Cited by 359Viral Infections and Immunology ResearchCardiomyopathy and Myosin StudiesCardiovascular Effects of Exercise

The Quest for New Approaches in Myocarditis and Inflammatory Cardiomyopathy

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Heymans, Stephane, Eriksson, Urs, Lehtonen, Jukka, Cooper, Leslie T.·2016·Journal of the American College of Cardiology

Abstract

Myocarditis is a diverse group of heart-specific immune processes classified by clinical and histopathological manifestations. Up to 40% of dilated cardiomyopathy is associated with inflammation or viral infection. Recent experimental studies revealed complex regulatory roles for several microribonucleic acids and T-cell and macrophage subtypes. Although the prevalence of myocarditis remained stable between 1990 and 2013 at about 22 per 100,000 people, overall mortality from cardiomyopathy and myocarditis has decreased since 2005. The diagnostic and prognostic value of cardiac magnetic resonance has increased with new, higher-sensitivity sequences. Positron emission tomography has emerged as a useful tool for diagnosis of cardiac sarcoidosis. The sensitivity of endomyocardial biopsy may be increased, especially in suspected sarcoidosis, by the use of electrogram guidance to target regions of abnormal signal. Investigational treatments on the basis of mechanistic advances are entering clinical trials. Revised management recommendations regarding athletic participation after acute myocarditis have heightened the importance of early diagnosis.

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Crossref · 10.1016/j.jacc.2016.09.937

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  • The monocyte and macrophage lineage constitute the most abundant immune cell population in the hearts of healthy adults and under myocarditis conditions.

    “The monocyte and macrophage lineage constitute the most abundant immune cell population in the hearts of healthy adults and under myocarditis conditions”

    From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [107]

    The Innate Mechanisms section (page unavailable) describes macrophages and heart-infiltrating monocytic precursors in myocardial inflammation, and the Role of T-Cell Subsets section says T cells are a minority of infiltrating cells in myocarditis. Neither passage establishes that the monocyte–macrophage lineage is the most abundant immune-cell population in myocarditis or in healthy adult hearts. (LLM, conf=0.78)

    Experimental — accuracy not yet measured
  • In preclinical animal models for myocarditis, monocytes and macrophages were predominant populations in heart infiltrates.

    “in preclinical animal models for myocarditis, monocytes and macrophages were predominant populations in the heart infiltrates”

    From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [107]

    The Innate Mechanisms section describes heart-infiltrating monocytic precursors as a source of acute inflammation and says M2 macrophages predominate during myocardial healing. The Role of T-Cell Subsets section says T cells are a minority of heart-infiltrating cells in mouse myocarditis models. Neither passage establishes that monocytes and macrophages together are the predominant infiltrating populations across preclinical myocarditis models. (LLM, conf=0.82)

    Experimental — accuracy not yet measured
  • An unnoticed history of viral infection may contribute to the migration and activation of autoreactive T cells in the heart.

    “an unnoticed history of viral infection may contribute to the migration and activation of autoreactive T cells in the heart. 7,10,31,107”

    From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [107]

    The “Role of T-Cell Subsets in Myocarditis” section (page not provided) says that T-cell responses can turn initial myocarditis into an autoimmune response after an infectious agent is cleared, and that dendritic cells promote expansion of autoreactive T cells and heart-specific inflammation. It does not establish that the earlier viral infection was unnoticed or specifically describe migration of autoreactive T cells into the heart. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

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Research works printed but not linked: 87

