Evidence map›Paper›PMID 28810874›Full record

ReviewJournal of biomedical science2017

Sudden cardiac death: focus on the genetics of channelopathies and cardiomyopathies.

Simona Magi, Vincenzo Lariccia, Marta Maiolino, Salvatore Amoroso, Santo Gratteri

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of biomedical science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  10. Article
  11. Article
  12. Article
  13. Epicardial ablation in genetic cardiomyopathies: a new frontier.European heart journal supplements : journal of the European Society of Cardiology · 2019
    Article
  14. Genetics of Dilated Cardiomyopathy.Current cardiology reports · 2018
    Review
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 2 institutions in 1 country.

Simona MagiDepartment of Biomedical Sciences and Public Health, School of Medicine, University "Politecnica delle Marche", Via Tronto 10/A, 60126, Ancona, Italy. s.magi@univpm.it.ORCID http://orcid.org/0000-0002-8115-8226
Vincenzo LaricciaDepartment of Biomedical Sciences and Public Health, School of Medicine, University "Politecnica delle Marche", Via Tronto 10/A, 60126, Ancona, Italy.
Marta MaiolinoDepartment of Biomedical Sciences and Public Health, School of Medicine, University "Politecnica delle Marche", Via Tronto 10/A, 60126, Ancona, Italy.
Salvatore AmorosoDepartment of Biomedical Sciences and Public Health, School of Medicine, University "Politecnica delle Marche", Via Tronto 10/A, 60126, Ancona, Italy.
Santo GratteriDepartment of Health Sciences, University "Magna Graecia", 88100, Catanzaro, Italy.
Marche Polytechnic University · ITMagna Graecia University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sudden cardiac death (SCD) describes a natural and unexpected death from cardiac causes occurring within a short period of time (generally within 1 h of symptom onset) in the absence of any other potentially lethal condition. Most SCD-related diseases have a genetic basis; in particular congenital cardiac channelopathies and cardiomyopathies have been described as leading causes of SCD. Congenital cardiac channelopathies are primary electric disorders caused by mutations affecting genes encoding cardiac ion channels or associated proteins, whereas cardiomyopathies are related to mutations in genes encoding several categories of proteins, including those of sarcomeres, desmosomes, the cytoskeleton, and the nuclear envelope. The purpose of this review is to provide a general overview of the main genetic variants that have been linked to the major congenital cardiac channelopathies and cardiomyopathies. Functional alterations of the related proteins are also described.

Indexed as

Genetic VariationCardiomyopathiesCaveolin 3ChannelopathiesDeath, Sudden, CardiacHumansMutationCAV3 protein, humanCaveolin 3CardiomyopathiesCaveolinsChannelopathiesGeneticsSudden cardiac death

Identifiers

PMID28810874
PMCPMC5556354
OpenAlexW2749167448

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.