Evidence map›Paper›PMID 33413413›Full record

ArticleCardiovascular diabetology2021

Dual SGLT-1 and SGLT-2 inhibition improves left atrial dysfunction in HFpEF.

David Bode, Lukas Semmler, Paulina Wakula, Niklas Hegemann, Uwe Primessnig, Nicola Beindorff, David Powell, Raphael Dahmen, Hartmut Ruetten, Christian Oeing and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 4 pooled it
11.7field-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

71 citing papers in PubMed, 4 syntheses or guidelines pooled it, 109 citations in OpenAlex.

  1. Pooled it
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  16. Observational
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  19. Atrial cardiomyopathy.ESC heart failure · 2025
    Article
  20. Mitochondrial Dysfunction in HFpEF: Potential Interventions Through Exercise.Journal of cardiovascular translational research · 2025
    Review

11 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

15 authors at 4 institutions in 2 countries.

David BodeDepartment of Internal Medicine and Cardiology, Charité University Medicine, Campus Virchow-Klinikum, Augustenburgerplatz 1, 13353, Berlin, Germany.
Lukas SemmlerDepartment of Internal Medicine and Cardiology, Charité University Medicine, Campus Virchow-Klinikum, Augustenburgerplatz 1, 13353, Berlin, Germany.
Paulina WakulaDepartment of Internal Medicine and Cardiology, Charité University Medicine, Campus Virchow-Klinikum, Augustenburgerplatz 1, 13353, Berlin, Germany.
Niklas HegemannDepartment of Internal Medicine and Cardiology, Charité University Medicine, Campus Virchow-Klinikum, Augustenburgerplatz 1, 13353, Berlin, Germany.
Uwe PrimessnigDepartment of Internal Medicine and Cardiology, Charité University Medicine, Campus Virchow-Klinikum, Augustenburgerplatz 1, 13353, Berlin, Germany.
Nicola BeindorffBerlin Experimental Radionuclide Imaging Center (BERIC), Charité-Universitaetsmedizin Berlin, Berlin, Germany.
David PowellLexicon Pharmaceuticals, Metabolism Research, Houston, TX, USA.
Raphael DahmenSanofi-Aventis Deutschland GmbH, Research & Development, 65926, Frankfurt am Main, Germany.
Hartmut RuettenSanofi-Aventis Deutschland GmbH, Research & Development, 65926, Frankfurt am Main, Germany.
Christian OeingDepartment of Internal Medicine and Cardiology, Charité University Medicine, Campus Virchow-Klinikum, Augustenburgerplatz 1, 13353, Berlin, Germany.
Alessio AlognaDepartment of Internal Medicine and Cardiology, Charité University Medicine, Campus Virchow-Klinikum, Augustenburgerplatz 1, 13353, Berlin, Germany.
Daniel MessroghliDepartment of Internal Medicine and Cardiology, Charité University Medicine, Campus Virchow-Klinikum, Augustenburgerplatz 1, 13353, Berlin, Germany.
Burkert M PieskeDepartment of Internal Medicine and Cardiology, Charité University Medicine, Campus Virchow-Klinikum, Augustenburgerplatz 1, 13353, Berlin, Germany.
Frank R HeinzelDepartment of Internal Medicine and Cardiology, Charité University Medicine, Campus Virchow-Klinikum, Augustenburgerplatz 1, 13353, Berlin, Germany.
Felix HohendannerDepartment of Internal Medicine and Cardiology, Charité University Medicine, Campus Virchow-Klinikum, Augustenburgerplatz 1, 13353, Berlin, Germany. felix.hohendanner@charite.de.ORCID 0000-0002-0194-4615
German Centre for Cardiovascular Research · DESanofi (Germany) · DECharité - Universitätsmedizin Berlin · DELexicon Pharmaceuticals (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSodium-glucose linked transporter type 2 (SGLT-2) inhibition has been shown to reduce cardiovascular mortality in heart failure independently of glycemic control and prevents the onset of atrial arrhythmias, a common co-morbidity in heart failure with preserved ejection fraction (HFpEF). The mechanism behind these effects is not fully understood, and it remains unclear if they could be further enhanced by additional SGLT-1 inhibition. We investigated the effects of chronic treatment with the dual SGLT-1&2 inhibitor sotagliflozin on left atrial (LA) remodeling and cellular arrhythmogenesis (i.e. atrial cardiomyopathy) in a metabolic syndrome-related rat model of HFpEF.

methods17 week-old ZSF-1 obese rats, a metabolic syndrome-related model of HFpEF, and wild type rats (Wistar Kyoto), were fed 30 mg/kg/d sotagliflozin for 6 weeks. At 23 weeks, LA were imaged in-vivo by echocardiography. In-vitro, Ca

resultsSotagliflozin ameliorated LA enlargement in HFpEF in-vivo. In-vitro, LA cardiomyocytes in HFpEF showed an increased incidence and amplitude of arrhythmic spontaneous Ca

conclusionThe SGLT-1&2 inhibitor sotagliflozin ameliorated LA remodeling in metabolic HFpEF. It also improved distinct features of Ca

Indexed as

AnimalsArrhythmias, CardiacAtrial Function, LeftAtrial RemodelingCalcium SignalingDisease Models, AnimalGlycosidesHeart AtriaHeart FailureMetabolic SyndromeMitochondria, HeartMitochondrial DynamicsMitochondrial SwellingRatsRats, Inbred WKYRats, Zucker(2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-ethoxybenzyl)phenyl)-6-(methylthio)tetrahydro-2H-pyran-3,4,5-triolGlycosidesReactive Oxygen SpeciesSlc5a1 protein, ratSlc5a2 protein, ratSodium-Calcium ExchangerSodium-Glucose Transporter 1Sodium-Glucose Transporter 2Sodium-Glucose Transporter 2 InhibitorsAtrial cardiomyopathyAtrial remodelingCalcium cyclingHeart failure with preserved ejection fractionLeft atrial cardiomyocytesMitochondriaSGLT inhibition

Identifiers

PMID33413413
PMCPMC7792219
OpenAlexW3120249811

What OpenQuestion holds

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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 OpenQuestion graph.