaminase]] ([[AST]])


:[[AST]] is considered to be the most sensitive marker of myocarditis<ref name="pmid18055677">{{cite journal| author=Freedman SB, Haladyn JK, Floh A, Kirsh JA, Taylor G, Thull-Freedman J| title=Pediatric myocarditis: emergency department clinical findings and diagnostic evaluation. | journal=Pediatrics | year= 2007 | volume= 120 | issue= 6 | pages= 1278-85 | pmid=18055677 | doi=10.1542/peds.2007-1073 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18055677  }} </ref> with the sensitivity of 85%. However, the specificities of AST and ALT are low in patients with myocarditis as they may be elevated secondary to other coexisting systemic or organ dysfunction<ref name="pmid18381554">{{cite journal| author=Lippi G, Salvagno GL, Guidi GC| title=Cardiac troponins in pediatric myocarditis. | journal=Pediatrics | year= 2008 | volume= 121 | issue= 4 | pages= 864; author reply 864-5 | pmid=18381554 | doi=10.1542/peds.2008-0031 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18381554  }} </ref>.
'''Note:''' [[AST]] is considered to be the most sensitive [[marker]] of myocarditis with the [[sensitivity]] of 85%. However, the specificities of [[AST]] and [[ALT]] are low in [[patients]] with myocarditis as they may be [[Elevation|elevated]] [[secondary]] to other coexisting [[systemic]] or [[Organ (biology)|organ]] [[dysfunction]].


==Inflammatory Markers==
===Inflammatory Markers===
The following inflammatory markers are often elevated:
The following [[inflammatory]] markers are often [[Elevation|elevated]]:<ref>{{Cite journal
 
| author = [[Giovanni Donato Aquaro]], [[Matteo Perfetti]], [[Giovanni Camastra]], [[Lorenzo Monti]], [[Santo Dellegrottaglie]], [[Claudio Moro]], [[Alessia Pepe]], [[Giancarlo Todiere]], [[Chiara Lanzillo]], [[Alessandra Scatteia]], [[Mauro Di Roma]], [[Gianluca Pontone]], [[Martina Perazzolo Marra]], [[Andrea Barison]] & [[Gianluca Di Bella]]
*[[Complete Blood Count|CBC]]: [[Leukocytosis]] or [[eosinophilia]] in hypersensitive [[myocarditis]].
| title = Cardiac MR With Late Gadolinium Enhancement in Acute Myocarditis With Preserved Systolic Function: ITAMY Study
| journal = [[Journal of the American College of Cardiology]]
| volume = 70
| issue = 16
| pages = 1977–1987
| year = 2017
| month = October
| doi = 10.1016/j.jacc.2017.08.044
| pmid = 29025554
}}</ref><ref>{{Cite journal
| author = [[Michela Brambatti]], [[Maria Vittoria Matassini]], [[Eric D. Adler]], [[Karin Klingel]], [[Paolo G. Camici]] & [[Enrico Ammirati]]
| title = Eosinophilic Myocarditis: Characteristics, Treatment, and Outcomes
| journal = [[Journal of the American College of Cardiology]]
| volume = 70
| issue = 19
| pages = 2363–2375
| year = 2017
| month = November
| doi = 10.1016/j.jacc.2017.09.023
| pmid = 29096807
}}</ref>
*[[Complete Blood Count|CBC]]: [[leukocytosis]] or [[eosinophilia]] in [[hypersensitive]] [[myocarditis]].
*[[C-reactive protein]]
*[[C-reactive protein]]
*Erythrocyte sedimentation rate ([[ESR]])
*[[Erythrocyte sedimentation rate]] ([[ESR]])


