Evidence map›Paper›PMID 20161734›Full record

SynthesisPloS one2010

Causal relationship of susceptibility genes to ischemic stroke: comparison to ischemic heart disease and biochemical determinants.

Paul Bentley, George Peck, Liam Smeeth, John Whittaker, Pankaj Sharma

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 9 pooled it
6.5field-weighted citation impact, top 3% 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

33 citing papers in PubMed, 9 syntheses or guidelines pooled it, 84 citations in OpenAlex.

  1. Pooled it
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  3. A Meta-Prediction ofInternational journal of environmental research and public health · 2018
    Pooled it
  4. Guideline
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  9. Paraoxonase 1 polymorphisms and ischemic stroke risk: A systematic review and meta-analysis.Genetics in medicine : official journal of the American College of Medical Genetics · 2010
    Pooled it
  10. Trial
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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

5 authors at 3 institutions in 1 country.

Paul BentleyImperial College Cerebrovascular Research Unit, Clinical Neurosciences, Charing Cross Hospital, Imperial College London, London, United Kingdom. p.bentley@imperial.ac.uk
George Peck
Liam Smeeth
John Whittaker
Pankaj Sharma
Charing Cross Hospital · GBLondon School of Hygiene & Tropical Medicine · GBImperial College London · GB

Funding

Wellcome Trust 082178
6 · The paper itself

Abstract

Interrelationships between genetic and biochemical factors underlying ischemic stroke and ischemic heart disease are poorly understood. We: 1) undertook the most comprehensive meta-analysis of genetic polymorphisms in ischemic stroke to date; 2) compared genetic determinants of ischemic stroke with those of ischemic heart disease, and 3) compared effect sizes of gene-stroke associations with those predicted from independent biochemical data using a mendelian randomization strategy. Electronic databases were searched up to January 2009. We identified: 1) 187 ischemic stroke studies (37,481 cases; 95,322 controls) interrogating 43 polymorphisms in 29 genes; 2) 13 meta-analyses testing equivalent polymorphisms in ischemic heart disease; and 3) for the top five gene-stroke associations, 146 studies (65,703 subjects) describing equivalent gene-biochemical relationships, and 28 studies (46,928 subjects) describing biochemical-stroke relationships. Meta-analyses demonstrated positive associations with ischemic stroke for factor V Leiden Gln506, ACE I/D, MTHFR C677T, prothrombin G20210A, PAI-1 5G allele and glycoprotein IIIa Leu33Pro polymorphisms (ORs: 1.11 - 1.60). Most genetic associations show congruent levels of risk comparing ischemic stroke with ischemic heart disease, but three genes--glycoprotein IIIa, PAI-1 and angiotensinogen--show significant dissociations. The magnitudes of stroke risk observed for factor V Leiden, ACE, MTHFR and prothrombin, but not PAI-1, polymorphisms, are consistent with risks associated with equivalent changes in activated protein C resistance, ACE activity, homocysteine, prothrombin, and PAI-1 levels, respectively. Our results demonstrate causal relationships for four of the most robust genes associated with stroke while also showing that PAI-1 4G/5G polymorphism influences cardiovascular risk via a mechanism not simply related to plasma levels of PAI-1 (or tPA) alone.

Indexed as

Polymorphism, GeneticCarbon-Nitrogen LigasesCausalityFactor VGenetic Predisposition to DiseaseGenotypeHumansMyocardial IschemiaOdds RatioPhenotypePlasminogen Activator Inhibitor 1ProthrombinRisk FactorsStroke5,10-methenyltetrahydrofolate synthetaseCarbon-Nitrogen LigasesFactor Vfactor V LeidenPlasminogen Activator Inhibitor 1Prothrombin

Identifiers

PMID20161734
PMCPMC2817726
OpenAlexW2058180580

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.