Evidence map›Paper›PMID 34718532›Full record

ArticleEuropace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology2022

Pacing therapy for atrioventricular dromotropathy: a combined computational-experimental-clinical study.

Floor C W M Salden, Peter R Huntjens, Rick Schreurs, Erik Willemen, Marion Kuiper, Philippe Wouters, Jos G Maessen, Pierre Bordachar, Tammo Delhaas, Justin Luermans and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in 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, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
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  5. Impact of myocardial phenotype on optimal atrioventricular delay settings during biventricular and left bundle branch pacing at rest and during exercise: insights from a virtual patient study.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
  6. Article
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  8. Early effects of left bundle branch area pacing on ventricular activation by speckle tracking echocardiography.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2024
    Article
  9. Article
  10. Review
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  12. Frontiers in conduction system pacing: treatment of long PR in patients with heart failure.European heart journal supplements : journal of the European Society of Cardiology · 2023
    Article
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  14. Review
  15. Atrioventricular dromotropathy: an important substrate for complete resynchronization therapy-Authors' reply.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 · 2022
    Article
  16. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 7 institutions in 3 countries.

Floor C W M SaldenDepartment of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Centre+ (MUMC+), Maastricht, The Netherlands.
Peter R HuntjensDepartment of Biomedical Engineering, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.ORCID 0000-0002-1845-6837
Rick SchreursDepartment of Physiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.ORCID 0000-0003-4799-5132
Erik WillemenDepartment of Biomedical Engineering, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
Marion KuiperDepartment of Physiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.
Philippe WoutersDepartment of Cardiology, University Medical Centre Utrecht (UMC Utrecht), Utrecht, The Netherlands.ORCID 0000-0002-3406-4083
Jos G MaessenDepartment of Cardiothoracic Surgery, Maastricht University Medical Centre+ (MUMC+), Maastricht, The Netherlands.
Pierre BordacharDepartment of Cardiology, Electrophysiology and Heart Modeling Institute (LIRYC), Bordeaux University, Pessac, France.
Tammo DelhaasDepartment of Biomedical Engineering, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
Justin LuermansDepartment of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Centre+ (MUMC+), Maastricht, The Netherlands.
Mathias MeineDepartment of Cardiology, University Medical Centre Utrecht (UMC Utrecht), Utrecht, The Netherlands.ORCID 0000-0002-1102-2155
Cornelis P AllaartDepartment of Cardiology, Amsterdam University Medical Centre (Amsterdam UMC), Amsterdam, The Netherlands.ORCID 0000-0002-0506-9512
Antonius M W van StipdonkDepartment of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Centre+ (MUMC+), Maastricht, The Netherlands.
Frits W PrinzenDepartment of Physiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.ORCID 0000-0001-8917-9032
Joost LumensDepartment of Biomedical Engineering, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.ORCID 0000-0001-8129-7384
Kevin VernooyDepartment of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Centre+ (MUMC+), Maastricht, The Netherlands.ORCID 0000-0002-8818-5964
Maastricht University · NLMaastricht University Medical Centre · NLUniversity Medical Center Utrecht · NLAmsterdam University Medical Centers · NLElectrophysiology and Heart Modeling Institute · FRRadboud University Nijmegen · NLWashington University in St. Louis · US

Funding

AbbottDutch Heart Foundation 2015T082European Union's Horizon 2020 Research and InnovationFrench Government Agence National de la Recherche ANR-10-IAHU-04Marie Sklodowska-Curie 860745Netherlands Organisation for Scientific Research 016.176.340
6 · The paper itself

Abstract

aimsInvestigate haemodynamic effects, and their mechanisms, of restoring atrioventricular (AV)-coupling using pacemaker therapy in normal and failing hearts in a combined computational-experimental-clinical study. METHODS AND

resultsComputer simulations were performed in the CircAdapt model of the normal and failing human heart and circulation. Experiments were performed in a porcine model of AV dromotropathy. In a proof-of-principle clinical study, left ventricular (LV) pressure and volume were measured in 22 heart failure (HF) patients (LV ejection fraction <35%) with prolonged PR interval (>230 ms) and narrow or non-left bundle branch block QRS complex. Computer simulations and animal studies in normal hearts showed that restoring of AV-coupling with unchanged ventricular activation sequence significantly increased LV filling, mean arterial pressure, and cardiac output by 10-15%. In computer simulations of failing hearts and in HF patients, reducing PR interval by biventricular (BiV) pacing (patients: from 300 ± 61 to 137 ± 30 ms) resulted in significant increases in LV stroke volume and stroke work (patients: 34 ± 40% and 26 ± 31%, respectively). However, worsening of ventricular dyssynchrony by using right ventricular (RV) pacing abrogated the benefit of restoring AV-coupling. In model simulations, animals and patients, the increase of LV filling and associated improvement of LV pump function coincided with both larger mitral inflow (E- and A-wave area) and reduction of diastolic mitral regurgitation.

conclusionRestoration of AV-coupling by BiV pacing in normal and failing hearts with prolonged AV conduction leads to considerable haemodynamic improvement. These results indicate that BiV or physiological pacing, but not RV pacing, may improve cardiac function in patients with HF and prolonged PR interval.

Indexed as

Atrioventricular BlockCardiac Resynchronization TherapyHeart FailureAnimalsCardiac Pacing, ArtificialHeart VentriclesHumansStroke VolumeSwineVentricular Function, LeftBiventricular pacingComputer modellingFirst-degree atrioventricular blockHaemodynamicsHeart failure

Identifiers

PMID34718532
PMCPMC9071072
OpenAlexW3210505356

What OpenQuestion holds

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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.