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

Abstract

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 singlecenter 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 \ 0.01) and LDL cholesterol (105.8 ± 7.6 vs. 89.5 ± 8.0 mg/dL; p \ 0.01) decreased significantly during the observational period. No serious adverse effects were reported by any of the participants. Conclusions Our observation suggests an inhibitory effect of GT and/or GTE on the progression of cardiac amyloidosis. We propose a randomized placebo-controlled investigation to confirm our observation. K. Altland, H. A. Katus contributed equally to this work.Electronic supplementary material The online version of this article (doi:10.1007/s00392-012-0463-z) contains supplementary material, which is available to authorized users.

Modulators of amyloid protein aggregation and toxicity: EGCG and CLR01

“…Left ventricular function is positively correlated with better prognosis in cardiac amyloidosis [158]. Though this study was very preliminary, without a control cohort, and the increase in left ventricular mass varied [159], the authors also found an increase in the mean mitral annular systolic velocity, a restorative effect, and a decrease in the total and low-density lipoprotein-associated cholesterol levels with no serious adverse events, suggesting that treatment with EGCG might be beneficial in these patients [157].…”

“…EGCG: A single-center observational study conducted in patients with familial amyloidotic TTR cardiomyopathy with an intake of 500-700 mg EGCG per day for 12 months, reported either no increase or a decrease in the left ventricular myocardial mass [157]. Left ventricular function is positively correlated with better prognosis in cardiac amyloidosis [158].…”

Light chain amyloidosis 2012: a new era

“…Following the observations that (-)-epigallocatechin-3-gallate (EGCG), the main polyphenolic constituent of green tea, reduces cerebral amyloidosis in Alzheimer transgenic mice (Rezai-Zadeh et al, 2005), and inhibits fibril formation of amyloid- (Ehrnhoefer et al, 2008), Dr Werner Hunstein, former professor of haematology at the University of Heidelberg, who was suffering from AL amyloidosis, observed an improvement in his cardiac symptoms while he was purposely drinking high amounts of green tea (Hunstein, 2007). The clinical activity of EGCG was then confirmed in retrospective case series both in AL amyloidosis and in transthyretin-related amyloidosis (ATTR) (Mereles et al, 2010;Kristen et al, 2012). A randomized clinical trial is ongoing to evaluate the ability of EGCG in promoting regression of residual cardiac damage in patients with AL amyloidosis who have completed chemotherapy.…”

Amyloidosis

“…Epigallocatechin-3-gallate (EGCG), a green tea extract, seems to have an inhibitory effect on the formation of AL and ATTR amyloid. [82][83][84] A clinical trial has started to evaluate a possible role of EGCG in promoting regression of residual cardiac damage in patients with AL amyloidosis who have successfully completed chemotherapy. 67 An interesting development is the combined use of a drug called CPHPC and anti-SAP antibodies.…”