Evidence map›Paper›PMID 23478099›Full record

SynthesisHypertension (Dallas, Tex. : 1979)2013

Genetic predisposition to higher blood pressure increases coronary artery disease risk.

Wolfgang Lieb, Henning Jansen, Christina Loley, Michael J Pencina, Christopher P Nelson, Christopher Newton-Cheh, Sekar Kathiresan, Muredach P Reilly, Themistocles L Assimes, Eric Boerwinkle and 14 more

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in Hypertension (Dallas, Tex. : 1979), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 4 pooled it
9.0field-weighted citation impact, top 2% 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

38 citing papers in PubMed, 4 syntheses or guidelines pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Metabolic Syndrome and Coronary Artery Disease Risk: A Meta-Analysis of Observational Studies.International journal of environmental research and public health · 2021
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
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  9. Review
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  13. Review
  14. Studies in Zebrafish Demonstrate ThatFrontiers in cardiovascular medicine · 2020
    Article
  15. Article
  16. Atherosclerotic diseases and lung cancer - a ten-year cross-sectional study in Cyprus.Archives of medical sciences. Atherosclerotic diseases · 2020
    Article
  17. Article
  18. Article
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  20. 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

24 authors at 4 institutions in 3 countries.

Wolfgang LiebUniversity Clinic Schleswig Holstein, Institute of Epidemiology, Campus Kiel, Germany.
Henning Jansen
Christina Loley
Michael J Pencina
Christopher P Nelson
Christopher Newton-Cheh
Sekar Kathiresan
Muredach P Reilly
Themistocles L Assimes
Eric Boerwinkle
Alistair S Hall
Christian Hengstenberg
Reijo Laaksonen
Ruth McPherson
Unnur Thorsteinsdottir
Andreas Ziegler
Annette Peters
John R Thompson
Inke R König
Jeanette Erdmann
Nilesh J Samani
Ramachandran S Vasan
Heribert Schunkert
CARDIoGRAM
Harvard University Press · USUniversity Hospitals of Leicester NHS Trust · GBDean College · USdeCODE Genetics (Iceland) · IS

Funding

Regression of Atherosclerosis CoreP01HL098055 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI FISHER, EDWARD A · 2010 to 2014
$12.1M
REGULATION OF MONOCYTE 15-LIPOXYGENASE EXPRESSIONP01HL087018 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI MCINTYRE, THOMAS M · 2007 to 2011
$11.4M
A Genome-wide Association Study for Early-Onset Myocardial InfarctionR01HL087676 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ALTSHULER, DAVID · 2007 to 2009
$4.7M
Whole Genome Association for Early Coronary Artery Disease and Related PhenotypesR01HL087647 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2006 to 2008
$4.6M
Biomarkers for Complications in Type 1 Diabetes (DCCT/EDIC)R01DK080732 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI HAZEN, STANLEY L · 2009 to 2010
$1.4M
COMMUNITY AND COHORT SURVEILLANCE PROGRAMS-N01HC55015N01HC055015 · HC · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI CHAMBLESS, LLOYD E · 1985 to 2006
$1.1M
COMMUNITY AND COHORT SURVEILLANCE PROGRAMN01HC055016 · HC · BAYLOR COLLEGE OF MEDICINE · PI BALLANTYNE, CHRISTIE M · 1985 to 2000
$785k
FIELD CENTER FOR CCSPN01HC055019 · HC · UNIVERSITY OF MINNESOTA TWIN CITIES · PI FOLSOM, AARON R · 1985 to 2000
$748k
FIELD CENTERN01HC055021 · HC · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI JONES, DANIEL W · 1985 to 2000
$617k
CCSP-FIELD CENTERN01HC055020 · HC · JOHNS HOPKINS UNIVERSITY · PI NIETO, F JAVIER · 1985 to 2000
$334k
CENTRAL HEMOSTATIS LABORATORY FOR CCSPN01HC055022 · HC · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI WU, KENNETH K · 1985 to 2000
$264k
CCSP--FIELD CENTER AND ULTRASOUND READING CENTERN01HC055018 · HC · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI HEISS, GERARDO · 1985 to 2000
$104k
British Heart FoundationCancer Research UKCIHR CIHR #MOP172605CIHR CIHR #MOP77682CIHR CIHR #MOP‐‐82810Intramural NIH HHSMedical Research CouncilNHLBI NIH HHS 1R01HL103931‐01NHLBI NIH HHS HL087647NHLBI NIH HHS N01 HC025195NHLBI NIH HHS N01-HC-25195NHLBI NIH HHS N01‐HC‐55015NHLBI NIH HHS N01‐HC‐55016NHLBI NIH HHS N01‐HC‐55018NHLBI NIH HHS N01‐HC‐55019NHLBI NIH HHS N01‐HC‐55020NHLBI NIH HHS N01‐HC‐55021NHLBI NIH HHS N01‐HC‐55022NHLBI NIH HHS P01HL076491‐06NHLBI NIH HHS P01HL087018NHLBI NIH HHS P01 HL098055NHLBI NIH HHS R01 HL087676NHLBI NIH HHS R01HL089650‐02NIA NIH HHS N01‐AG‐12100NIDDK NIH HHS R01DK080732Wellcome Trust
6 · The paper itself

Abstract

Hypertension is a risk factor for coronary artery disease. Recent genome-wide association studies have identified 30 genetic variants associated with higher blood pressure at genome-wide significance (P<5 × 10(-8)). If elevated blood pressure is a causative factor for coronary artery disease, these variants should also increase coronary artery disease risk. Analyzing genome-wide association data from 22 233 coronary artery disease cases and 64 762 controls, we observed in the Coronary ARtery DIsease Genome-Wide Replication And Meta-Analysis (CARDIoGRAM) consortium that 88% of these blood pressure-associated polymorphisms were likewise positively associated with coronary artery disease, that is, they had an odds ratio >1 for coronary artery disease, a proportion much higher than expected by chance (P=4 × 10(-5)). The average relative coronary artery disease risk increase per each of the multiple blood pressure-raising alleles observed in the consortium was 3.0% for systolic blood pressure-associated polymorphisms (95% confidence interval, 1.8%-4.3%) and 2.9% for diastolic blood pressure-associated polymorphisms (95% confidence interval, 1.7%-4.1%). In substudies, individuals carrying most systolic blood pressure- and diastolic blood pressure-related risk alleles (top quintile of a genetic risk score distribution) had 70% (95% confidence interval, 50%-94%) and 59% (95% confidence interval, 40%-81%) higher odds of having coronary artery disease, respectively, as compared with individuals in the bottom quintile. In conclusion, most blood pressure-associated polymorphisms also confer an increased risk for coronary artery disease. These findings are consistent with a causal relationship of increasing blood pressure to coronary artery disease. Genetic variants primarily affecting blood pressure contribute to the genetic basis of coronary artery disease.

Indexed as

AdultAgedAllelesBlood PressureCase-Control StudiesCoronary Artery DiseaseFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansHypertensionMaleMiddle AgedPolymorphism, Single NucleotideRisk Factors

Identifiers

PMID23478099
PMCPMC3855241
OpenAlexW2110227655

What OpenQuestion holds

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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.