Evidence map›Paper›PMID 26839654›Full record

ReviewWorld journal of cardiology2016

Genetics of coronary artery disease and myocardial infarction.

Xuming Dai, Szymon Wiernek, James P Evans, Marschall S Runge

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 8 pooled it
12.1field-weighted citation impact, top 1% 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

82 citing papers in PubMed, 8 syntheses or guidelines pooled it, 224 citations in OpenAlex.

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  16. Treating Cardiovascular Disorders with Personalized Medicine.Cardiovascular & hematological disorders drug targets · 2025
    Review
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22 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Xuming DaiXuming Dai, Szymon Wiernek, Marschall S Runge, Division of Cardiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States.
Szymon WiernekXuming Dai, Szymon Wiernek, Marschall S Runge, Division of Cardiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States.
James P EvansXuming Dai, Szymon Wiernek, Marschall S Runge, Division of Cardiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States.
Marschall S RungeXuming Dai, Szymon Wiernek, Marschall S Runge, Division of Cardiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States.
University of North Carolina at Chapel Hill · US

Funding

UNC-Clinician-Scientist Training Program in Cardiovascular MedicineT32HL083828 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI STOUFFER, GEORGE A · 2006 to 2015
$2.0M
NHLBI NIH HHS T32 HL083828
6 · The paper itself

Abstract

Atherosclerotic coronary artery disease (CAD) comprises a broad spectrum of clinical entities that include asymptomatic subclinical atherosclerosis and its clinical complications, such as angina pectoris, myocardial infarction (MI) and sudden cardiac death. CAD continues to be the leading cause of death in industrialized society. The long-recognized familial clustering of CAD suggests that genetics plays a central role in its development, with the heritability of CAD and MI estimated at approximately 50% to 60%. Understanding the genetic architecture of CAD and MI has proven to be difficult and costly due to the heterogeneity of clinical CAD and the underlying multi-decade complex pathophysiological processes that involve both genetic and environmental interactions. This review describes the clinical heterogeneity of CAD and MI to clarify the disease spectrum in genetic studies, provides a brief overview of the historical understanding and estimation of the heritability of CAD and MI, recounts major gene discoveries of potential causal mutations in familial CAD and MI, summarizes CAD and MI-associated genetic variants identified using candidate gene approaches and genome-wide association studies (GWAS), and summarizes the current status of the construction and validations of genetic risk scores for lifetime risk prediction and guidance for preventive strategies. Potential protective genetic factors against the development of CAD and MI are also discussed. Finally, GWAS have identified multiple genetic factors associated with an increased risk of in-stent restenosis following stent placement for obstructive CAD. This review will also address genetic factors associated with in-stent restenosis, which may ultimately guide clinical decision-making regarding revascularization strategies for patients with CAD and MI.

Indexed as

AtherosclerosisCoronary artery diseaseGeneticsGenome-wide association studyHeritabilityIn-stent restenosisMyocardial infarction

Identifiers

PMID26839654
PMCPMC4728103
OpenAlexW2411477905

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.