Evidence map›Paper›PMID 25700702›Full record

ArticleActa diabetologica2015

Analysis of a cardiovascular disease genetic risk score in the Diabetes Heart Study.

Laura M Raffield, Amanda J Cox, J Jeffrey Carr, Barry I Freedman, Pamela J Hicks, Carl D Langefeld, Fang-Chi Hsu, Donald W Bowden

Abstract read
In one paragraph

Article in Acta diabetologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 2 pooled it
1.2field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Genetic Risk Score for Coronary Heart Disease: Review.Journal of personalized medicine · 2020
    Review
  7. Article
  8. 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

8 authors at 2 institutions in 1 country.

Laura M RaffieldMolecular Genetics and Genomics Program, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Amanda J Cox
J Jeffrey Carr
Barry I Freedman
Pamela J Hicks
Carl D Langefeld
Fang-Chi Hsu
Donald W Bowden
Wake Forest University · USVanderbilt University Medical Center · US

Funding

Epidemiology of cardiovascular disease in diabetesR01HL067348 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BOWDEN, DONALD W · 2001 to 2004
$4.3M
Genetic Epidemiology of Cerebrovascular Disease and Cognition in DiabetesR01NS058700 · NINDS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BOWDEN, DONALD W · 2008 to 2012
$3.0M
Whole Genome Association Analysis of the Diabetes Heart StudyR01HL092301 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BOWDEN, DONALD W · 2010 to 2013
$2.7M
Genetics of Bone and Vascular Calcium in Type 2 DiabetesR01AR048797 · NIAMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CARR, JOHN JEFFREY · 2001 to 2004
$1.3M
Analysis of Coding Variants Associated with Age-Related PhenotypesF31AG044879 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RAFFIELD, LAURA M · 2013 to 2015
$86k
NHLBI NIH HHS R01 HL067348NHLBI NIH HHS R01 HL092301NHLBI NIH HHS R01 HL67348NIAMS NIH HHS R01 AR048797NIAMS NIH HHS R01 AR48797NIA NIH HHS F31 AG044879NINDS NIH HHS R01 NS058700
6 · The paper itself

Abstract

aimsIt remains unclear whether the high cardiovascular disease (CVD) burden in people with type 2 diabetes (T2D) is associated with genetic variants that contribute to CVD in general populations. Recent studies have examined genetic risk scores of single-nucleotide polymorphisms (SNPs) identified by genome-wide association studies for their cumulative contribution to CVD-related traits. Most analyses combined SNPs associated with a single phenotypic class, e.g., lipids. In the present analysis, we examined a more comprehensive risk score comprised of SNPs associated with a broad range of CVD risk phenotypes.

methodsThe composite risk score was analyzed for potential associations with subclinical CVD, self-reported CVD events, and mortality in 983 T2D-affected individuals of European descent from 466 Diabetes Heart Study (DHS) families. Genetic association was examined using marginal models with generalized estimating equations for subclinical CVD and prior CVD events and Cox proportional hazards models with sandwich-based variance estimation for mortality; analyses were adjusted for age and sex.

resultsAn increase in genetic risk score was significantly associated with higher levels of coronary artery calcified plaque (p = 1.23 × 10(-4)); however, no significant associations with self-reported myocardial infarction and CVD events and all-cause and CVD mortality were observed.

conclusionsThese results suggest that a genetic risk score of SNPs associated with CVD events and risk factors does not significantly account for CVD risk in the DHS, highlighting the limitations of applying current genetic markers for CVD in individuals with diabetes.

Indexed as

Polymorphism, Single NucleotideAdultAgedAged, 80 and overCardiovascular DiseasesDiabetes Mellitus, Type 2FamilyFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMaleMiddle AgedPhenotypePlaque, AtheroscleroticQuantitative Trait, Heritable

Identifiers

PMID25700702
PMCPMC4506855
OpenAlexW1983025806

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.