Evidence mapPaperPMID 39516499Full record

ArticleScientific reports2024

Metformin associates with higher myocardial perfusion reserve and survival in type 2 diabetes mellitus patients.

Noor Sharrack, Kristopher D Knott, Gaurav S Gulsin, Tushar Kotecha, Louise A E Brown, Jian L Yeo, Aldostefano Porcari, Robert D Adam, Sharmaine Thirunavukarasu, Amrit Chowdhary and 11 more

Abstract readMulticenter Study
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
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

21 authors.

Noor SharrackDepartment of Biomedical Imaging Science, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, LS2 9JT, UK. n.sharrack@leeds.ac.uk.
Kristopher D KnottBarts Heart Centre, St Bartholomew's Hospital, London, UK.
Gaurav S GulsinDepartment of Cardiovascular Sciences, Cardiovascular Biomedical Research Centre, University of Leicester and the NIHR Leicester, University Hospitals of Leicester NHS Trust, Glenfield Hospital, Leicester, UK.
Tushar KotechaInstitute of Cardiovascular Science, University College London, London, UK.
Louise A E BrownDepartment of Biomedical Imaging Science, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, LS2 9JT, UK.
Jian L YeoDepartment of Cardiovascular Sciences, Cardiovascular Biomedical Research Centre, University of Leicester and the NIHR Leicester, University Hospitals of Leicester NHS Trust, Glenfield Hospital, Leicester, UK.
Aldostefano PorcariDivision of Medicine, National Amyloidosis Centre, University College London, Royal Free Campus, London, UK.
Robert D AdamBarts Heart Centre, St Bartholomew's Hospital, London, UK.
Sharmaine ThirunavukarasuDepartment of Biomedical Imaging Science, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, LS2 9JT, UK.
Amrit ChowdharyDepartment of Biomedical Imaging Science, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, LS2 9JT, UK.
Eylem LeveltDepartment of Biomedical Imaging Science, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, LS2 9JT, UK.
James C MoonBarts Heart Centre, St Bartholomew's Hospital, London, UK.
Gerry P McCannDepartment of Cardiovascular Sciences, Cardiovascular Biomedical Research Centre, University of Leicester and the NIHR Leicester, University Hospitals of Leicester NHS Trust, Glenfield Hospital, Leicester, UK.
Marianna FontanaInstitute of Cardiovascular Science, University College London, London, UK.
Peter KellmanDepartment of Health and Human Services, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Theresa MunyombweLeeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK.
Chris P GaleLeeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK.
David L BuckleyDepartment of Biomedical Imaging Science, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, LS2 9JT, UK.
John P GreenwoodDepartment of Biomedical Imaging Science, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, LS2 9JT, UK.
Peter P SwobodaDepartment of Biomedical Imaging Science, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, LS2 9JT, UK.
Sven PleinDepartment of Biomedical Imaging Science, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, LS2 9JT, UK. s.plein@leeds.ac.uk.

Funding

British Heart Foundation 17/YH/0300British Heart Foundation 18/YH/0168British Heart Foundation CH/16/2/32089).British Heart Foundation FS/16/47/32190National Institute for Health and Care Research RP-2017-08-ST2-007Romanian society of cardiology 95/01.09.2020Wellcome Trust 221690/Z/20/Z
6 · The paper itself

Abstract

Metformin is an antihyperglycemic used to treat type 2 diabetes mellitus (T2DM). Patients with T2DM are at increased risk of cardiovascular disease. We explored the association between metformin use and cardiovascular magnetic resonance (CMR) derived stress myocardial blood flow (MBF), myocardial perfusion reserve (MPR) and major adverse cardiovascular events (MACE; all cause death, MI, stroke, heart failure hospitalisation and coronary revascularisation) in patients with T2DM. Multi-centre study of patients with T2DM, and healthy controls, underwent quantitative myocardial perfusion CMR using an artificial intelligence supported process. Multivariable regression analysis, and cox proportional hazard models of propensity score weighted patients quantified associations between metformin use, MBF, MPR, all cause death and MACE. Analysis included 572 patients with T2DM (68% prescribed metformin) with median follow-up 851 days (IQR 935 - 765). Metformin use was associated with an increase of MPR of 0.12 [0.08-0.40], p = 0.004. There were 82 MACE events (14.3%) including 25 (4.4%) deaths of which 16 were in those not prescribed metformin (8.7%), compared to 9 in patients prescribed metformin (2.3%): adjusted hazard ratio 0.24 (95% CI 0.08-0.70, p = 0.009). MACE events were similar between groups. This multicentre, inverse probability weighting propensity score analysis study showed that in patients with T2DM, metformin use is associated with higher MPR and improved all cause survival.

Indexed as

Diabetes Mellitus, Type 2Hypoglycemic AgentsMetforminAgedCoronary CirculationFemaleHumansMaleMiddle AgedMyocardial Perfusion ImagingHypoglycemic AgentsMetforminEndothelial dysfunctionMajor adverse cardiovascular events (MACE)MetforminMyocardial perfusion reserve (MPR)Stress myocardial blood flow (MBF)Type 2 diabetes mellitus (T2DM)

Identifiers

PMID39516499
PMCPMC11549305

What Socratic holds

Texttitle and abstract
LicenceCC BY
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Registered trials

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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 Socratic graph.