Evidence map›Paper›PMID 35629214›Full record

ArticleJournal of personalized medicine2022

Transthyretin Amyloid Cardiomyopathy: Impact of Transthyretin Amyloid Deposition in Myocardium on Cardiac Morphology and Function.

Tomoya Nakano, Kenji Onoue, Chiyoko Terada, Satoshi Terasaki, Satomi Ishihara, Yukihiro Hashimoto, Yasuki Nakada, Hitoshi Nakagawa, Tomoya Ueda, Ayako Seno and 7 more

Open access · goldAbstract read
In one paragraph

Article in Journal of personalized medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 42% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Observational
  5. Review
  6. Article
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

17 authors at 4 institutions in 1 country.

Tomoya NakanoDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara 634-8521, Nara, Japan.ORCID 0000-0001-7459-3070
Kenji OnoueDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara 634-8521, Nara, Japan.
Chiyoko TeradaDepartment of Diagnostic Pathology, Nara Medical University, Kashihara 634-8521, Nara, Japan.
Satoshi TerasakiDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara 634-8521, Nara, Japan.
Satomi IshiharaDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara 634-8521, Nara, Japan.
Yukihiro HashimotoDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara 634-8521, Nara, Japan.
Yasuki NakadaDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara 634-8521, Nara, Japan.
Hitoshi NakagawaDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara 634-8521, Nara, Japan.ORCID 0000-0002-1394-8509
Tomoya UedaDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara 634-8521, Nara, Japan.ORCID 0000-0002-0656-3336
Ayako SenoDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara 634-8521, Nara, Japan.
Taku NishidaDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara 634-8521, Nara, Japan.ORCID 0000-0001-7025-0310
Makoto WatanabeDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara 634-8521, Nara, Japan.
Yoshinobu HoshiiDepartment of Diagnostic Pathology, Yamaguchi University Hospital, Ube 755-0046, Yamaguchi, Japan.ORCID 0000-0003-0192-7791
Kinta HatakeyamaDepartment of Pathology, National Cerebral and Cardiovascular Center, Suita 564-8565, Osaka, Japan.ORCID 0000-0001-7729-1836
Yasuhiro SakaguchiDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara 634-8521, Nara, Japan.
Chiho OhbayashiDepartment of Diagnostic Pathology, Nara Medical University, Kashihara 634-8521, Nara, Japan.
Yoshihiko SaitoDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara 634-8521, Nara, Japan.
Nara Medical University · JPNational Cerebral and Cardiovascular Center · JPYamaguchi University Hospital · JPYamato Municipal Hospital · JP

Funding

AMED, Platform Program for Promotion of Genome Medicine JP19km0405009AMED, Practical Research Project for Life-Style related Diseases including Cardiovascular Diseases and Diabetes Mellitus JP19ek0210080, JP19ek0210118, JP19ek0210121, JP19ek0210115AMED, Practical Research Project for Rare/Intractable Diseases JP19ek0109367, JP19ek0109406Health Labour Sciences Research, Technology and the Ministry of Health, Labor, and Welfare of Japan 19189094, 17933459MEXT KAKENHI, Grants-in-aid from the Ministry of Education, Culture, Sports, Science JP19155855
6 · The paper itself

Abstract

backgroundTransthyretin (TTR) amyloid cardiomyopathy (ATTR-CM) is increasingly being recognized as a cause of left ventricular (LV) hypertrophy (LVH) and progressive heart failure in elderly patients. However, little is known about the cardiac morphology of ATTR-CM and the association between the degree of TTR amyloid deposition and cardiac dysfunction in these patients.

methodsWe studied 28 consecutive patients with ATTR-CM and analyzed the relationship between echocardiographic parameters and pathological features using endomyocardial biopsy samples.

resultsThe cardiac geometries of patients with ATTR-CM were mainly classified as concentric LVH (96.4%). The relative wall thickness, a marker of LVH, tended to be positively correlated with the degree of non-cardiomyocyte area. The extent of TTR deposition was positively correlated with enlargement of the non-cardiomyocyte area, and these were positively correlated with LV diastolic dysfunction. Additionally, the extent of the area containing TTR was positively correlated with the percentage of cardiomyocyte nuclei stained for 8-hydroxy-2'deoxyguanosine, a marker of reactive oxygen species (ROS). ROS accumulation in cardiomyocytes was positively correlated with LV systolic dysfunction.

conclusionPatients with ATTR-CM mainly displayed concentric LVH geometry. TTR amyloid deposition was associated with cardiac dysfunction via increased non-cardiomyocyte area and ROS accumulation in cardiomyocytes.

Indexed as

cardiac dysfunctionconcentric left ventricular hypertrophyendomyocardial biopsyhuman heart tissueimmunostainingreactive oxygen speciestransthyretin amyloid cardiomyopathy

Identifiers

PMID35629214
PMCPMC9147607
OpenAlexW4280588529

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.