  1. Leslie T. Cooper Jr., Cardiovascular Department, Mayo Clinic, 4500 San Pablo Road, Jacksonville, Florida 32224. E-mail: cooper.leslie@mayo.. F E R E N C E S 1. Cooper LT Jr. Myocarditis. N Engl J Med 2009; 360:1526-38.
  2. Dennert R, Crijns HJ, Heymans S. Acute viral myocarditis. Eur Heart J 2008;29:2073-82.
  3. Caforio ALP, Pankuweit S, Arbustini E, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a posi- tion statement of the European Society of Cardi- ology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 2013;34:2636-48.
  4. Global Burden of Disease Study 2013 Collabo- rators. Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet 2015;386:743-800.
  5. Cooper LT Jr., Keren A, Sliwa K, et al. The global burden of myocarditis: part 1: a systematic litera- ture review for the Global Burden of Diseases, Injuries, and Risk Factors 2010 study. Glob Heart 2014;9:121-9.
  6. Maron BJ, Udelson JE, Bonow RO, et al. Eligibility and disqualification recommendations for compet- itive athletes with cardiovascular abnormalities: Task Force 3: hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and other cardiomyopathies, and myocarditis: a scientific statement from the American Heart As- sociation and American College of Cardiology. J Am Coll Cardiol 2015;66:2362-71.
  7. Matoba R, Shikata I, Iwai K, et al. An epidemi- ologic and histopathological study of sudden car- diac death in Osaka Medical Examiner's Office. Jpn Circ J 1989;53:1581-8.
  8. Kandolin R, Lehtonen J, Airaksinen J, et al. Cardiac sarcoidosis: epidemiology, characteristics, and outcome over 25 years in a nationwide study. Circulation 2015;131:624-32.
  9. Roberts WC, McAllister HA Jr., Ferrans VJ. Sarcoidosis of the heart. A clinicopathologic study of 35 necropsy patients (group I) and review of 78 previously described necropsy patients (group II). Am J Med 1977;63:86-108.
  10. Hazebroek MR, Moors S, Dennert R, et al. Prognostic relevance of gene-environment in- teractions in patients with dilated cardiomyopa- thy: applying the MOGE(S) classification. J Am Coll Cardiol 2015;66:1313-23.
  11. Cooper LT Jr., Hare JM, Tazelaar HD, et al., for the Giant Cell Myocarditis Treatment Trial In- vestigators. Usefulness of immunosuppression for giant cell myocarditis. Am J Cardiol 2008;102: 1535-9.
  12. Kandolin R, Lehtonen J, Salmenkivi K, et al. Diagnosis, treatment, and outcome of giant-cell myocarditis in the era of combined immunosup- pression. Circ Heart Failure 2013;6:15-22.
  13. Whitehead R. Isolated myocarditis. Brit Heart J 1965;27:220-30.
  14. Kytö V, Saukko P, Lignitz E, et al. Diagnosis and presentation of fatal myocarditis. Hum Pathol 2005;36:1003-7.
  15. Davidoff R, Palacios I, Southern J, et al. Giant cell versus lymphocytic myocarditis. A comparison of their clinical features and long-term outcomes. Circulation 1991;83:953-61.
  16. Schultheiss HP, Kühl U, Cooper LT. The manage- ment of myocarditis. Eur Heart J 2011;32:2616-25.
  17. Andréoletti L, Lévêque N, Boulagnon C, et al. Viral causes of human myocarditis. Arch Car- diovasc Dis 2009;102:559-68.
  18. Pauschinger M, Phan MD, Doerner A, et al. Enteroviral RNA replication in the myocardium of patients with left ventricular dysfunction and clinically suspected myocarditis. Circulation 1999; 99:889-95.
  19. Baruteau AE, Boimond N, Ramful D. Myocar- ditis associated with 2009 influenza A (H1N1) virus in children. Cardiol Young 2010;20:351-2.
  20. Bowles NE, Ni J, Kearney DL, et al. Detection of viruses in myocardial tissues by polymerase chain reaction. Evidence of adenovirus as a com- mon cause of myocarditis in children and adults. J Am Coll Cardiol 2003;42:466-72.
  21. Pauschinger M, Bowles NE, Fuentes-Garcia FJ, et al. Detection of adenoviral genome in the myocardium of adult patients with idiopathic left ventricular dysfunction. Circulation 1999;99: 1348-54.
  22. Matsumori A, Yutani C, Ikeda Y, et al. Hepatitis C virus from the hearts of patients with myocar- ditis and cardiomyopathy. Lab Invest 2000;80: 1137-42.