==Other Biomarkers==
===Other Biomarkers===
*Serological markers such as [[Fas]], [[Fas ligand]], [[interleukin]]-10 or [[antimyosin autoantibodies]] are of prognostic value in myocarditis.  
*[[Serological]] [[Marker|markers]] such as [[Fas]], [[Fas ligand]], [[interleukin-10]] or antimyosin [[Autoantibody|autoantibodies]] are of [[prognostic]] value in myocarditis. <ref name="pmid16168288">{{cite journal| author=Sheppard R, Bedi M, Kubota T, Semigran MJ, Dec W, Holubkov R et al.| title=Myocardial expression of fas and recovery of left ventricular function in patients with recent-onset cardiomyopathy. | journal=J Am Coll Cardiol | year= 2005 | volume= 46 | issue= 6 | pages= 1036-42 | pmid=16168288 | doi=10.1016/j.jacc.2005.05.067 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16168288  }} </ref><ref name="pmid10636253">{{cite journal| author=Lauer B, Schannwell M, Kühl U, Strauer BE, Schultheiss HP| title=Antimyosin autoantibodies are associated with deterioration of systolic and diastolic left ventricular function in patients with chronic myocarditis. | journal=J Am Coll Cardiol | year= 2000 | volume= 35 | issue= 1 | pages= 11-8 | pmid=10636253 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10636253  }} </ref><ref name="pmid15364334">{{cite journal| author=Nishii M, Inomata T, Takehana H, Takeuchi I, Nakano H, Koitabashi T et al.| title=Serum levels of interleukin-10 on admission as a prognostic predictor of human fulminant myocarditis. | journal=J Am Coll Cardiol | year= 2004 | volume= 44 | issue= 6 | pages= 1292-7 | pmid=15364334 | doi=10.1016/j.jacc.2004.01.055 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15364334  }} </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>
**'''[[Fas]] and [[Fas ligand]]''' are markers of cell death ([[apoptosis]]) and are associated with [[cardiac dysfunction]]. A study evaluating the role of gene expression for predicting myocardial recovery in recent-onset cardiomyopathy, reported that patients in the highest tertile of Fas expression had minimal improvement at six months when compared with the intermediate and lowest tertiles<ref name="pmid16168288">{{cite journal| author=Sheppard R, Bedi M, Kubota T, Semigran MJ, Dec W, Holubkov R et al.| title=Myocardial expression of fas and recovery of left ventricular function in patients with recent-onset cardiomyopathy. | journal=J Am Coll Cardiol | year= 2005 | volume= 46 | issue= 6 | pages= 1036-42 | pmid=16168288 | doi=10.1016/j.jacc.2005.05.067 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16168288  }} </ref>.
**[[Fas]] and [[Fas ligand]] are [[Marker|markers]] of [[cell death]] ([[apoptosis]]) and are associated with [[cardiac dysfunction]].
**'''Antimyosin autoantibodies''' are associated with left ventricular systolic dysfunction and diastolic stiffness in patients with chronic myocarditis<ref name="pmid10636253">{{cite journal| author=Lauer B, Schannwell M, Kühl U, Strauer BE, Schultheiss HP| title=Antimyosin autoantibodies are associated with deterioration of systolic and diastolic left ventricular function in patients with chronic myocarditis. | journal=J Am Coll Cardiol | year= 2000 | volume= 35 | issue= 1 | pages= 11-8 | pmid=10636253 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10636253  }} </ref>.
**Antimyosin [[autoantibodies]] are associated with [[left ventricular systolic dysfunction]] and [[diastolic stiffness]] in [[patients]] with [[Chronic (medical)|chronic]] myocarditis.
**High levels of '''[[interleukin-10]]''' in fulminant myocarditis patients at admission may be predictive of subsequent development of [[cardiogenic shock]] (requiring mechanical cardiopulmonary support system) and mortality<ref name="pmid15364334">{{cite journal| author=Nishii M, Inomata T, Takehana H, Takeuchi I, Nakano H, Koitabashi T et al.| title=Serum levels of interleukin-10 on admission as a prognostic predictor of human fulminant myocarditis. | journal=J Am Coll Cardiol | year= 2004 | volume= 44 | issue= 6 | pages= 1292-7 | pmid=15364334 | doi=10.1016/j.jacc.2004.01.055 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15364334  }} </ref>.
**High levels of [[interleukin-10]] in [[fulminant]] myocarditis [[patients]] at [[Admission note|admission]] may be [[Predictive medicine|predictive]] of subsequent [[development]] of [[cardiogenic shock]] (requiring mechanical [[cardiopulmonary]] [[support]] [[system]]) and [[mortality]].
**[[Viral]] [[Antibody titer|antibody titers]] for [[coxsackie B virus]], [[Human Immunodeficiency Virus (HIV)|human immunodeficiency virus]] ([[HIV]]), [[cytomegalovirus]], [[Ebstein-Barr virus]], [[Hepatitis|hepatitis virus family]], and [[influenza virus]] may be useful in [[diagnosis]] the causative [[organism]]. However, the management of myocarditis due to a [[viral]] [[etiology]] seldom differs depending upon the [[virus]], and therefore, [[Antibody titer|antibody titers]] are rarely [[Indication (medicine)|indicated]] in the [[diagnostic]] evaluation of myocarditis.


*'''Viral antibody titers''' for [[coxsackie B virus]], human immunodeficiency virus ([[HIV]]), [[cytomegalovirus]], [[Ebstein-Barr virus]], [[hepatitis virus]] family, and [[influenza virus]] may be useful in diagnosing the causative organism. However, the management of myocarditis due to a viral etiology seldom differs depending upon the virus, and therefore, antibody titers are rarely indicated in the diagnostic evaluation of myocarditis.
*[[Autoantibodies|Auto-antibodies]] such as [[ANA]], [[rheumatoid factor]], and [[anti-topoisomerase antibodies]] may identify conditions that respond to [[immunosuppressive therapy]].


*'''Auto antibodies''' such as [[ANA]], [[rheumatoid factor]], and [[anti-topoisomerase antibodies]] may identify conditions that respond to immunosuppressive therapy.
*[[Polymerase chain reaction]] ([[PCR]]) may be used in the detection of and identification of [[viral infections]] from [[myocardial biopsy]], [[pericardial fluid]] or other [[body]] [[fluids]]. Persistence of a [[viral]] [[genome]] is indicative of a poor [[prognosis]].
 
