Evidence map›Paper›PMID 35929637›Full record

ArticleCardiovascular research2023

Transthyretin cardiac amyloidosis.

Aldostefano Porcari, Marianna Fontana, Julian D Gillmore

Open access · hybridAbstract read
In one paragraph

Article in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 2 pooled it
12.0field-weighted citation impact, top 1% 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

86 citing papers in PubMed, 2 syntheses or guidelines pooled it, 154 citations in OpenAlex.

  1. Pooled it
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  7. UniqueAnnals of laboratory medicine · 2026
    Article
  8. Classification of cardiomyopathies: bringing order to complexity.European heart journal supplements : journal of the European Society of Cardiology · 2026
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26 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

3 authors at 2 institutions in 2 countries.

Aldostefano PorcariNational Amyloidosis Centre, Division of Medicine, University College London, Royal Free Campus, Rowland Hill Street, London NW3 2PF, UK.ORCID 0000-0003-3307-0825
Marianna FontanaNational Amyloidosis Centre, Division of Medicine, University College London, Royal Free Campus, Rowland Hill Street, London NW3 2PF, UK.ORCID 0000-0002-9233-9831
Julian D GillmoreNational Amyloidosis Centre, Division of Medicine, University College London, Royal Free Campus, Rowland Hill Street, London NW3 2PF, UK.ORCID 0000-0001-6174-9232
The Royal Free Hospital · GBUniversity of Trieste · IT

Funding

British Heart Foundation FS/18/21/33447
6 · The paper itself

Abstract

Transthyretin cardiac amyloidosis (ATTR-CA) is an increasingly recognized cause of heart failure (HF) and mortality worldwide. Advances in non-invasive diagnosis, coupled with the development of effective treatments, have shifted ATTR-CA from a rare and untreatable disease to a relatively prevalent condition that clinicians should consider on a daily basis. Amyloid fibril formation results from age-related failure of homoeostatic mechanisms in wild-type ATTR (ATTRwt) amyloidosis (non-hereditary form) or destabilizing mutations in variant ATTR (ATTRv) amyloidosis (hereditary form). Longitudinal large-scale studies in the United States suggest an incidence of cardiac amyloidosis in the contemporary era of 17 per 100 000, which has increased from a previous estimate of 0.5 per 100 000, which was almost certainly due to misdiagnosis and underestimated. The presence and degree of cardiac involvement is the leading cause of mortality both in ATTRwt and ATTRv amyloidosis, and can be identified in up to 15% of patients hospitalized for HF with preserved ejection fraction. Associated features, such as carpal tunnel syndrome, can preceed by several years the development of symptomatic HF and may serve as early disease markers. Echocardiography and cardiac magnetic resonance raise suspicion of disease and might offer markers of treatment response at a myocardial level, such as extracellular volume quantification. Radionuclide scintigraphy with 'bone' tracers coupled with biochemical tests may differentiate ATTR from light chain amyloidosis. Therapies able to slow or halt ATTR-CA progression and increase survival are now available. In this evolving scenario, early disease recognition is paramount to derive the greatest benefit from treatment.

Indexed as

AmyloidosisCardiomyopathiesHeart FailureEchocardiographyHumansMagnetic Resonance ImagingPrealbuminPrealbuminCardiac magnetic resonanceCardiac scintigraphy with bone tracersPrognostic stratificationTherapyTransthyretin cardiac amyloidosisTTR

Identifiers

PMID35929637
PMCPMC9897687
OpenAlexW4289878937

What OpenQuestion holds

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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.