Evidence map›Paper›PMID 21596318›Full record

ReviewJACC. Cardiovascular interventions2011

Emerging genomic applications in coronary artery disease.

Samir B Damani, Eric J Topol

Open access · greenAbstract readReview
In one paragraph

Review in JACC. Cardiovascular interventions, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. PeerJ · 2024
    Article
  4. Review
  5. Review
  6. Lrp1 Regulation of Pulmonary Function. Follow-Up of Human GWAS in Mice.American journal of respiratory cell and molecular biology · 2021
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Cancer genomics and inherited risk.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2014
    Article
  14. Article
  15. Article
  16. Cardiovascular risk.British journal of clinical pharmacology · 2012
    Review
  17. Review
  18. 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 1 institution in 1 country.

Samir B DamaniDivision of Cardiovascular Diseases, Scripps Clinic, Scripps Translational Science Institute and the Scripps Research Institute, La Jolla, California 92037, USA.
Eric J Topol
Scripps Research Institute · US

Funding

Scripps Translational Science Institute (UL1)UL1TR000109 · NCATS · SCRIPPS RESEARCH INSTITUTE, THE · PI TOPOL, ERIC JEFFREY · 2012 to 2013
$4.0M
Scripps Translational Science Institute (KL2)KL2RR025773 · NCRR · SCRIPPS RESEARCH INSTITUTE, THE · PI TOPOL, ERIC JEFFREY · 2008 to 2011
$1.9M
NCATS NIH HHS UL1 TR000109NCRR NIH HHS KL2 RR025773
6 · The paper itself

Abstract

Over the last 4 years, an unprecedented number of studies illuminating the genomic underpinnings of common "polygenic" diseases including coronary artery disease have been published. Notably, these studies have established numerous deoxyribonucleic acid (DNA) variants within or near chromosome 9p21.3, the LPA, CXADR, and APOE genes, to name a few, as key coronary artery disease and sudden cardiac death susceptibility markers. Most importantly, many of these DNA variants confer over a 2-fold increase in risk for coronary artery disease, myocardial infarction, and ventricular fibrillation. Additionally, loss-of-function variants in the hepatic cytochrome 2C19 system have now been found to be the predominant genetic mediators of clopidogrel antiplatelet response, with variant carriers having a >3-fold increase in risk for stent thrombosis. In the near future, many additional rare polymorphisms, structural variants, and tissue-specific epigenetic features of the human genome including DNA methylation, histone modifications, and chromatin state will emerge as significant contributors to disease pathogenesis and drug response. In aggregate, these findings will have the potential to radically change the practice of cardiovascular medicine. However, only the individual clinician can ultimately enable the translation of these important discoveries to systematic implementation in clinical practice.

Indexed as

GenomicsAnimalsApolipoproteins EAryl Hydrocarbon HydroxylasesCoronary Artery DiseaseCytochrome P-450 CYP2C19Gene Expression ProfilingGenetic Predisposition to DiseaseHumansLipoprotein(a)PharmacogeneticsPhenotypePlatelet Aggregation InhibitorsPolymorphism, GeneticPrecision MedicineRisk AssessmentApolipoproteins EAryl Hydrocarbon HydroxylasesCYP2C19 protein, humanCytochrome P-450 CYP2C19Lipoprotein(a)Platelet Aggregation Inhibitors

Identifiers

PMID21596318
PMCPMC6072268
OpenAlexW2014472596

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.