*'''Polymerase chain reaction (PCR)''' may be used in the detection of and identification of viral infections from [[myocardial biopsy]], pericardial fluid or other body fluids. Persistence of a viral genome is indicative of a poor prognosis<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>.


==References==
==References==
{{reflist|2}}
{{reflist|2}}
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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

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.

Laboratory Findings

Markers of Myonecrosis

The following markers of myonecrosis are often elevated in myocarditis, particularly early on in the course of the disease:[1][2][3][4][5]

Note: AST is considered to be the most sensitive marker of myocarditis with the sensitivity of 85%. However, the specificities of AST and ALT are low in patients with myocarditis as they may be elevated secondary to other coexisting systemic or organ dysfunction.

Inflammatory Markers

The following inflammatory markers are often elevated:[6][7]

Other Biomarkers

References

  1. ↑ Smith SC, Ladenson JH, Mason JW, Jaffe AS (1997). "Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates". Circulation. 95 (1): 163–8. PMID 8994432.
  2. ↑ Lauer B, Niederau C, Kühl U, Schannwell M, Pauschinger M, Strauer BE; et al. (1997). "Cardiac troponin T in patients with clinically suspected myocarditis". J Am Coll Cardiol. 30 (5): 1354–9. PMID 9350939.
  3. ↑ Soongswang J, Durongpisitkul K, Ratanarapee S, Leowattana W, Nana A, Laohaprasitiporn D; et al. (2002). "Cardiac troponin T: its role in the diagnosis of clinically suspected acute myocarditis and chronic dilated cardiomyopathy in children". Pediatr Cardiol. 23 (5): 531–5. PMID 12211203.
  4. ↑ Freedman SB, Haladyn JK, Floh A, Kirsh JA, Taylor G, Thull-Freedman J (2007). "Pediatric myocarditis: emergency department clinical findings and diagnostic evaluation". Pediatrics. 120 (6): 1278–85. doi:10.1542/peds.2007-1073. PMID 18055677.
  5. ↑ Lippi G, Salvagno GL, Guidi GC (2008). "Cardiac troponins in pediatric myocarditis". Pediatrics. 121 (4): 864, author reply 864-5. doi:10.1542/peds.2008-0031. PMID 18381554.
  6. ↑ Giovanni Donato Aquaro, Matteo Perfetti, Giovanni Camastra, Lorenzo Monti, Santo Dellegrottaglie, Claudio Moro, Alessia Pepe, Giancarlo Todiere, Chiara Lanzillo, Alessandra Scatteia, Mauro Di Roma, Gianluca Pontone, Martina Perazzolo Marra, Andrea Barison & Gianluca Di Bella (2017). "Cardiac MR With Late Gadolinium Enhancement in Acute Myocarditis With Preserved Systolic Function: ITAMY Study". Journal of the American College of Cardiology. 70 (16): 1977–1987. doi:10.1016/j.jacc.2017.08.044. PMID 29025554. Unknown parameter |month= ignored (help)
  7. ↑ Michela Brambatti, Maria Vittoria Matassini, Eric D. Adler, Karin Klingel, Paolo G. Camici & Enrico Ammirati (2017). "Eosinophilic Myocarditis: Characteristics, Treatment, and Outcomes". Journal of the American College of Cardiology. 70 (19): 2363–2375. doi:10.1016/j.jacc.2017.09.023. PMID 29096807. Unknown parameter |month= ignored (help)
  8. ↑ Sheppard R, Bedi M, Kubota T, Semigran MJ, Dec W, Holubkov R; et al. (2005). "Myocardial expression of fas and recovery of left ventricular function in patients with recent-onset cardiomyopathy". J Am Coll Cardiol. 46 (6): 1036–42. doi:10.1016/j.jacc.2005.05.067. PMID 16168288.
  9. ↑ Lauer B, Schannwell M, Kühl U, Strauer BE, Schultheiss HP (2000). "Antimyosin autoantibodies are associated with deterioration of systolic and diastolic left ventricular function in patients with chronic myocarditis". J Am Coll Cardiol. 35 (1): 11–8. PMID 10636253.
  10. ↑ Nishii M, Inomata T, Takehana H, Takeuchi I, Nakano H, Koitabashi T; et al. (2004). "Serum levels of interleukin-10 on admission as a prognostic predictor of human fulminant myocarditis". J Am Coll Cardiol. 44 (6): 1292–7. doi:10.1016/j.jacc.2004.01.055. PMID 15364334.
  11. ↑ Kühl U, Pauschinger M, Seeberg B, Lassner D, Noutsias M, Poller W; et al. (2005). "Viral persistence in the myocardium is associated with progressive cardiac dysfunction". Circulation. 112 (13): 1965–70. doi:10.1161/CIRCULATIONAHA.105.548156. PMID 16172268.

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