Evidence map›Paper›PMID 28728756›Full record

ArticleAtherosclerosis2017

Circulating soluble urokinase plasminogen activator receptor levels and peripheral arterial disease outcomes.

Ayman Samman Tahhan, Salim S Hayek, Pratik Sandesara, Jamal Hajjari, Muhammad Hammadah, Wesley T O'Neal, Heval M Kelli, Ayman Alkhoder, Nima Ghasemzadeh, Yi-An Ko and 10 more

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In one paragraph

Article in Atherosclerosis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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  13. RAGE and αVβ3-integrin are essential for suPAR signaling in podocytes.Biochimica et biophysica acta. Molecular basis of disease · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 3 institutions in 1 country.

Ayman Samman TahhanEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Salim S HayekEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Pratik SandesaraEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Jamal HajjariEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Muhammad HammadahEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Wesley T O'NealEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Heval M KelliEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Ayman AlkhoderEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Nima GhasemzadehEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Yi-An KoDepartment of Biostatistics and Bioinformatics, Emory University, United States.
Hiroshi AidaEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Mohamad Mazen GafeerEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Naser AbdelhadiEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Kareem Hosny MohammedEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Keyur PatelEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Shipra AryaDepartment of Surgery, Emory University School of Medicine, United States.
Jochen ReiserDepartment of Medicine, Rush University Medical Center, United States.
Viola VaccarinoEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States; Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, United States.
Laurence SperlingEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States.
Arshed QuyyumiEmory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, United States. Electronic address: aquyyum@emory.edu.
Emory University · USEmory Healthcare · USRush University Medical Center · US

Funding

Serious Hazards of Transfusion & Cellular Therapies: Mechanisms and InterventionP01HL086773 · NHLBI · EMORY UNIVERSITY · PI ROBACK, JOHN D · 2008 to 2019
$17.9M
Vascular Responses During Mental StressP01HL101398 · NHLBI · EMORY UNIVERSITY · PI QUYYUMI, ARSHED A · 2010 to 2015
$11.0M
Mental Stress and Myocardial Ischemia after MI: Sex Differences, Mechanisms and PrognosisR01HL109413 · NHLBI · EMORY UNIVERSITY · PI VACCARINO, VIOLA · 2012 to 2023
$6.9M
Multidisciplinary Research Training to Reduce Inequities in Cardiovascular HealthT32HL130025 · NHLBI · EMORY UNIVERSITY · PI Tené T Lewis, Viola Vaccarino · 2016 to 2026
$6.4M
Cell therapy for diabetic peripheral neurovascular complicationsDP3DK094346 · NIDDK · EMORY UNIVERSITY · PI CHENG, XIAODONG, YOON, YOUNG-SUP · 2011 to 2011
$6.1M
The role of the renin-angiotensin-endothelial pathway in ADRF1AG051633 · NIA · EMORY UNIVERSITY · PI HAJJAR, IHAB M, QUYYUMI, ARSHED A · 2015 to 2017
$6.0M
Adverse effects of RBC transfusions: A unifying hypothesisR01HL095479 · NHLBI · EMORY UNIVERSITY · PI ROBACK, JOHN D · 2009 to 2017
$5.2M
Mechanisms Linking Depression to Cardiovascular RiskR01HL068630 · NHLBI · EMORY UNIVERSITY · PI VACCARINO, VIOLA · 2001 to 2010
$4.8M
Metabolomics of subclinical and clinical cardiovascular diseaseP20HL113451 · NHLBI · EMORY UNIVERSITY · PI JONES, DEAN PAUL · 2012 to 2016
$4.3M
PTSD and Ischemic Heart Disease Progression: A Longitudinal Twin StudyR01HL125246 · NHLBI · EMORY UNIVERSITY · PI VACCARINO, VIOLA · 2015 to 2018
$3.4M
Posttraumatic Stress Disorder and Cardiovascular DiseaseR01AG026255 · NIA · EMORY UNIVERSITY · PI VACCARINO, VIOLA · 2004 to 2007
$2.8M
Heart Failure Clinical Trials NetworkU10HL110302 · NHLBI · EMORY UNIVERSITY · PI SMITH, ANDREW · 2012 to 2018
$2.5M
NHLBI NIH HHS F32 HL134290NHLBI NIH HHS K24 HL077506NHLBI NIH HHS P01 HL086773NHLBI NIH HHS P01 HL101398NHLBI NIH HHS P20 HL113451NHLBI NIH HHS R01 HL068630NHLBI NIH HHS R01 HL089650NHLBI NIH HHS R01 HL095479NHLBI NIH HHS R01 HL109413NHLBI NIH HHS R01 HL125246NHLBI NIH HHS R56 HL126558NHLBI NIH HHS RC2 HL101515NHLBI NIH HHS T32 HL130025NHLBI NIH HHS U10 HL110302NIA NIH HHS R01 AG026255NIA NIH HHS RF1 AG051633NIDDK NIH HHS DP3 DK094346NINDS NIH HHS R01 NS064162
6 · The paper itself

Abstract

BACKGROUND AND

aimsCirculating soluble urokinase plasminogen activator receptor (suPAR) is a marker of immune activation associated with atherosclerosis. Whether suPAR levels are associated with prevalent peripheral arterial disease (PAD) and its adverse outcomes remains unknown and is the aim of the study.

methodsSuPAR levels were measured in 5810 patients (mean age 63 years, 63% male, 77% with obstructive coronary artery disease [CAD]) undergoing cardiac catheterization. The presence of PAD (n = 967, 17%) was classified as carotid (36%), lower/upper extremities (30%), aortic (15%) and multisite disease (19%). Multivariable logistic and Cox regression models were used to determine independent predictors of prevalent PAD and outcomes including all-cause death, cardiovascular death and PAD-related events after adjustment for age, gender, race, body mass index, smoking, diabetes, hypertension, hyperlipidemia, renal function, heart failure history, and obstructive CAD.

resultsPlasma suPAR levels were 22.5% (p < 0.001) higher in patients with PAD compared to those without PAD. Plasma suPAR was higher in patients with more extensive PAD (≥2 compared to single site) p < 0.001. After multivariable adjustment, suPAR was associated with prevalent PAD; odds ratio (OR) for highest compared to lowest tertile of 2.0, 95% CI (1.6-2.5) p < 0.001. In Cox survival analyses adjusted for clinical characteristics and medication regimen, suPAR (in the highest vs. lowest tertile) remained an independent predictor of all-cause death [HR 3.1, 95% CI (1.9-5.3)], cardiovascular death [HR 3.5, 95% CI (1.8-7.0)] and PAD-related events [HR = 1.8, 95% CI (1.3-2.6) p < 0.001 for all].

conclusionsPlasma suPAR level is predictive of prevalent PAD and of incident cardiovascular and PAD-related events. Whether SuPAR measurement can help screen, risk stratify, or monitor therapeutic responses in PAD requires further investigation.

Indexed as

AgedBiomarkersCase-Control StudiesChi-Square DistributionCoronary Artery DiseaseFemaleGeorgiaHumansIncidenceKaplan-Meier EstimateLogistic ModelsMaleMiddle AgedMultivariate AnalysisOdds RatioPeripheral Arterial DiseaseBiomarkersPLAUR protein, humanReceptors, Urokinase Plasminogen ActivatorAtherosclerosisCADCardiovascular outcomesPADPAD-Related outcomesSuPAR

Identifiers

PMID28728756
PMCPMC5808930
OpenAlexW2623947131

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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.