Dr. Gräni receives funding from the Swiss National Science foundation, InnoSuisse, Center for Artificial Intelligence Grant from the University of Bern and the GAMBIT foundation.
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Introduction
We illustrate the findings of multimodality imaging (i.e., DPD-scintigraphy, 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET), cardiac magnetic resonance (CMR)) in endomyocardial biopsy proofed cardiac sarcoidosis and cardiac transthyretin amyloidosis (ATTR).
Case presentation
A 79-year-old female presented with fatigue, dyspnea, elevated NT-proBNP, and recurrent exudative pleural effusion of unknown origin without bacteria or neoplastic cells. Pulmonary embolism, pneumonia, and tumor were ruled out by computed tomography. Echocardiography showed slightly reduced left ventricular ejection fraction with diffuse hypokinesia and apical sparing. Light-chain amyloidosis was ruled out and DPD-scintigraphy showed cardiac ATTR. As diagnostic thoracoscopy revealed no malignancy, but non-necrotizing granulomas in the lung, a FDG-PET was performed, which suggested multiorgan sarcoidosis. CMR showed diffuse fibrosis and multifocal late gadolinium enhancement (LGE) suggesting cardiac ATTR. However, the extensive LGE and multifocal inflammation would also be in accordance with cardiac sarcoidosis. Endomyocardial biopsy was performed, and histological analysis confirmed the diagnosis of both cardiac sarcoidosis and cardiac ATTR (differentiation revealed wild-type ATTR). Tafamidis and immunosuppressant therapy were initiated.
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Discussion
The main differentials according to the imaging findings were (a) FDG-PET uptake in LV-myocardium: cardiac ATTR mimicking cardiac sarcoidosis?1 (b) DPD-scintigraphy uptake in LV-myocardium: cardiac sarcoidosis mimicking cardiac ATTR?2 (c) Simultaneous presence of both entities, which, to our knowledge, has not yet been described in the literature. Multimodality imaging and endomyocardial biopsy could establish the diagnosis of the simultaneous occurrence of cardiac ATTR and cardiac involvement of systemic sarcoidosis and helped to guide optimal medical therapy of this patient (Figure 1).
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Disclosures
Dr. Caobelli receives grants and speaker honoraria from Siemens Healthineers and Bracco AG for matters not related to the present paper All other authors have nothing to disclose.
Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
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