  23. Omura T, Yoshiyama M, Hayashi T, et al. Core protein of hepatitis C virus induces cardiomyopa- thy. Circ Res 2005;96:148-50.
  24. Chimenti C, Russo A, Pieroni M, et al. Intra- myocyte detection of Epstein-Barr virus genome by laser capture microdissection in patients with inflammatory cardiomyopathy. Circulation 2004; 110:3534-9.
  25. Breinholt JP, Moulik M, Dreyer WJ, et al. Viral epidemiologic shift in inflammatory heart disease: the increasing involvement of parvovirus B19 in the myocardium of pediatric cardiac transplant patients. J Heart Lung Transplant 2010;29: 739-46.
  26. Kühl U, Pauschinger M, Noutsias M, et al. High prevalence of viral genomes and multiple viral infections in the myocardium of adults with "idiopathic" left ventricular dysfunction. Circula- tion 2005;111:887-93.
  27. Ellis NM, Kurahara DK, Vohra H, et al. Priming the immune system for heart disease: a perspec- tive on group A streptococci. J Infect Dis 2010; 202:1059-67.
  28. Marin-Neto JA, Cunha-Neto E, Maciel BC, et al. Pathogenesis of chronic Chagas heart dis- ease. Circulation 2007;115:1109-23.
  29. Burke A, Saenger J, Mullick F, et al. Hyper- sensitivity myocarditis. Arch Pathol Lab Med 1991; 115:764-9.
  30. Haas SJ, Hill R, Krum H, et al. Clozapine- associated myocarditis: a review of 116 cases of suspected myocarditis associated with the use of clozapine in Australia during 1993-2003. Drug Safety 2007;30:47-57.
  31. Cook SC, Ferguson BA, Cotes RO, et al. Clozapine-induced myocarditis: prevention and considerations in rechallenge. Psychosomatics 2015;56:685-90.
  32. Zawadowski G, Klarich K, Moder K, et al. A contemporary case series of lupus myocarditis. Lupus 2012;21:1378-84.
  33. Maleszewski JJ, Orellana VM, Hodge DO, et al. Long-term risk of recurrence, morbidity and mor- tality in giant cell myocarditis. Am J Cardiol 2015; 115:1733-8.
  34. Ciháková D, Sharma RB, Fairweather D, et al. Animal models for autoimmune myocarditis and autoimmune thyroiditis. Methods Mol Med 2004; 102:175-93.
  35. Chow LH, Beisel KW, McManus BM. Entero- viral infection of mice with severe combined immunodeficiency. Evidence for direct viral pathogenesis of myocardial injury. Lab Invest 1992;66:24-31.
  36. Kaya Z, Katus HA, Rose NR. Cardiac troponins and autoimmunity: their role in the pathogenesis of myocarditis and of heart failure. Clin Immunol 2010;134:80-8.
  37. Watanabe K, Arumugam S, Sreedhar R, et al. Small interfering RNA therapy against carbohy- drate sulfotransferase 15 inhibits cardiac remod- eling in rats with dilated cardiomyopathy. Cell Signal 2015;27:1517-24.
  38. Kandolf R, Canu A, Hofschneider PH. Cox- sackie B3 virus can replicate in cultured human foetal heart cells and is inhibited by interferon. J Mol Cell Cardiol 1985;17:167-81.
  39. Bergelson JM, Cunningham JA, Droguett G, et al. Isolation of a common receptor for Coxsackie B viruses and adenoviruses 2 and 5. Science 1997; 275:1320-3.
  40. Martino TA, Petric M, Brown M, et al. Car- diovirulent coxsackieviruses and the decay- accelerating factor (CD55) receptor. Virology 1998;244:302-14.
  41. Fairweather D, Frisancho-Kiss S, Rose N. Vi- ruses as adjuvants for autoimmunity: evidence from Coxsackievirus-induced myocarditis. Rev Med Virol 2005;15:17-27.
  42. Bonney K, Engman D. Autoimmune patho- genesis of Chagas heart disease: looking back, looking ahead. Am J Pathol 2015;185:1537-47.
  43. Mocelin A, Issa V, Bacal F, et al. The influence of aetiology on inflammatory and neurohumoral activation in patients with severe heart failure: a prospective study comparing Chagas' heart dis- ease and idiopathic dilated cardiomyopathy. Eur J Heart Failure 2005;7:869-73.
  44. Yuan J, Liu Z, Lim T, et al. CXCL10 inhibits viral replication through recruitment of natural killer cells in coxsackievirus B3-induced myocarditis. Circ Res 2009;104:628-38.
  45. Jenke A, Holzhauser L, Löbel M, et al. Adipo- nectin promotes coxsackievirus B3 myocarditis by suppression of acute anti-viral immune responses. Basic Res Cardiol 2014;109:408.
