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

Department of Cardiology, Angiology, and Respiratory Medicine, University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany, .
Clinical Research in Cardiology (Impact Factor: 4.17). 05/2012; 101(10):805-13. DOI: 10.1007/s00392-012-0463-z
Source: PubMed

ABSTRACT 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.
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.
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.
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.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Mediterranean and Asian diets are currently considered as the most healthy traditional feeding habits effective against risk of age-associated, particularly cardiovascular and neurodegenerative, diseases. A common feature of these two regimens is the abundance of foods and beverages of plant origin (green tea, extra virgin olive oil, red wine, spices, berries, and aromatic herbs) that are considered responsible for the observed beneficial effects. Epidemiological data suggest that the phenolic component remarkably enriched in these foods plays an important role in reducing the incidence of amyloid diseases, pathological conditions associated to tissue deposition of toxic protein aggregates responsible for progressive functional deterioration. Great effort is being spent to provide knowledge on the effects of several natural phenols in this context, moving from the test tube to animal models and, more slowly, to the patient's bed. An emerging feature that makes these molecules increasingly attractive for amyloid disease prevention and therapy is their wide spectrum of activity: recent pieces of evidence suggest that they can inhibit the production of amyloidogenic peptides from precursors, increase antioxidant enzyme activity, activate autophagy and reduce inflammation. Our concept should than shift from considering natural phenols simply as antioxidants or, at the best, as amyloid aggregation inhibitors, to describing them as potentially multitargeting drugs. A main concern is the low bioavailability of such compounds and efforts aimed at improving it are underway, with encapsulation strategies being the most promising ones. © 2014 BioFactors, 00(00):000–000, 2014
    BioFactors 06/2014; · 3.09 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hereditary amyloidosis is an autosomal dominant fatal multisystem disease caused by extracellular deposition of misfolded proteins and, therefore represents a hereditary protein folding or deposition disease that leads to progressive organ damage and eventually death. In most instances mutations within the transthyretin gene are the underlying cause. The main manifestation is a rapidly progressing axonal sensorimotor and autonomic polyneuropathy (familial amyloid polyneuropathy, FAP). Cardiac involvement is frequent in FAP and additional manifestations include the gastrointestinal tract and the eyes. A second manifestation type is cardiomyopathy with little or no polyneuropathy (familial amyloid cardiomyopathy, FAC). For therapy, orthotopic liver transplantation has been established for 25 years. Recently, the oral agent tafamidis, a transthyretin stabilizer, was licensed for treatment of stage 1 polyneuropathy. Additional treatment options are currently being studied.
    Der Nervenarzt 08/2014; · 0.86 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Introduction: Transthyretin (TTR)-related hereditary amyloidosis is an adult-onset, dominantly inherited, systemic neurodegenerative disease endemic in some populations. Stabilization of the native structure of TTR by small-molecule ligands has recently proved effective in slowing neurological progression. Two drugs, tafamidis and diflunisal, are now available for most patients, particularly in the early stage of the disease. However, this disorder remains life threatening with several unmet needs. There are great expectations for a number of novel agents undergoing investigation. Areas covered: The authors review the current investigational drugs for the treatment of TTR amyloidosis according to the different steps of the fibrillogenesis process they target. Innovative approaches include suppression of TTR secretion, prevention of TTR misfolding by stronger stabilizers identified through structure-based design and high-throughput screening methodologies as well as the redirection of pathogenic aggregates toward nontoxic species and reabsorption of deposits through amyloid disrupters and immunotherapy. Expert opinion: Suppression of TTR synthesis by antisense oligonucleotides and small-interfering RNA is presently one of the most promising therapeutic approaches. However, well-designed clinical trials are required to establish their safety and efficacy compared with liver transplantation, tafamidis and diflunisal. With a longer time frame, it may be possible to develop combination therapies that target multiple steps of the aggregation process that could provide the best long-life effective treatments for this devastating disease.
    Expert Opinion on Investigational Drugs 07/2014; · 4.74 Impact Factor


Available from
May 20, 2014