Monitoring treatment response to tafamidis by serial native T1 and extracellular volume in transthyretin amyloid cardiomyopathy
| Autor: | Hideaki Kanzaki, Yoshiki Sekijima, Yasuhiro Shintani, Chisato Izumi, Hiroyuki Takahama, Yasuhiro Hamatani, Satoshi Yasuda, Masashi Amano, Atsushi Okada, Keiko Ohta-Ogo, Chihiro Shimazaki, Makoto Amaki, Takuya Hasegawa, Masahide Yazaki, Tsuneaki Yoshinaga, Hatsue Ishibashi-Ueda, Yoshiaki Morita |
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| Rok vydání: | 2018 |
| Předmět: |
Tafamidis
endocrine system medicine.diagnostic_test biology business.industry Amyloidosis nutritional and metabolic diseases Tafamidis Meglumine 030204 cardiovascular system & hematology Pharmacology medicine.disease 03 medical and health sciences chemistry.chemical_compound Transthyretin 0302 clinical medicine chemistry Cardiac amyloidosis Cardiac magnetic resonance imaging Heart failure medicine biology.protein 030212 general & internal medicine Cardiology and Cardiovascular Medicine Amyloid cardiomyopathy business |
| Zdroj: | ESC Heart Failure. 6:232-236 |
| ISSN: | 2055-5822 |
| DOI: | 10.1002/ehf2.12382 |
| Popis: | Tafamidis meglumine, a transthyretin (TTR) stabilizer, is effective in delaying the progression of neuropathy in TTR amyloidosis with Val30Met mutations. However, its efficacy in TTR amyloid cardiomyopathy is not fully elucidated. Herein, we report a 73-year-old Japanese man with a diagnosis of TTR amyloid cardiomyopathy with Val30Met mutation treated with tafamidis. To evaluate treatment response, cardiac magnetic resonance imaging was performed before and after 12 months of tafamidis treatment. Native T1, extracellular volume, and left ventricular mass showed no obvious worsening, and findings of other diagnostic studies also supported the efficacy of tafamidis to delay the progression of amyloid cardiomyopathy. Our case suggests that serial native T1 and extracellular volume may be novel non-invasive imaging methods to monitor the treatment response to TTR stabilizers in cardiac amyloidosis and also that tafamidis may be effective in suppressing cardiac progression in TTR amyloid cardiomyopathy with Val30Met mutation. |
| Databáze: | OpenAIRE |
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