Evidence map›Paper›PMID 22496207›Full record

Trial reportVascular medicine (London, England)2012

Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease.

Corey E Tabit, Monica Holbrook, Sherene M Shenouda, Mustali M Dohadwala, Michael E Widlansky, Alissa A Frame, Brian H Kim, Mai-Ann Duess, Matthew A Kluge, Aaron Levit and 3 more

Open access · bronzeAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Vascular medicine (London, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

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  20. Angiopoietin-like 2 promotes atherogenesis in mice.Journal of the American Heart Association · 2013
    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

13 authors at 3 institutions in 1 country.

Corey E TabitEvans Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Monica Holbrook
Sherene M Shenouda
Mustali M Dohadwala
Michael E Widlansky
Alissa A Frame
Brian H Kim
Mai-Ann Duess
Matthew A Kluge
Aaron Levit
John F Keaney
Joseph A Vita
Naomi M Hamburg
Boston University · USMedical College of Wisconsin · USUniversity of Massachusetts Chan Medical School · US

Funding

Redox regulation in Endothelial Progenitor CellsP01HL081587 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI HAMBURG, NAOMI MIRIAM · 2005 to 2015
$21.5M
Multidisciplinary Training in Cardiovascular ResearchT32HL007224 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI HAMBURG, NAOMI MIRIAM, WAINFORD, RICHARD DAVID · 1985 to 2020
$12.3M
Vascular Consequences of Insulin Resistance and ObesityP50HL083801 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI VITA, JOSEPH A. · 2006 to 2010
$11.2M
Clinical Utility of Endothelial Function in PADR01HL075795 · NHLBI · BOSTON MEDICAL CENTER · PI VITA, JOSEPH A. · 2003 to 2007
$4.9M
Nox4 and Vascular HomeostasisR01HL098407 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KEANEY, JOHN FRANCIS · 2010 to 2017
$3.8M
Boston University Medical Center Leadership Program in Vascular MedicineK12HL083781 · NHLBI · BOSTON MEDICAL CENTER · PI EBERHARDT, ROBERT THOMAS · 2007 to 2013
$3.4M
Inflammation and Vascular Dysfunction in ObesityR01HL084213 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GOKCE, NOYAN · 2007 to 2011
$2.3M
Adipose inflammation, mitochondrial function & endothelial phenotypes in obesityR01HL114675 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GOKCE, NOYAN · 2012 to 2016
$2.3M
Obesity, Adipocytokines, and Endothelial DysfunctionR01HL074097 · NHLBI · BOSTON MEDICAL CENTER · PI GOKCE, NOYAN · 2003 to 2007
$2.2M
Endothelial Insulin Resistance, Inflammation and Vascular Function in DiabetesR01HL102299 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI HAMBURG, NAOMI MIRIAM · 2010 to 2014
$2.0M
Determinants of Shear Stress-Mediated Arterial RemodelingR01HL083269 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI VITA, JOSEPH A. · 2006 to 2009
$1.9M
MicroRNA Profile in Peripheral Artery DiseaseR21HL109790 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI HAMBURG, NAOMI MIRIAM · 2012 to 2013
$455k
NHLBI NIH HHS HL074097NHLBI NIH HHS HL081587NHLBI NIH HHS HL083269NHLBI NIH HHS HL083801NHLBI NIH HHS HL084213NHLBI NIH HHS HL102299NHLBI NIH HHS HL75795NHLBI NIH HHS K12 HL083781NHLBI NIH HHS P01 HL081587NHLBI NIH HHS P50 HL083801NHLBI NIH HHS R01 HL074097NHLBI NIH HHS R01 HL075795NHLBI NIH HHS R01 HL083269NHLBI NIH HHS R01 HL084213NHLBI NIH HHS R01 HL098407NHLBI NIH HHS R01 HL102299NHLBI NIH HHS R01 HL114675NHLBI NIH HHS R21 HL109790NHLBI NIH HHS T32 HL007224
6 · The paper itself

Abstract

Inflammation is critical for atherosclerosis development and may be a target for risk-reduction therapy. In experimental studies, activation of the inflammatory regulator, nuclear factor kappa B (NFlB), contributes to endothelial activation and reduced nitric oxide production. We treated patients with coronary artery disease with sulfasalazine, an inhibitor of NFκB, and placebo in a randomized, double-blind, crossover study design. Brachial artery flow-mediated dilation (FMD) and digital vascular function were measured at baseline and after each 6-week treatment period. Of the 53 patients enrolled in the crossover study, 32 (age 60 ± 10, 22% female) completed all the visits, with a high rate of study withdrawal due to gastrointestinal side effects. In a subset of 10 participants, we compared the effects of 4 days of sulfasalazine treatment (n = 5) to no treatment (n = 5) on NFκB-regulated gene expression in peripheral blood mononuclear cells. Tumor necrosis factor α-stimulated expression of CD69 and NFlB subunit p50 was significantly blunted after 4 days of sulfasalazine treatment but not after no treatment. However, FMD and digital vasodilator response did not significantly change from baseline with long-term sulfasalazine treatment. Short-term sulfasalazine inhibited NFlB activity; however, long-term treatment was poorly tolerated and did not improve endothelial function. Our findings suggest that sulfasalazine therapy is not the optimal anti-inflammatory treatment for reversing endothelial dysfunction in cardiovascular disease. Further studies are warranted to investigate the potential for NFlB inhibition to reduce cardiovascular risk.

Indexed as

AgedAnalysis of VarianceAnti-Inflammatory Agents, Non-SteroidalBiomarkersBostonBrachial ArteryCoronary Artery DiseaseCross-Over StudiesDouble-Blind MethodEndothelium, VascularFemaleFingersHumansInflammation MediatorsLeukocytesMaleAnti-Inflammatory Agents, Non-SteroidalBiomarkersInflammation MediatorsNF-kappa BSulfasalazine

Identifiers

PMID22496207
PMCPMC3632403
OpenAlexW2154722823

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.