Myocarditis laboratory findings: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
m (Bot: Removing from Primary care)
 
(40 intermediate revisions by 8 users not shown)
Line 1: Line 1:
__NOTOC__
{{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>
*'''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>.  
*[[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]].


Persistently elevated cTnT or CK-MB is suggestive of ongoing necrosis. Cardiac enzymes may also be useful in differentiating myocarditis from [[dilated cardiomyopathy]] as demonstrated in a series in Thailand<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>. CK-MB and cTnT levels were found to be higher in myocarditis than [[dilated cardiomyopathy]].
*[[Lactate dehydrogenase]] ([[LDH]])
*[[Alanine transaminase]] ([[ALT]])
*[[Aspartate transaminase]] ([[AST]])


'''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==
*Serological markers such as [[Fas]], [[Fas ligand]], [[interleukin]]-10 or [[antimyosin autoantibodies]] are of prognostic value in myocarditis.
**'''[[Fas]] and [[Fas ligand]]''' can lead to apoptotic  death of myocytes and thus causing 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>.
**'''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>.
**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>.


*'''Viral antibody titers''' for [[coxsackie B virus]], human immunodeficiency virus ([[HIV]]), [[cytomegalovirus]], [[Ebstein-Barr virus]], [[hepatitis virus]] family, and [[influenza virus]] assist in recognizing the causative organism. However, the management of myocarditis of viral etiology seldom differ with the virus and hence, antibody titers are rarely indicated in the diagnosis.
===Other Biomarkers===
*[[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 [[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 (medical)|chronic]] myocarditis.
**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.


*'''Auto antibodies''' such as [[ANA]], [[rheumatoid factor]], and [[anti-topoisomerase antibodies]] help in determining the etiology of [[myocarditis]] and thus help in effective management of the condition with immunosuppressants if needed.
*[[Autoantibodies|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 detection and identification of viral infections from [[myocardial biopsy]], pericardial fluid or other body fluids. Persistence of viral genome is indicative of 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>.  
*[[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]].


==References==
==References==
{{reflist|2}}
{{reflist|2}}
{{WS}}
{{WH}}


[[Category:Medicine]]
[[Category:Cardiology]]
[[Category:Cardiology]]
[[Category:Laboratory Test]]
[[Category:Up-To-Date]]
[[Category:Up to date]]
[[Category:Emergency medicine]]
[[Category:Up to date cardiology]]
[[Category:Intensive care medicine]]
[[Category:Overview complete]]
 
{{WS}}
{{WH}}

Latest revision as of 22:51, 29 July 2020

Myocarditis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Adrenergic Myocarditis
Giant Cell Myocarditis

Causes

Differentiating Myocarditis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Myocarditis laboratory findings On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Google Images

American Roentgen Ray Society Images of Myocarditis laboratory findings

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Myocarditis laboratory findings

CDC on Myocarditis laboratory findings

Myocarditis laboratory findings in the news

Blogs on Myocarditis laboratory findings

Directions to Hospitals Treating Type page name here

Risk calculators and risk factors for Myocarditis laboratory findings

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.

Template:WS Template:WH

Retrieved from "https://www.wikidoc.org/index.php?title=Myocarditis_laboratory_findings&oldid=1641008"