Evidence map›Paper›PMID 21150009›Full record

ReviewThe Indian journal of medical research2010

Genomic approaches to coronary artery disease.

Sandosh Padmanabhan, Claire Hastie, Dorairaj Prabhakaran, Anna F Dominczak

Abstract readReview
In one paragraph

Review in The Indian journal of medical research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Association Between Paraoxonase 2 Ser311Cys Polymorphism and Coronary Heart Disease Risk: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Pooled it
  2. Meta-Analysis on the Correlation Between APOM rs805296 Polymorphism and Risk of Coronary Artery Disease.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Pooled it
  3. Trial
  4. Article
  5. Journal of cardiovascular development and disease · 2018
    Article
  6. Analysis of the mutations in exon 10 ofJournal of cardiovascular and thoracic research · 2018
    Article
  7. Article
  8. Telomere length as a potential biomarker of coronary artery disease.The Indian journal of medical research · 2017
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
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.

Sandosh PadmanabhanInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom. sp24g@clinmed.gla.ac.uk
Claire Hastie
Dorairaj Prabhakaran
Anna F Dominczak

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronary artery disease (CAD) is a leading cause of death and disability worldwide. In addition to lifestyle and environmental factors which are major aetiologic determinants, there is considerable familial clustering of the disease indicating a genetic component in its causation. Although the total genetic contribution to CAD risk can be quantified, the determination of the size and number of contributing effects is impossible without identifying all CAD susceptibility genes. However, despite extensive studies, strong evidence of a molecular genetic association with coronary artery disease or myocardial infarction remains elusive. Genome wide association studies have been successful in identifying robust associations of single nucleotide polymorphisms (SNP) with CAD. Identifying the causal variant and dissecting pathways linking these variants to disease process is a major challenge. Technologies from whole genome sequencing, proteomics, transcriptomics and metabolomics are now available to extend analysis to a more complete range of potential susceptibility variants, and to support more explicit modelling of the joint effects of genes and environment. The availability of these high throughput technologies does not diminish the importance of rigorous phenotyping and appropriate study designs in all the endeavours to understand the aetiopathogenesis of CAD. Combining classical epidemiology with modern genomics will require collaborative efforts within the cardiovascular disease community at both bench and bedside and this will have the potential to expand our understanding of CAD and translate discoveries into clinically useful applications that will have a major impact on public health.

Indexed as

Genetic LinkageGenome-Wide Association StudyResearch DesignCoronary Artery DiseaseGenetic Predisposition to DiseaseGenomicsHumansPolymorphism, Single Nucleotide

Identifiers

PMID21150009
PMCPMC3028944

What OpenQuestion holds

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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.