Evidence map›Paper›PMID 34729530›Full record

ArticleJACC. CardioOncology2021

Effect of Tafamidis on Serum Transthyretin Levels in Non-Trial Patients With Transthyretin Amyloid Cardiomyopathy.

Rodney H Falk, Mia Haddad, Crystal R Walker, Sharmila Dorbala, Sarah A M Cuddy

Open access · goldAbstract read
In one paragraph

Article in JACC. CardioOncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 35 citations in OpenAlex.

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  14. QuantitativeJournal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2024
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  19. Tafamidis polyneuropathy amelioration requires modest increases in transthyretin stability even though increases in plasma native TTR and decreases in non-native TTR do not predict response.Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2023
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Rodney H FalkAmyloidosis Program, Division of Cardiology, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Mia HaddadAmyloidosis Program, Division of Cardiology, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Crystal R WalkerAmyloidosis Program, Division of Cardiology, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Sharmila DorbalaAmyloidosis Program, Division of Cardiology, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Sarah A M CuddyAmyloidosis Program, Division of Cardiology, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Brigham and Women's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTransthyretin amyloid (ATTR) cardiomyopathy is slowed by tafamidis, which stabilizes the TTR molecule and reduces the formation of amyloidogenic oligomers. Stabilizers in clinical doses raise serum TTR, which may be a surrogate for the degree of stabilization.

objectivesThis study aims to determine, in a non-trial, unselected population of patients with ATTR cardiomyopathy, the effect of tafamidis on serum levels of TTR, and to compare these with published data of changes in TTR.

methodsTTR levels were measured before therapy and 3 to 12 months following initiation of tafamidis therapy in all patients seen between May 20, 2019, and March 1, 2021, who had a follow-up visits within 12 months of therapy initiation.

resultsAmong 72 patients with ATTR cardiomyopathy (67 patients with wild-type and 5 patients with variant TTR), administration of tafamidis increased serum TTR from 21.8 mg ± 0.7 mg/dL to 29.3 ± 0.86 mg/dL, an increase of 34.5%. In 5 patients with variant TTR, the increase was 70.9%, compared to 32.0% in the wild-type patients. Mean N-terminal pro-brain natriuretic peptide increased over a mean follow-up of 21 ± 1.2 weeks, but the change was not statistically significant. Over the same period there was a small increase in high-sensitivity troponin T that was of borderline statistical significance

conclusionsTafamidis consistently increases serum TTR levels in patients with ATTR cardiomyopathy, consistent with its effect on stabilizing TTR. Measurement of TTR level change post-TTR stabilizing therapy might be a surrogate for stabilization and could be a more accurate measure of drug efficacy than an in vitro nonphysiologic test of stabilization.

Indexed as

amyloid cardiomyopathyATTR, transthyretin amyloidATTRv, variant transthyretin amyloidosisNT-proBNP, N-terminal pro-brain natriuretic peptidetafamidistransthyretinTTR, transthyretin

Identifiers

PMID34729530
PMCPMC8543137
OpenAlexW3205720016

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.