Evidence map›Paper›PMID 38170280›Full record

ArticleBasic research in cardiology2024

Acute antiarrhythmic effects of SGLT2 inhibitors-dapagliflozin lowers the excitability of atrial cardiomyocytes.

Amelie Paasche, Felix Wiedmann, Manuel Kraft, Fitzwilliam Seibertz, Valerie Herlt, Pablo L Blochberger, Natasa Jávorszky, Moritz Beck, Leo Weirauch, Timon Seeger and 9 more

Open access · hybridAbstract read
In one paragraph

Article in Basic research in cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
12.5field-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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Understanding the Diseased Atria.Physiology (Bethesda, Md.) · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Transforming atrial fibrillation management by targeting comorbidities and reducing atrial fibrillation burden: the 10th AFNET/EHRA consensus conference.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025
    Article
  13. Review
  14. Review
  15. Disease mechanism and novel drug therapies for atrial fibrillation.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2025
    Article
  16. Observational
  17. Article
  18. Observational
  19. Review
  20. 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

19 authors at 2 institutions in 1 country.

Amelie Paasche *Department of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Felix Wiedmann *Department of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Manuel KraftDepartment of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Fitzwilliam SeibertzInstitute of Pharmacology and Toxicology, University Medical Center Göttingen, Robert Koch Strasse 42a, 37075, Göttingen, Germany.
Valerie HerltDepartment of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Pablo L BlochbergerDepartment of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Natasa JávorszkyDepartment of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Moritz BeckDepartment of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Leo WeirauchDepartment of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Timon SeegerDepartment of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Antje BlankDepartment of Clinical Pharmacology and Pharmacoepidemiology, University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Walter E HaefeliDepartment of Clinical Pharmacology and Pharmacoepidemiology, University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Rawa ArifDepartment of Cardiac Surgery, University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Anna L MeyerDepartment of Cardiac Surgery, University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Gregor WarneckeDepartment of Cardiac Surgery, University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Matthias KarckDepartment of Cardiac Surgery, University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Niels VoigtInstitute of Pharmacology and Toxicology, University Medical Center Göttingen, Robert Koch Strasse 42a, 37075, Göttingen, Germany.
Norbert FreyDepartment of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Constanze SchmidtDepartment of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany. Constanze.Schmidt@med.uni-heidelberg.de.ORCID 0000-0001-5897-237X
Heidelberg University · DEUniversitätsmedizin Göttingen · DE

Funding

Deutsche Forschungsgemeinschaft SCHM 3358/1-1Deutsche Forschungsgemeinschaft VO 1568/3-1Deutsche Forschungsgemeinschaft VO 1568/4-1Deutsche Gesellschaft für Kardiologie-Herz und Kreislaufforschung. Clinician Scientist ProgramDeutsche Stiftung für Herzforschung F/03/19Else Kröner-Fresenius-Stiftung Clinician Scientist Professorship
6 · The paper itself

Abstract

In recent years, SGLT2 inhibitors have become an integral part of heart failure therapy, and several mechanisms contributing to cardiorenal protection have been identified. In this study, we place special emphasis on the atria and investigate acute electrophysiological effects of dapagliflozin to assess the antiarrhythmic potential of SGLT2 inhibitors. Direct electrophysiological effects of dapagliflozin were investigated in patch clamp experiments on isolated atrial cardiomyocytes. Acute treatment with elevated-dose dapagliflozin caused a significant reduction of the action potential inducibility, the amplitude and maximum upstroke velocity. The inhibitory effects were reproduced in human induced pluripotent stem cell-derived cardiomyocytes, and were more pronounced in atrial compared to ventricular cells. Hypothesizing that dapagliflozin directly affects the depolarization phase of atrial action potentials, we examined fast inward sodium currents in human atrial cardiomyocytes and found a significant decrease of peak sodium current densities by dapagliflozin, accompanied by a moderate inhibition of the transient outward potassium current. Translating these findings into a porcine large animal model, acute elevated-dose dapagliflozin treatment caused an atrial-dominant reduction of myocardial conduction velocity in vivo. This could be utilized for both, acute cardioversion of paroxysmal atrial fibrillation episodes and rhythm control of persistent atrial fibrillation. In this study, we show that dapagliflozin alters the excitability of atrial cardiomyocytes by direct inhibition of peak sodium currents. In vivo, dapagliflozin exerts antiarrhythmic effects, revealing a potential new additional role of SGLT2 inhibitors in the treatment of atrial arrhythmias.

Indexed as

Atrial FibrillationBenzhydryl CompoundsGlucosidesInduced Pluripotent Stem CellsSodium-Glucose Transporter 2 InhibitorsAction PotentialsAnimalsAnti-Arrhythmia AgentsHumansMyocytes, CardiacSodiumSwineAnti-Arrhythmia AgentsBenzhydryl CompoundsdapagliflozinGlucosidesSodiumSodium-Glucose Transporter 2 InhibitorsAtrial action potentialAtrial fibrillationDapagliflozinNaV1.5SGLT2 inhibitors

Identifiers

PMID38170280
PMCPMC10837223
OpenAlexW4390544606

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.