Evidence map›Paper›PMID 33771149›Full record

Trial reportCardiovascular diabetology2021

Dapagliflozin effect on endothelial dysfunction in diabetic patients with atherosclerotic disease: a randomized active-controlled trial.

Andrei C Sposito, Ikaro Breder, Alexandre A S Soares, Sheila T Kimura-Medorima, Daniel B Munhoz, Riobaldo M R Cintra, Isabella Bonilha, Daniela C Oliveira, Jessica Cunha Breder, Pamela Cavalcante and 9 more

Open access · goldFull text readComparative StudyRandomized Controlled Trial
In one paragraph

Trial report in Cardiovascular diabetology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 5 pooled it
9.5field-weighted citation impact, top 1% 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

45 citing papers in PubMed, 5 syntheses or guidelines pooled it, 80 citations in OpenAlex.

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  17. Endothelial dysfunction in chronic kidney disease: a clinical perspective.American journal of physiology. Heart and circulatory physiology · 2025
    Review
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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

19 authors at 1 institution in 1 country.

Andrei C SpositoAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil. sposito@unicamp.br.ORCID 0000-0001-7127-2052
Ikaro BrederAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Alexandre A S SoaresAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Sheila T Kimura-MedorimaAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Daniel B MunhozAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Riobaldo M R CintraAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Isabella BonilhaAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Daniela C OliveiraAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Jessica Cunha BrederAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Pamela CavalcanteAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Camila MoreiraAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Filipe A MouraAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Jose Carlos de Lima-JuniorAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Helison R P do CarmoAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Joaquim BarretoAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Wilson NadruzAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Luiz Sergio F CarvalhoAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
Thiago QuinagliaAterosclerose and Vascular Biology Laboratory (Aterolab), Cardiology Division, State University of Campinas Medical School, Rua Tessalia Vieira de Camargo 126, Cidade Universitaria Zeferino Vaz, Campinas, SP, 13084-971, Brazil.
ADDENDA-BHS2 trial investigators
Universidade Estadual de Campinas (UNICAMP) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe glucose-lowering independent effect of sodium glucose cotransporter-2 inhibitors (SGLT2i) on arterial wall function has not yet been clarified. This study aims to assess whether SGLT2i treatment can attenuate endothelial dysfunction related to type 2 diabetes mellitus (T2D) compared with glucose-lowering equivalent therapy.

methodsIn a prospective, open-label, single-center, randomized clinical trial, 98 patients with T2DM and carotid intima-media thickness above the 75th percentile were randomized 1:1 to 12 weeks of therapy with dapagliflozin or glibenclamide in addition to metformin in glucose-lowering equivalent regimens. The coprimary endpoints were 1-min flow-mediated dilation (FMD) at rest and 1-min FMD after 15 min of ischemia followed by 15 min of reperfusion time (I/R).

resultsNinety-seven patients (61% males, 57 ± 7 years) completed the study. The median HbA1c decreased by - 0.8 (0.7)% and -0.7 (0.95)% following dapagliflozin and glibenclamide, respectively. The first coprimary endpoint, i.e., rest FMD changed by + 3.3(8.2)% and - 1.2(7.5)% for the dapagliflozin and glibenclamide arms, respectively (p = 0.0001). Differences between study arms in the second coprimary endpoint were not significant. Plasma nitrite 1 min after rest FMD was higher for dapagliflozin [308(220) nmol/L] than for glibenclamide (258[110] nmol/L; p = 0.028). The resistive indices at 1 min [0.90 (0.11) vs. 0.93 (0.07); p = 0.03] and 5 min [0.93 (0.07) vs. 0.95 (0.05); p = 0.02] were higher for the glibenclamide group than for the dapagliflozin group. Plasma biomarkers for inflammation and oxidative stress did not differ between the treatments.

conclusionsDapagliflozin improved micro- and macrovascular endothelial function compared to glibenclamide, regardless of glycemic control in patients with T2DM and subclinical carotid atherosclerotic disease.

Indexed as

AdultAgedBenzhydryl CompoundsBiomarkersBlood GlucoseBrazilCarotid Artery DiseasesDiabetes Mellitus, Type 2Drug Therapy, CombinationEndothelium, VascularFemaleGlucosidesGlyburideGlycated HemoglobinHumansMaleBenzhydryl CompoundsBiomarkersBlood GlucosedapagliflozinGlucosidesGlyburideGlycated Hemoglobinhemoglobin A1c protein, humanMetforminSodium-Glucose Transporter 2 InhibitorsEndothelial functionNitric oxideSGLT2Type 2 diabetes

Identifiers

PMID33771149
PMCPMC8004411
OpenAlexW3139496483

What Socratic holds

Textfull text, public
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 Socratic graph.