  46. Deonarain R, Cerullo D, Fuse K, et al. Protec- tive role for interferon-b in coxsackievirus B3 infection. Circulation 2004;110:3540-3.
  47. Huber SA, Sartini D, Exley M. Vg4þT cells promote autoimmune CD8þ cytolytic T-lymphocyte activation in coxsackievirus B3- induced myocarditis in mice: role for CD4þ Th1 cells. J Virol 2002;76:10785-90.
  48. Noutsias M, Rohde M, Göldner K, et al. Expression of functional T-cell markers and T-cell receptor Vbeta repertoire in endomyocardial bi- opsies from patients presenting with acute myocarditis and dilated cardiomyopathy. Eur J Heart Failure 2011;13:611-8.
  49. Valaperti A, Marty RR, Kania G, et al. CD11bþ monocytes abrogate Th17 CD4þ T cell-mediated experimental autoimmune myocarditis. J Immunol 2008;180:2686-95.
  50. Caforio AL, Marcolongo R, Jahns R, et al. Immune-mediated and autoimmune myocarditis: clinical presentation, diagnosis and management. Heart Fail Rev 2013;18:715-32.
  51. Mahrholdt H, Wagner A, Deluigi C, et al. Pre- sentation, patterns of myocardial damage, and clinical course of viral myocarditis. Circulation 2006;114:1581-90.
  52. Caforio AL, Mahon NJ, McKenna WJ. Cardiac autoantibodies to myosin and other heart-specific autoantigens in myocarditis and dilated cardio- myopathy. Autoimmunity 2001;34:199-204.
  53. Cunha-Neto E, Bilate AM, Hyland KV, et al. Induction of cardiac autoimmunity in Chagas heart disease: a case for molecular mimicry. Autoim- munity 2006;39:41-54.
  54. Blyszczuk P, Kania G, Dieterle T, et al. Myeloid differentiation factor-88/interleukin-1 signaling controls cardiac fibrosis and heart failure pro- gression in inflammatory dilated cardiomyopathy. Circ Res 2009;105:912-20.
  55. Kania G, Blyszczuk P, Eriksson U. Mechanisms of cardiac fibrosis in inflammatory heart disease. Trends Cardiovasc Med 2009;19:247-52.
  56. Frieler RA, Mortensen RM. Immune cell and other noncardiomyocyte regulation of cardiac hy- pertrophy and remodeling. Circulation 2015;131: 1019-30.
  57. Delgado C, Ruiz-Hurtado G, Gómez- Hurtado N, et al. NOD1, a new player in cardiac function and calcium handling. Cardiovasc Res 2015;106:375-86.
  58. Gratchev A, Kzhyshkowska J, Kothe K, et al. Mphi1 and Mphi2 can be re-polarized by Th2 or Th1 cytokines, respectively, and respond to exogenous danger signals. Immunobiology 2006;211:473-86.
  59. Cheung C, Luo H, Yanagawa B, et al. Matrix metalloproteinases and tissue inhibitors of met- alloproteinases in coxsackievirus-induced myocarditis. Cardiovasc Pathol 2006;15:63-74.
  60. Rienks M, Papageorgiou AP. Novel regulators of cardiac inflammation: matricellular proteins expand their repertoire. J Mol Cell Cardiol 2016; 91:172-8.
  61. Epelman S, Liu PP, Mann DL. Role of innate and adaptive immune mechanisms in cardiac injury and repair. Nat Rev Immunol 2015;15:117-29.
  62. Jenke A, Wilk S, Poller W, et al. Adiponectin protects against Toll-like receptor 4-mediated cardiac inflammation and injury. Cardiovasc Res 2013;99:422-31.
  63. Riad A, Meyer zu Schwabedissen H, Weitmann K, et al. Variants of Toll-like receptor 4 predict cardiac recovery in patients with dilated cardiomyopathy. J Biol Chem 2012;287:27236-43.
  64. Pagni PP, Traub S, Demaria O, et al. Contri- bution of TLR7 and TLR9 signaling to the sus- ceptibility of MyD88-deficient mice to myocarditis. Autoimmunity 2010;43:275-87.
  65. Abston ED, Coronado MJ, Bucek A, et al. TLR3 deficiency induces chronic inflammatory cardio- myopathy in resistant mice following coxsack- ievirus B3 infection: role for IL-4. Am J Physiol Regul Integr Comp Physiol 2013;304:R267-77.
  66. Gorbea C, Makar KA, Pauschinger M, et al. A role for Toll-like receptor 3 variants in host susceptibility to enteroviral myocarditis and dilated cardiomyopathy. J Biol Chem 2010;285: 23208-23.
  67. Weithauser A, Bobbert P, Antoniak S, et al. Protease-activated receptor-2 regulates the innate immune response to viral infection in a coxsackievirus B3-induced myocarditis. J Am Coll Cardiol 2013;62:1737-45.
