Evidence map›Paper›PMID 21430528›Full record

ReviewCurrent opinion in cardiology2011

Genetics of sudden cardiac death syndromes.

Nagesh Chopra, Björn C Knollmann

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Desmoplakin Cardiomyopathy.The international journal of cardiovascular imaging · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. The Crossroad of Ion Channels and Calmodulin in Disease.International journal of molecular sciences · 2019
    Review
  9. Article
  10. Article
  11. De NovoJournal of the American Heart Association · 2017
    Article
  12. SK4 KEMBO molecular medicine · 2017
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Genetics of sudden cardiac death.Current cardiology reports · 2015
    Review
  20. 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

2 authors at 1 institution in 1 country.

Nagesh ChopraDivision of Cardiology, Department of Medicine, Oates Institute for Experimental Therapeutics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Björn C Knollmann
Vanderbilt University · US

Funding

Troponin T mutations and Sudden Cardiac DeathR01HL071670 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KNOLLMANN, BJORN C · 2003 to 2017
$4.5M
Calsequestrin in Ventricular Arrhythmia and Sudden DeathR01HL088635 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KNOLLMANN, BJORN C · 2007 to 2015
$3.2M
NHLBI NIH HHS HL71670NHLBI NIH HHS HL88635NHLBI NIH HHS R01 HL071670NHLBI NIH HHS R01 HL088635
6 · The paper itself

Abstract

purpose of reviewTo survey recent developments in the field of genetics encompassing discovery of new candidate genes, new diagnostic strategies, and new therapies for sudden cardiac death (SCD) syndromes. RECENT

findingsIn addition to new mutations in known SCD genes, several novel genes not previously implicated in SCD causation have been found, particularly in long QT syndrome (e.g., KCNJ5, AKAP9, SNTA1), idiopathic ventricular fibrillation (e.g., DPP6, KCNJ8), dilated cardiomyopathy (e.g., NEBL), and hypertrophic cardiomyopathy (HCM; e.g., NEXN). Genetic SCD animal models have provided novel insights into the cellular mechanism and pathogenesis of nearly all the major SCD syndromes, which has led to several new drug therapies for patients with genetic arrhythmia syndromes (e.g., flecainide in catecholaminergic polymorphic ventricular tachycardia). Furthermore, genetic contributions to acquired heart diseases are increasingly being recognized. For example, a 21q21 locus is strongly associated with ventricular fibrillation after myocardial infarction. Near this locus is CXADR, a gene encoding a viral receptor implicated in myocarditis and dilated cardiomyopathy. Finally, common variants in cardiac ion channels and proteins likely contribute to common cardiac phenotypes. SUMMARY: Major strides have been made in uncovering new genes, mechanisms, and syndromes that have significantly advanced the diagnosis and treatment of genetic SCD disorders.

Indexed as

Brugada SyndromeCardiomyopathiesDeath, Sudden, CardiacHumansLong QT SyndromeMutationPolymorphic Catecholaminergic Ventricular TachycardiaRisk FactorsTachycardia, VentricularVentricular Fibrillation

Identifiers

PMID21430528
PMCPMC3145336
OpenAlexW2049980274

What OpenQuestion holds

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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.