Evidence map›Paper›PMID 23766260›Full record

SynthesisArteriosclerosis, thrombosis, and vascular biology2013

Risk scores of common genetic variants for lipid levels influence atherosclerosis and incident coronary heart disease.

Aaron Isaacs, Sara M Willems, Daniel Bos, Abbas Dehghan, Albert Hofman, M Arfan Ikram, André G Uitterlinden, Ben A Oostra, Oscar H Franco, Jacqueline C Witteman and 1 more

Open access · bronzeAbstract readMeta-AnalysisMulticenter Study
PubMed Publisher
In one paragraph

Synthesis in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.6field-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

26 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Experimental and therapeutic medicine · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Genetic Risk Score for Coronary Heart Disease: Review.Journal of personalized medicine · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Genetic Markers for Coronary Artery Disease.Medicina (Kaunas, Lithuania) · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Systems Biology and Noninvasive Imaging of Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2016
    Review
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Aaron IsaacsGenetic Epidemiology Unit, Department of Epidemiology, Erasmus Medical Center, Rotterdam, The Netherlands. a.isaacs@erasmusmc.nl
Sara M Willems
Daniel Bos
Abbas Dehghan
Albert Hofman
M Arfan Ikram
André G Uitterlinden
Ben A Oostra
Oscar H Franco
Jacqueline C Witteman
Cornelia M van Duijn
Centre for Medical Systems Biology · NLErasmus University Rotterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveCirculating levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol, and triglycerides are recognized risk factors for cardiovascular disease. We tested the hypothesis that the cumulative effects of common genetic variants for lipids are collectively associated with subclinical atherosclerosis and incident coronary heart disease. APPROACH AND

resultsParticipants were drawn from the Erasmus Rucphen Family Study (n=2269) and the Rotterdam Study (n=8130). Linear regression and Cox proportional hazards models were applied to assess the influence of 4 risk scores derived from common genetic variants for lipids (total cholesterol, LDL-C, high-density lipoprotein cholesterol, and triglycerides) on carotid plaque, intima-media thickness, incident myocardial infarction, and coronary heart disease. Adjusted for age and sex, all 4 risk scores were associated with carotid plaque. This relationship was the strongest for the LDL-C score, which increased plaque score by 0.102 per SD increase in genetic risk score (P=3.2 × 10(-8)). The LDL-C score was also nominally associated with intima-media thickness, which increased 0.006 mm per SD increase in score (P=0.05). Both the total cholesterol and LDL-C scores were associated with incident myocardial infarction and coronary heart disease with hazard ratios between 1.10 and 1.13 per SD increase in score. Inclusion of additional risk factors as covariates minimally affected these results.

conclusionsCommon genetic variants with small effects on lipid levels are, in combination, significantly associated with subclinical and clinical cardiovascular outcomes. As knowledge of genetic variation increases, preclinical genetic screening tools might enhance the prediction and prevention of clinical events.

Indexed as

Polymorphism, Single NucleotideAdultAgedAsymptomatic DiseasesBiomarkersCarotid Artery DiseasesCarotid Intima-Media ThicknessCholesterolCholesterol, HDLCholesterol, LDLCoronary DiseaseFemaleGene FrequencyGenetic Predisposition to DiseaseHumansIncidenceBiomarkersCholesterolCholesterol, HDLCholesterol, LDLLipidsTriglyceridesatherosclerosiscarotid artery plaquecarotid intima-media thicknesscoronary diseasegenetic screeninglipidsmyocardial infarction

Identifiers

PMID23766260
OpenAlexW2104557985

What OpenQuestion holds

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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.