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Extensive cardiac FDG uptake in a patient with AL amyloidosis
Cardiac AL amyloidosis is a medical emergency causing rapid deterioration of cardiac function; however, it remains to be a diagnostic challenge especially when presenting with unusual symptoms and clinical findings. We present case of a 44-year-old patient with typical angina, persistently elevated...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10022573/ https://www.ncbi.nlm.nih.gov/pubmed/36930456 http://dx.doi.org/10.1007/s12350-023-03243-1 |
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author | Hatipoglu, Suzan Wechalekar, Ashutosh D. Wechalekar, Kshama |
author_facet | Hatipoglu, Suzan Wechalekar, Ashutosh D. Wechalekar, Kshama |
author_sort | Hatipoglu, Suzan |
collection | PubMed |
description | Cardiac AL amyloidosis is a medical emergency causing rapid deterioration of cardiac function; however, it remains to be a diagnostic challenge especially when presenting with unusual symptoms and clinical findings. We present case of a 44-year-old patient with typical angina, persistently elevated troponin and normal epicardial coronary arteries. He was initially treated for myocarditis due to chest pain with troponin rise. However, CMR finding of subendocardial enhancement, increased native T1 values as well as extensive diffuse FDG uptake on PET-CT also suggested inflammatory cardiac conditions. Rapid decline in LV function and clinical deterioration led to further investigations including serum free light chains and bone marrow biopsy which confirmed systemic AL amyloidosis. Although the pathophysiology of unusual FDG PET-CT findings remains unknown, marked myocardial FDG uptake might have been caused by various features that were associated with AL amyloidosis including myocardial cell toxicity/inflammation or microvascular dysfunction. Awareness of these features specific to AL amyloidosis among physicians and description of associated cardiac FDG uptake findings has a potential to aid early diagnosis. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12350-023-03243-1. |
format | Online Article Text |
id | pubmed-10022573 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Springer International Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-100225732023-03-17 Extensive cardiac FDG uptake in a patient with AL amyloidosis Hatipoglu, Suzan Wechalekar, Ashutosh D. Wechalekar, Kshama J Nucl Cardiol Case Presentation Corner Cardiac AL amyloidosis is a medical emergency causing rapid deterioration of cardiac function; however, it remains to be a diagnostic challenge especially when presenting with unusual symptoms and clinical findings. We present case of a 44-year-old patient with typical angina, persistently elevated troponin and normal epicardial coronary arteries. He was initially treated for myocarditis due to chest pain with troponin rise. However, CMR finding of subendocardial enhancement, increased native T1 values as well as extensive diffuse FDG uptake on PET-CT also suggested inflammatory cardiac conditions. Rapid decline in LV function and clinical deterioration led to further investigations including serum free light chains and bone marrow biopsy which confirmed systemic AL amyloidosis. Although the pathophysiology of unusual FDG PET-CT findings remains unknown, marked myocardial FDG uptake might have been caused by various features that were associated with AL amyloidosis including myocardial cell toxicity/inflammation or microvascular dysfunction. Awareness of these features specific to AL amyloidosis among physicians and description of associated cardiac FDG uptake findings has a potential to aid early diagnosis. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12350-023-03243-1. Springer International Publishing 2023-03-17 /pmc/articles/PMC10022573/ /pubmed/36930456 http://dx.doi.org/10.1007/s12350-023-03243-1 Text en © The Author(s) under exclusive licence to American Society of Nuclear Cardiology 2023, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. |
spellingShingle | Case Presentation Corner Hatipoglu, Suzan Wechalekar, Ashutosh D. Wechalekar, Kshama Extensive cardiac FDG uptake in a patient with AL amyloidosis |
title | Extensive cardiac FDG uptake in a patient with AL amyloidosis |
title_full | Extensive cardiac FDG uptake in a patient with AL amyloidosis |
title_fullStr | Extensive cardiac FDG uptake in a patient with AL amyloidosis |
title_full_unstemmed | Extensive cardiac FDG uptake in a patient with AL amyloidosis |
title_short | Extensive cardiac FDG uptake in a patient with AL amyloidosis |
title_sort | extensive cardiac fdg uptake in a patient with al amyloidosis |
topic | Case Presentation Corner |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10022573/ https://www.ncbi.nlm.nih.gov/pubmed/36930456 http://dx.doi.org/10.1007/s12350-023-03243-1 |
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