Evidence map›Paper›PMID 28550093›Full record

SynthesisJournal of the American Heart Association2017

Causal Effect of Plasminogen Activator Inhibitor Type 1 on Coronary Heart Disease.

Ci Song, Stephen Burgess, John D Eicher, Christopher J O'Donnell, Andrew D Johnson

Open access · goldAbstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 3 pooled it
5.1field-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

76 citing papers in PubMed, 3 syntheses or guidelines pooled it, 132 citations in OpenAlex.

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16 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Ci SongFramingham Heart Study, Framingham, MA ci.song@nih.gov.
Stephen BurgessDepartment of Public Health and Primary Care, University of Cambridge, United Kingdom.
John D EicherFramingham Heart Study, Framingham, MA.
Christopher J O'DonnellFramingham Heart Study, Framingham, MA.
Andrew D JohnsonFramingham Heart Study, Framingham, MA.
National Heart Lung and Blood Institute · USFramingham Heart Study · USUniversity of Cambridge · GBVA Boston Healthcare System · US

Funding

Cardiovascular Genomics and Bioinformatics projectsZIAHL006170 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI JOHNSON, ANDREW · 2013 to 2025
$25.3M
British Heart Foundation RG/08/014/24067Medical Research Council MC_UP_0801/1Medical Research Council MC_UU_00002/7Medical Research Council MR/K013351/1Medical Research Council MR/L003120/1Wellcome Trust 100114Wellcome Trust 204623/Z/16/Z
6 · The paper itself

Abstract

backgroundPlasminogen activator inhibitor type 1 (PAI-1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI-1 levels are associated with increased risk of coronary heart disease (CHD). However, it is unclear whether the association reflects a causal influence of PAI-1 on CHD risk. METHODS AND

resultsTo evaluate the association between PAI-1 and CHD, we applied a 3-step strategy. First, we investigated the observational association between PAI-1 and CHD incidence using a systematic review based on a literature search for PAI-1 and CHD studies. Second, we explored the causal association between PAI-1 and CHD using a Mendelian randomization approach using summary statistics from large genome-wide association studies. Finally, we explored the causal effect of PAI-1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta-analysis, the highest quantile of blood PAI-1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age- and sex-adjusted model. The effect size was reduced in studies using a multivariable-adjusted model (odds ratio=1.46; 95% CI: 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI-1 level on CHD risk (odds ratio=1.22 per unit increase of log-transformed PAI-1; 95% CI: 1.01, 1.47). In addition, we also detected a causal effect of PAI-1 on elevating blood glucose and high-density lipoprotein cholesterol.

conclusionsOur study indicates a causal effect of elevated PAI-1 level on CHD risk, which may be mediated by glucose dysfunction.

Indexed as

FibrinolysisBiomarkersBlood GlucoseCoronary DiseaseGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansIncidenceLipoproteins, HDLMendelian Randomization AnalysisMultivariate AnalysisObservational Studies as TopicOdds RatioPlasminogen Activator Inhibitor 1Polymorphism, Single NucleotideRisk AssessmentBiomarkersBlood GlucoseLipoproteins, HDLPlasminogen Activator Inhibitor 1SERPINE1 protein, humancoronary heart diseasegenome‐wide association studyMendelian randomizationplasminogen activator inhibitor type 1single nucleotide polymorphism

Identifiers

PMID28550093
PMCPMC5669150
OpenAlexW2613753174

What OpenQuestion holds

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LicenceCC BY
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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.