Evidence map›Paper›PMID 29884292›Full record

ArticleInternational journal of cardiology2018

Role of genetic heart disease in sentinel sudden cardiac arrest survivors across the age spectrum.

John R Giudicessi, Michael J Ackerman

Open access · greenAbstract read
In one paragraph

Article in International journal of cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Guideline
  2. Review
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  5. Idiopathic ventricular fibrillation: is it a case for genetic testing?Herzschrittmachertherapie & Elektrophysiologie · 2024
    Review
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  7. Review
  8. The genetic basis of apparently idiopathic ventricular fibrillation: a retrospective overview.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023
    Article
  9. Review
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  16. [Adult advanced life support].Notfall & rettungsmedizin · 2021
    Review
  17. 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 2 institutions in 1 country.

John R GiudicessiDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, United States; Department of Internal Medicine (Clinician-Investigator Training Program), Mayo Clinic, Rochester, MN, United States.
Michael J AckermanDepartment of Cardiovascular Medicine (Division of Heart Rhythm Services), Mayo Clinic, Rochester, MN, United States; Department of Pediatric and Adolescent Medicine (Division of Pediatric Cardiology), Mayo Clinic, Rochester, MN, United States; Department of Molecular Pharmacology & Experimental Therapeutics (Windland Smith Rice Sudden Death Genomics Laboratory), Mayo Clinic, Rochester, MN, United States. Electronic address: ackerman.michael@mayo.edu.
Mayo Clinic · USWinnMed · US

Funding

Cardiac Channel Mutations in Sudden Infant Death Syndrome (SIDS)R01HD042569 · NICHD · MAYO CLINIC ROCHESTER · PI ACKERMAN, MICHAEL JOHN · 2002 to 2017
$6.9M
NICHD NIH HHS R01 HD042569
6 · The paper itself

Abstract

backgroundSudden cardiac arrest (SCA) may be the sentinel expression of a sudden cardiac death-predisposing genetic heart disease (GHD). Although shown to underlie many unexplained SCAs in the young, the contribution of GHDs to sentinel SCA has never been quantified across the age spectrum. Thus, we sought to determine the contribution of GHDs in single-center referral cohort of non-ischemic SCA survivors. METHODS AND

resultsRetrospective analysis of 3037 patients was used to identify all individuals who experienced a sentinel event of SCA. Following exclusion of patients with ischemic or complex congenital heart disease, cases were classified by clinical diagnoses. Overall, 180 (5.9%) referral patients experienced a sentinel SCA (average age at SCA 28 ± 15 years, 99 females). An etiology was identified in 113/180 patients (62.8%) including channelopathies in 26.7%, arrhythmogenic bileaflet mitral valve prolapse in 10.6%, cardiomyopathies in 9.4%, other etiologies in 6.7%, acquired long QT syndrome in 6.7%, and multiple disorders in 2.8%. The remaining 67/180 (37.2%) cases were classified as idiopathic ventricular fibrillation (IVF). Interestingly, the contribution of GHDs declined precipitously after the first decade of life [90.0% (age 0-9; n = 20), 58.7% (age 10-19; n = 46), 28.1% (age 20-29; n = 32), 23.8% (age 30-39; n = 42), 16.7% (age 40-49; n = 24), and 12.5% (age 50+; n = 16)].

conclusionsWithin a referral population enriched for GHDs, the ability of a comprehensive cardiac evaluation, including genetic testing, to elucidate a root cause in non-ischemic SCA survivors declined with age. Although rare, GHDs can underlie SCA into adulthood and merit consideration across the age spectrum.

Indexed as

SurvivorsAdolescentAdultChildChild, PreschoolCohort StudiesDeath, Sudden, CardiacFemaleGenetic Predisposition to DiseaseHeart DiseasesHumansInfantInfant, NewbornMaleMiddle AgedRetrospective StudiesArrhythmiaCardiomyopathyGeneticsGenetic testingSudden cardiac arrestSudden cardiac death

Identifiers

PMID29884292
PMCPMC6364980
OpenAlexW2806488444

What OpenQuestion holds

Textmetadata
LicenceTDM
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.