Evidence map›Paper›PMID 29874179›Full record

ArticleCirculation. Genomic and precision medicine2018

Polygenic Risk Score for Coronary Heart Disease Modifies the Elevated Risk by Cigarette Smoking for Disease Incidence.

George Hindy, Frans Wiberg, Peter Almgren, Olle Melander, Marju Orho-Melander

Open access · hybridAbstract read
In one paragraph

Article in Circulation. Genomic and precision medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.8field-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

20 citing papers in PubMed, 37 citations in OpenAlex.

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  14. Gene-Environment Interactions for Cardiovascular Disease.Current atherosclerosis reports · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

George HindyFrom the Department of Clinical Sciences in Malmö, Lund University, Sweden (G.H., F.W., P.A., O.M., M.O.-M.); and Program in Medical and Population Genetics, The Broad Institute, Cambridge, MA (G.H.).
Frans WibergFrom the Department of Clinical Sciences in Malmö, Lund University, Sweden (G.H., F.W., P.A., O.M., M.O.-M.); and Program in Medical and Population Genetics, The Broad Institute, Cambridge, MA (G.H.).
Peter AlmgrenFrom the Department of Clinical Sciences in Malmö, Lund University, Sweden (G.H., F.W., P.A., O.M., M.O.-M.); and Program in Medical and Population Genetics, The Broad Institute, Cambridge, MA (G.H.).
Olle MelanderFrom the Department of Clinical Sciences in Malmö, Lund University, Sweden (G.H., F.W., P.A., O.M., M.O.-M.); and Program in Medical and Population Genetics, The Broad Institute, Cambridge, MA (G.H.).
Marju Orho-MelanderFrom the Department of Clinical Sciences in Malmö, Lund University, Sweden (G.H., F.W., P.A., O.M., M.O.-M.); and Program in Medical and Population Genetics, The Broad Institute, Cambridge, MA (G.H.). marju.orho-melander@med.lu.se.
Malmö University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCoronary heart disease (CHD) is a multifactorial disease with both genetic and environmental components. Smoking is the most important modifiable risk factor for CHD. Our aim was to test whether the increased CHD incidence by smoking is modified by genetic predisposition to CHD. METHODS AND

resultsOur study included 24 443 individuals from the MDCS (Malmö Diet and Cancer Study). A weighted polygenic risk score (PRS) was created by summing the number of risk alleles for 50 single-nucleotide polymorphisms associated with CHD. Individuals were classified as current, former, or never smokers. Interactions were primarily tested between smoking status and PRS and secondarily with individual single-nucleotide polymorphisms. Then, the predictive use of PRS for CHD incidence was tested among different smoking categories. During a median follow-up time of 19.4 years, 3217 incident CHD cases were recorded. The association between smoking and CHD was modified by the PRS (

conclusionsGenetic predisposition to CHD modifies the associated increased CHD risk by smoking. The PRS has a better predictive use among never smokers compared with smokers.

Indexed as

AgedAllelesArea Under CurveCoronary DiseaseFemaleGenetic Predisposition to DiseaseGenotypeHistone DeacetylasesHumansIncidenceMaleMiddle AgedOdds RatioPhosphatidate PhosphatasePolymorphism, Single NucleotideProspective StudiesHDAC9 protein, humanHistone DeacetylasesPhosphatidate PhosphatasePLPP3 protein, humanRepressor Proteinscigarette smokingcoronary diseasegene-environment interactiongenetic predisposition to diseaseppolymorphism, geneticsmoking

Identifiers

PMID29874179
PMCPMC6319562
OpenAlexW2783198044

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.