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

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.

Automated summary

In this article, we present a complex case of an 81-year-old female patient who experienced persistently high levels of troponin after immunotherapy and displayed amyloid deposition in the myocardium. However, histological examination revealed minimal T-lymphocyte infiltration and no myocyte necrosis, indicating transthyretin cardiac amyloidosis rather than immune checkpoint inhibitor myocarditis. This case highlights the importance of evaluating other causes of elevated troponin levels and the necessity of comprehensive histological and immunohistochemical examinations when cardiovascular magnetic resonance imaging is inconclusive.