  68. Su Z, Zhang P, Yu Y, et al. HMGB1 facilitated macrophage reprogramming towards a proin- flammatory M1-like phenotype in experimental autoimmune myocarditis development. Sci Rep 2016;6:21884.
  69. Zhang P, Cox CJ, Alvarez KM, et al. Cutting edge: cardiac myosin activates innate immune re- sponses through TLRs. J Immunol 2009;183: 27-31.
  70. Barin JG, Baldeviano GC, Talor MV, et al. Macrophages participate in IL-17-mediated inflammation. Eur J Immunol 2012;42:726-36.
  71. Leuschner F, Courties G, Dutta P, et al. Silencing of CCR2 in myocarditis. Eur Heart J 2015; 36:1478-88.
  72. Cooper LT Jr., Fairweather D. Nano-scale treatment for a macro-scale disease: nanoparticle- delivered siRNA silences CCR2 and treats myocarditis. Eur Heart J 2015;36:1434-6.
  73. Göser S, Ottl R, Brodner A, et al. Critical role for monocyte chemoattractant protein-1 and macrophage inflammatory protein-1a in induction of experimental autoimmune myocarditis and effective anti-monocyte chemoattractant protein- 1 gene therapy. Circulation 2005;112:3400-7.
  74. Biswas SK, Mantovani A. Macrophage plas- ticity and interaction with lymphocyte subsets: cancer as a paradigm. Nat Immunol 2010;11: 889-96.
  75. Martinez FO, Sica A, Mantovani A, et al. Macrophage activation and polarization. Front Biosci 2008;13:453-61.
  76. Barin JG, Rose NR, Ciháková D. Macrophage diversity in cardiac inflammation: a review. Immunobiology 2012;217:468-75.
  77. Cihakova D, Barin JG, Afanasyeva M, et al. Interleukin-13 protects against experimental autoimmune myocarditis by regulating macro- phage differentiation. Am J Pathol 2008;172: 1195-208.
  78. Kania G, Blyszczuk P, Stein S, et al. Heart- infiltrating prominin-1þ/CD133þ progenitor cells represent the cellular source of transforming growth factor b-mediated cardiac fibrosis in experimental autoimmune myocarditis. Circ Res 2009;105:462-70.
  79. Afanasyeva M, Georgakopoulos D, Belardi DF, et al. Quantitative analysis of myocardial inflam- mation by flow cytometry in murine autoimmune myocarditis: correlation with cardiac function. Am J Pathol 2004;164:807-15.
  80. Cihakova D, Rose NR. Pathogenesis of myocarditis and dilated cardiomyopathy. Adv Immunol 2008;99:95-114.
  81. Huber SA. Viral myocarditis and dilated car- diomyopathy: etiology and pathogenesis. Curr Pharm Des 2016;22:408-26.
  82. Marty RR, Dirnhofer S, Mauermann N, et al. MyD88 signaling controls autoimmune myocar- ditis induction. Circulation 2006;113:258-65.
  83. Nindl V, Maier R, Ratering D, et al. Coopera- tion of Th1 and Th17 cells determines transition from autoimmune myocarditis to dilated cardio- myopathy. Eur J Immunol 2012;42:2311-21.
  84. Chen P, Baldeviano GC, Ligons DL, et al. Sus- ceptibility to autoimmune myocarditis is associ- ated with intrinsic differences in CD4þ T cells. Clin Exp Immunol 2012;169:79-88.
  85. Eriksson U, Kurrer MO, Sebald W, et al. Dual role of the IL-12/IFN-g axis in the development of autoimmune myocarditis: induction by IL-12 and protection by IFN-g. J Immunol 2001;167:5464-9.
  86. Barin JG, Baldeviano GC, Talor MV, et al. Fatal eosinophilic myocarditis develops in the absence of IFN-g and IL-17A. J Immunol 2013;191: 4038-47.
  87. Eriksson U, Kurrer MO, Bingisser R, et al. Le- thal autoimmune myocarditis in interferon-g receptor-deficient mice: enhanced disease severity by impaired inducible nitric oxide synthase induc- tion. Circulation 2001;103:18-21. 100. Afanasyeva M, Wang Y, Kaya Z, et al. Interleukin-12 receptor/STAT4 signaling is requ- ired for the development of autoimmune myocarditis in mice by an interferon-g-indepen- dent pathway. Circulation 2001;104:3145-51. 101. Silverio JC, Pereira IR, Cipitelli Mda C, et al. CD8þ T-cells expressing interferon gamma or perforin play antagonistic roles in heart injury in experimental Trypanosoma cruzi-elicited cardio- myopathy. PLoS Pathog 2012;8:e1002645. 102.

