Subtle‐but‐smouldering myocardial injury after immune checkpoint inhibitor treatment accompanied by amyloid deposits

Abstract Although cardiac troponin is a highly specific biomarker for myocardial cell injury, it is important to recognize the pitfalls of this test in the diagnosis and management of immune checkpoint inhibitor (ICI) myocarditis. We describe the challenging case of an 81‐year‐old woman with persist...

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Main Authors: Mizuki Ida, Shiro Nakamori, Shinya Yamamoto, Seimi Watanabe, Kyoko Imanaka‐Yoshida, Masaki Ishida, Hajime Sakuma, Keiichi Yamanaka, Kaoru Dohi
Format: Article
Language:English
Published: Wiley 2022-06-01
Series:ESC Heart Failure
Subjects:
Online Access:https://doi.org/10.1002/ehf2.13915
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author Mizuki Ida
Shiro Nakamori
Shinya Yamamoto
Seimi Watanabe
Kyoko Imanaka‐Yoshida
Masaki Ishida
Hajime Sakuma
Keiichi Yamanaka
Kaoru Dohi
author_facet Mizuki Ida
Shiro Nakamori
Shinya Yamamoto
Seimi Watanabe
Kyoko Imanaka‐Yoshida
Masaki Ishida
Hajime Sakuma
Keiichi Yamanaka
Kaoru Dohi
author_sort Mizuki Ida
collection DOAJ
description Abstract Although cardiac troponin is a highly specific biomarker for myocardial cell injury, it is important to recognize the pitfalls of this test in the diagnosis and management of immune checkpoint inhibitor (ICI) myocarditis. We describe the challenging case of an 81‐year‐old woman with persistently high troponin after undergoing immunotherapy with ipilimumab and nivolumab, and histological evidence of amyloid deposition in the myocardium. The patient received immunosuppressive treatments based on the magnitude of troponin changes because myocarditis was clinically suspected. However, histological examination revealed the deposition of transthyretin amyloid fibrils with only minimal T‐lymphocyte infiltration and no myocyte necrosis, suggesting transthyretin cardiac amyloidosis rather than ICI myocarditis. This case highlights the importance of assessing other causes of persistently high troponin, and the necessity of incorporating comprehensive histological and immunohistochemical examinations of the endomyocardial biopsy, especially when cardiovascular magnetic resonance imaging is inconclusive.
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spelling doaj.art-3a935b9ef6bd4657b257e483da4571ef2022-12-22T03:03:59ZengWileyESC Heart Failure2055-58222022-06-01932027203110.1002/ehf2.13915Subtle‐but‐smouldering myocardial injury after immune checkpoint inhibitor treatment accompanied by amyloid depositsMizuki Ida0Shiro Nakamori1Shinya Yamamoto2Seimi Watanabe3Kyoko Imanaka‐Yoshida4Masaki Ishida5Hajime Sakuma6Keiichi Yamanaka7Kaoru Dohi8Department of Cardiology and Nephrology Mie University Graduate School of Medicine 174 Edobashi Tsu Mie 5148507 JapanDepartment of Cardiology and Nephrology Mie University Graduate School of Medicine 174 Edobashi Tsu Mie 5148507 JapanDepartment of Dermatology Mie University Graduate School of Medicine Tsu JapanDepartment of Dermatology Mie University Graduate School of Medicine Tsu JapanDepartment of Pathology Mie University Graduate School of Medicine Tsu JapanDepartment of Radiology Mie University Graduate School of Medicine Tsu JapanDepartment of Radiology Mie University Graduate School of Medicine Tsu JapanDepartment of Dermatology Mie University Graduate School of Medicine Tsu JapanDepartment of Cardiology and Nephrology Mie University Graduate School of Medicine 174 Edobashi Tsu Mie 5148507 JapanAbstract Although cardiac troponin is a highly specific biomarker for myocardial cell injury, it is important to recognize the pitfalls of this test in the diagnosis and management of immune checkpoint inhibitor (ICI) myocarditis. We describe the challenging case of an 81‐year‐old woman with persistently high troponin after undergoing immunotherapy with ipilimumab and nivolumab, and histological evidence of amyloid deposition in the myocardium. The patient received immunosuppressive treatments based on the magnitude of troponin changes because myocarditis was clinically suspected. However, histological examination revealed the deposition of transthyretin amyloid fibrils with only minimal T‐lymphocyte infiltration and no myocyte necrosis, suggesting transthyretin cardiac amyloidosis rather than ICI myocarditis. This case highlights the importance of assessing other causes of persistently high troponin, and the necessity of incorporating comprehensive histological and immunohistochemical examinations of the endomyocardial biopsy, especially when cardiovascular magnetic resonance imaging is inconclusive.https://doi.org/10.1002/ehf2.13915AmyloidCardiovascular magnetic resonance imagingEndomyocardial biopsyImmune checkpoint inhibitorImmunosuppressive therapyMyocarditis
spellingShingle Mizuki Ida
Shiro Nakamori
Shinya Yamamoto
Seimi Watanabe
Kyoko Imanaka‐Yoshida
Masaki Ishida
Hajime Sakuma
Keiichi Yamanaka
Kaoru Dohi
Subtle‐but‐smouldering myocardial injury after immune checkpoint inhibitor treatment accompanied by amyloid deposits
ESC Heart Failure
Amyloid
Cardiovascular magnetic resonance imaging
Endomyocardial biopsy
Immune checkpoint inhibitor
Immunosuppressive therapy
Myocarditis
title Subtle‐but‐smouldering myocardial injury after immune checkpoint inhibitor treatment accompanied by amyloid deposits
title_full Subtle‐but‐smouldering myocardial injury after immune checkpoint inhibitor treatment accompanied by amyloid deposits
title_fullStr Subtle‐but‐smouldering myocardial injury after immune checkpoint inhibitor treatment accompanied by amyloid deposits
title_full_unstemmed Subtle‐but‐smouldering myocardial injury after immune checkpoint inhibitor treatment accompanied by amyloid deposits
title_short Subtle‐but‐smouldering myocardial injury after immune checkpoint inhibitor treatment accompanied by amyloid deposits
title_sort subtle but smouldering myocardial injury after immune checkpoint inhibitor treatment accompanied by amyloid deposits
topic Amyloid
Cardiovascular magnetic resonance imaging
Endomyocardial biopsy
Immune checkpoint inhibitor
Immunosuppressive therapy
Myocarditis
url https://doi.org/10.1002/ehf2.13915
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