Evidence map›Paper›PMID 31553132›Full record

ReviewESC heart failure2019

Transthyretin cardiac amyloidosis: an update on diagnosis and treatment.

Hiroyuki Yamamoto, Tomoki Yokochi

Open access · goldAbstract readReview
In one paragraph

Review in ESC heart failure, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed, 3 pooled it
7.4field-weighted citation impact, top 2% 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

103 citing papers in PubMed, 3 syntheses or guidelines pooled it, 191 citations in OpenAlex.

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43 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Hiroyuki YamamotoDepartment of Cardiovascular Medicine, Narita-Tomisato Tokushukai Hospital, 1-1-1 Hiyoshidai, Tomisato, Chiba, 286-0201, Japan.ORCID 0000-0003-4742-7653
Tomoki YokochiDepartment of Clinical Research, Chiba Tokushukai Hospital, Chiba, Japan.
Fukuoka Tokushukai Hospital · JPTomitahama Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transthyretin cardiac amyloidosis (ATTR-CA) demonstrates progressive, potentially fatal, and infiltrative cardiomyopathy caused by extracellular deposition of transthyretin-derived insoluble amyloid fibrils in the myocardium. Two distinct types of transthyretin (wild type or variant) become unstable, and misfolding forms aggregate, resulting in amyloid fibrils. ATTR-CA, which has previously been underrecognized and considered to be rare, has been increasingly recognized as a cause of heart failure with preserved ejection fraction among elderly persons. With the advanced technology, the diagnostic tools have been improving for cardiac amyloidosis. Recently, the efficacy of several disease-modifying agents focusing on the amyloidogenic process has been demonstrated. ATTR-CA has been changing from incurable to treatable. Nevertheless, there are still no prognostic improvements due to diagnostic delay or misdiagnosis because of phenotypic heterogeneity and co-morbidities. Thus, it is crucial for clinicians to be aware of this clinical entity for early diagnosis and proper treatment. In this mini-review, we focus on recent advances in diagnosis and treatment of ATTR-CA.

Indexed as

AmyloidosisCardiomyopathiesPrealbuminAgedAmyloidFemaleHeartHeart FailureHumansMaleMiddle AgedMyocardiumAmyloidPrealbuminAmyloidosisCardiomyopathyDiagnosisDisease-modifying agentsHeart failureRed-flagsTransthyretin

Identifiers

PMID31553132
PMCPMC6989279
OpenAlexW2976060034

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.