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Authors
Heymans, S., Eriksson, U., Lehtonen, J., & Cooper, L. T.
Affiliations
  • Maastricht University Medical Centre (NL)
  • University of Zurich (CH)
  • Helsinki University Hospital (FI)
  • Mayo Clinic in Florida (US)
Corresponding author
Cooper, Leslie T.
Venue
Journal of the American College of Cardiology
Publisher
Elsevier BV
Published
2016-11
Volume
68
Issue
21
Pages
2348-2364
ISSN
0735-1097 (ISSN-L)
OpenAlex
W2555072060
Cited by
359
References
13
Citations by year
2026: 17 · 2025: 38 · 2024: 33 · 2023: 49 · 2022: 55 · 2021: 41 · 2020: 50 · 2019: 36 · 2018: 21 · 2017: 18 · 2016: 1
FWCI
4.47
Type
journal article
Language
en
Open access
Locations
  • Journal of the American College of Cardiology (publishedVersion)
  • PubMed (publishedVersion)
  • Research Publications (Maastricht University) (publishedVersion, other-oa)
  • Työväentutkimus Vuosikirja (submittedVersion, other-oa)
  • Research Publications (Maastricht University) (submittedVersion, other-oa)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Effects of Exercise
Keywords
myocarditis, inflammatory cardiomyopathy, dilated cardiomyopathy, cardiac sarcoidosis, microRNA, T cell subsets, macrophages, cardiac magnetic resonance, positron emission tomography, endomyocardial biopsy, viral infection, mortality trends, early diagnosis
MeSH terms
Biopsy, Humans, Immunity, Cellular, Cardiomyopathies, Myocarditis, Myocardium, Prognosis, T-Lymphocytes, Virus Diseases, Global Health, Incidence

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