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Reverse cardiac remodelling and dysfunction in A97S transthyretin cardiac amyloidosis after tafamidis treatment

Transthyretin cardiomyopathy (ATTR‐CM) is an under‐recognized cause of heart failure, but it has received increasing attention due to the availability of treatment options. We present a case of hereditary transthyretin cardiomyopathy (A97S, an under‐represented variant in current clinical studies) w...

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Detalles Bibliográficos
Autores principales: Wu, Yuan‐Kun (Aden), Tsai, Cheng‐Hsuan, Su, Mao‐Yuan, Chao, Chi‐Chao, Cheng, Mei‐Fang, Shun, Chia‐Tung, Hsieh, Sung‐Tsang, Lin, Yen‐Hung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9773766/
https://www.ncbi.nlm.nih.gov/pubmed/36128649
http://dx.doi.org/10.1002/ehf2.14165
Descripción
Sumario:Transthyretin cardiomyopathy (ATTR‐CM) is an under‐recognized cause of heart failure, but it has received increasing attention due to the availability of treatment options. We present a case of hereditary transthyretin cardiomyopathy (A97S, an under‐represented variant in current clinical studies) who presented with heart failure. Timely diagnosis and intervention with tafamidis demonstrated reversed cardiac remodelling via multiple imaging techniques (echocardiography, cardiac magnetic resonance imaging and technetium‐99m pyrophosphate scintigraphy). The echocardiography and cardiac magnetic resonance imaging demonstrated improved global strain. Cardiac magnetic resonance imaging showed decreased extracellular volume. The technetium‐99m pyrophosphate scintigraphy demonstrated decreased heart‐to‐contralateral ratio. This case highlights the potential reversible effect of tafamidis on A97S amyloidosis cardiomyopathy.