Evidence map›Paper›PMID 30726294›Full record

ArticlePloS one2019

Association of genetic variants previously implicated in coronary artery disease with age at onset of coronary artery disease requiring revascularizations.

Charlotte Andersson, Maria Lukács Krogager, Regitze Kuhr Skals, Emil Vincent Rosenbaum Appel, Christian Theil Have, Niels Grarup, Oluf Pedersen, Jørgen L Jeppesen, Ole Dyg Pedersen, Helena Dominguez and 11 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 32% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

21 authors at 8 institutions in 2 countries.

Charlotte AnderssonDepartment of Cardiology, Herlev and Gentofte Hospital, Hellerup, Denmark.ORCID 0000-0001-6019-8627
Maria Lukács KrogagerUnit of Epidemiology and biostatistics, Aalborg University Hospital, Aalborg, Denmark.
Regitze Kuhr SkalsUnit of Epidemiology and biostatistics, Aalborg University Hospital, Aalborg, Denmark.
Emil Vincent Rosenbaum AppelThe Novo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Christian Theil HaveThe Novo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.ORCID 0000-0002-8634-4781
Niels GrarupThe Novo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Oluf PedersenThe Novo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Jørgen L JeppesenDepartment of Internal Medicine, Section of Cardiology, Amager and Hvidovre Hospital Glostrup, Glostrup, Denmark.
Ole Dyg PedersenDepartment of Cardiology, Roskilde Hospital, Roskilde, Denmark.
Helena DominguezDepartment of Cardiology, Bispebjerg and Frederiksberg Hospital, Bispebjerg, Denmark.ORCID 0000-0002-7089-2636
Ulrik DixenDepartment of Cardiology, Amager and Hvidovre Hospital Hvidovre, Hvidovre, Denmark.
Thomas EngstrømDepartment of Cardiology, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark.
Niels TønderDepartment of Cardiology, Nephrology, and Endocrinology, Hillerød Hospital, Hillerød, Denmark.
Dan M RodenDepartments of Medicine, Pharmacology, and Biomedical Informatics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Steen StenderDepartment of Clinical Biochemistry, Copenhagen University Hospital, Gentofte, Denmark.
Gunnar H GislasonDepartment of Cardiology, Herlev and Gentofte Hospital, Hellerup, Denmark.
Henrik Enghusen-PoulsenLaboratory of Clinical Pharmacology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Torben HansenThe Novo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Lars KøberDepartment of Cardiology, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark.
Christian Torp-PedersenUnit of Epidemiology and biostatistics, Aalborg University Hospital, Aalborg, Denmark.
Peter E WeekeDepartment of Cardiology, Bispebjerg and Frederiksberg Hospital, Bispebjerg, Denmark.
University of Copenhagen · DKAalborg University Hospital · DKCopenhagen University Hospital · DKGentofte Hospital · DKHvidovre Hospital · DKFrederiksberg Hospital · DKUniversity of Southern Denmark · DKVanderbilt University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe relation between burden of risk factors, familial coronary artery disease (CAD), and known genetic variants underlying CAD and low-density lipoprotein cholesterol (LDL-C) levels is not well-explored in clinical samples. We aimed to investigate the association of these measures with age at onset of CAD requiring revascularizations in a clinical sample of patients undergoing first-time coronary angiography.

methods1599 individuals (mean age 64 years [min-max 29-96 years], 28% women) were genotyped (from blood drawn as part of usual clinical care) in the Copenhagen area (2010-2014). The burden of common genetic variants was measured as aggregated genetic risk scores (GRS) of single nucleotide polymorphisms (SNPs) discovered in genome-wide association studies.

resultsSelf-reported familial CAD (prevalent in 41% of the sample) was associated with -3.2 years (95% confidence interval -4.5, -2.2, p<0.0001) earlier need of revascularization in sex-adjusted models. Patients with and without familial CAD had similar mean values of CAD-GRS (unweighted scores 68.4 vs. 68.0, p = 0.10, weighted scores 67.7 vs. 67.5, p = 0.49) and LDL-C-GRS (unweighted scores 58.5 vs. 58.3, p = 0.34, weighted scores 63.3 vs. 61.1, p = 0.41). The correlation between the CAD-GRS and LDL-C-GRS was low (r = 0.14, p<0.001). In multivariable adjusted regression models, each 1 standard deviation higher values of LDL-C-GRS and CAD-GRS were associated with -0.70 years (95% confidence interval -1.25, -0.14, p = 0.014) and -0.51 years (-1.07, 0.04, p = 0.07) earlier need for revascularization, respectively.

conclusionsYoung individuals presenting with CAD requiring surgical interventions had a higher genetic burden of SNPs relating to LDL-C and CAD (although the latter was statistically non-significant), compared with older individuals. However, the absolute difference was modest, suggesting that genetic screening can currently not be used as an effective prediction tool of when in life a person will develop CAD. Whether undiscovered genetic variants can still explain a "missing heritability" in early-onset CAD warrants more research.

Indexed as

AdultAgedAged, 80 and overAge of OnsetCoronary AngiographyCoronary DiseaseFemaleGenetic Predisposition to DiseaseHumansMaleMiddle AgedPercutaneous Coronary InterventionPolymorphism, Single Nucleotide

Identifiers

PMID30726294
PMCPMC6364925
OpenAlexW2914478152

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.