Evidence map›Paper›PMID 26026997›Full record

ReviewCurrent cardiology reports2015

Genetics of sudden cardiac death.

Marwan M Refaat, Mostafa Hotait, Barry London

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current cardiology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.4field-weighted citation impact, top 7% 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, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. NovelFrontiers in cardiovascular medicine · 2021
    Article
  8. Review
  9. Competence of general practitioners in requesting and interpreting ECGs - a case vignette study.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2018
    Article
  10. Article
  11. IDENTIFYING NEW SUDDEN DEATH GENES.Transactions of the American Clinical and Climatological Association · 2018
    Article
  12. Article
  13. Article
  14. Review
  15. Molecular mechanisms in the pathogenesis of arrhythmogenic cardiomyopathy.Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
    Review
  16. 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

3 authors at 2 institutions in 2 countries.

Marwan M RefaatDepartment of Internal Medicine (Cardiology Division), American University of Beirut Medical Center, Beirut, Lebanon, mr48@aub.edu.lb.
Mostafa Hotait
Barry London
American University of Beirut Medical Center · LBUniversity of Iowa · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sudden cardiac death (SCD) is defined by the World Health Organization (WHO) as death within 1 h of symptom onset (witnessed) or within 24 h of being observed alive and symptom free (unwitnessed). It affects more than 3 million people annually worldwide and affects approximately 1/1000 people each year in the USA. Familial studies of syndromes with Mendelian inheritance, candidate genes analyses, and genome-wide association studies (GWAS) have helped our understanding of the genetics of SCD. We will review the genetics of arrhythmogenic hereditary syndromes with Mendelian inheritance from familial studies with structural heart disease (hypertrophic cardiomyopathy, dilated cardiomyopathy, and arrhythmogenic cardiomyopathy) as well as primary electrical causes (long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, and short QT syndrome). In addition, we will review the genetics of intermediate phenotypes for SCD such as coronary artery disease and electrocardiographic variables (QT interval, QRS duration, and RR interval). Finally, we will review rare and common variants that are associated with SCD in the general population and were identified from candidate gene analyses and GWAS. Our understanding of the genetics of SCD will improve by the use of next-generation sequencing/whole-exome sequencing as well as whole-genome sequencing which have the potential to discover unsuspected common and rare genetic variants that might be associated with SCD.

Indexed as

Arrhythmias, CardiacDeath, Sudden, CardiacElectrocardiographyGenetic Diseases, InbornGenetic Predisposition to DiseaseGenetic TestingGenome-Wide Association StudyHeart Conduction SystemHigh-Throughput Nucleotide SequencingHumansMendelian Randomization AnalysisPedigreePhenotypePopulation SurveillanceUnited States

Identifiers

PMID26026997
OpenAlexW1498957673

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.