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Green tea halts progression of cardiac transthyretin amyloidosis: an observational report

Background Treatment options in patients with amyloidotic transthyretin (ATTR) cardiomyopathy are limited. Epigallocatechin-3-gallate (EGCG), the most abundant catechin in green tea (GT), inhibits fibril formation from several amyloidogenic proteins in vitro. Thus, it might also halt progression of...

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Published in:Clinical research in cardiology 2012-10, Vol.101 (10), p.805-813
Main Authors: Kristen, Arnt V., Lehrke, Stephanie, Buss, Sebastian, Mereles, Derliz, Steen, Henning, Ehlermann, Philipp, Hardt, Stefan, Giannitsis, Evangelos, Schreiner, Rupert, Haberkorn, Uwe, Schnabel, Philipp A., Linke, Reinhold P., Röcken, Christoph, Wanker, Erich E., Dengler, Thomas J., Altland, Klaus, Katus, Hugo A.
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Language:English
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Summary:Background Treatment options in patients with amyloidotic transthyretin (ATTR) cardiomyopathy are limited. Epigallocatechin-3-gallate (EGCG), the most abundant catechin in green tea (GT), inhibits fibril formation from several amyloidogenic proteins in vitro. Thus, it might also halt progression of TTR amyloidosis. This is a single-center observational report on the effects of GT consumption in patients with ATTR cardiomopathy. Methods 19 patients with ATTR cardiomyopathy were evaluated by standard blood tests, echocardiography, and cardiac MRI ( n  = 9) before and after consumption of GT and/or green tea extracts (GTE) for 12 months. Results Five patients were not followed up for reasons of death ( n  = 2), discontinuation of GT/GTE consumption ( n  = 2), and heart transplantation ( n  = 1). After 12 months no increase of left ventricular (LV) wall thickness and LV myocardial mass was observed by echocardiography. In the subgroup of patients evaluated by cardiac MRI a mean decrease of LV myocardial mass (−12.5 %) was detected in all patients. This was accompanied by an increase of mean mitral annular systolic velocity of 9 % in all 14 patients. Total cholesterol (191.9 ± 8.9 vs. 172.7 ± 9.4 mg/dL; p  
ISSN:1861-0684
1861-0692
DOI:10.1007/s00392-012-0463-z