Evidence map›Paper›PMID 34031597›Full record

ReviewNature reviews. Cardiology2021

Genetics and genomics of arrhythmic risk: current and future strategies to prevent sudden cardiac death.

Chiara Scrocco, Connie R Bezzina, Michael J Ackerman, Elijah R Behr

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Article
  4. What Should a Clinical Cardiologist Know About Cardiogenetics?Journal of the American Heart Association · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Discerning the Ambiguous Role of MissenseJournal of personalized medicine · 2022
    Article
  15. Article
  16. Generation of a Triadin KnockOut Syndrome Zebrafish Model.International journal of molecular sciences · 2021
    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

4 authors at 3 institutions in 3 countries.

Chiara ScroccoCardiovascular Clinical Academic Group, Molecular and Clinical Sciences Institute, St George's University of London and St George's University Hospitals NHS Foundation Trust, London, UK.ORCID http://orcid.org/0000-0001-7739-4042
Connie R BezzinaAmsterdam University Medical Center, University of Amsterdam, Amsterdam, Netherlands.
Michael J AckermanDepartments of Cardiovascular Medicine, Pediatric and Adolescent Medicine, and Molecular Pharmacology & Experimental Therapeutics; Divisions of Heart Rhythm Services and Pediatric Cardiology, Mayo Clinic, Rochester, MN, USA.
Elijah R BehrCardiovascular Clinical Academic Group, Molecular and Clinical Sciences Institute, St George's University of London and St George's University Hospitals NHS Foundation Trust, London, UK. ebehr@sgul.ac.uk.ORCID http://orcid.org/0000-0002-8731-2853
St George's, University of London · GBAmsterdam University Medical Centers · NLMayo Clinic · US

Funding

British Heart Foundation SP/20/4/35124
6 · The paper itself

Abstract

A genetic risk of sudden cardiac arrest and sudden death due to an arrhythmic cause, known as sudden cardiac death (SCD), has become apparent from epidemiological studies in the general population and in patients with ischaemic heart disease. However, genetic susceptibility to sudden death is greatest in young people and is associated with uncommon, monogenic forms of heart disease. Despite comprehensive pathology and genetic evaluations, SCD remains unexplained in a proportion of young people and is termed sudden arrhythmic death syndrome, which poses challenges to the identification of relatives from affected families who might be at risk of SCD. In this Review, we assess the current understanding of the epidemiology and causes of SCD and evaluate both the monogenic and the polygenic contributions to the risk of SCD in the young and SCD associated with drug therapy. Finally, we analyse the potential clinical role of genomic testing in the prevention of SCD in the general population.

Indexed as

Arrhythmias, CardiacDeath, Sudden, CardiacAdolescentGenetic Predisposition to DiseaseGenomicsHumans

Identifiers

PMID34031597
OpenAlexW3165138237

What OpenQuestion holds

Textmetadata
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.