Evidence map›Paper›PMID 35747946›Full record

Trial reportESC heart failure2022

Impact of different training modalities on high-density lipoprotein function in HFpEF patients: a substudy of the OptimEx trial.

Pamela W Sowa, Ephraim B Winzer, Jennifer Hommel, Anita Männel, Emeline M van Craenenbroeck, Ulrik Wisløff, Burkert Pieske, Martin Halle, Axel Linke, Volker Adams

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in ESC heart failure, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 3 pooled it
1.5field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 3 syntheses or guidelines pooled it, 9 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
  4. Trial
  5. Review
  6. 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

10 authors at 5 institutions in 3 countries.

Pamela W SowaLaboratory of Molecular and Experimental Cardiology, Technische Universität Dresden, Heart Center Dresden, Dresden, Germany.
Ephraim B WinzerLaboratory of Molecular and Experimental Cardiology, Technische Universität Dresden, Heart Center Dresden, Dresden, Germany.
Jennifer HommelLaboratory of Molecular and Experimental Cardiology, Technische Universität Dresden, Heart Center Dresden, Dresden, Germany.
Anita MännelLaboratory of Molecular and Experimental Cardiology, Technische Universität Dresden, Heart Center Dresden, Dresden, Germany.
Emeline M van CraenenbroeckResearch Group Cardiovascular Diseases, GENCOR, University of Antwerp, Antwerp, Belgium.
Ulrik WisløffThe Cardiac Exercise Research Group at Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway.
Burkert PieskeDepartment Internal Medicine and Cardiology, Campus Virchow Klinikum, Charité Universitätsmedizin Berlin, Berlin, Germany.
Martin HalleDepartment of Prevention and Sports Medicine, University Hospital Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Axel LinkeLaboratory of Molecular and Experimental Cardiology, Technische Universität Dresden, Heart Center Dresden, Dresden, Germany.
Volker AdamsLaboratory of Molecular and Experimental Cardiology, Technische Universität Dresden, Heart Center Dresden, Dresden, Germany.
Technische Universität Dresden · DECharité - Universitätsmedizin Berlin · DENorwegian University of Science and Technology · NOTechnical University of Munich · DEUniversity of Antwerp · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsIn heart failure with preserved ejection fraction (HFpEF), the reduction of nitric oxide (NO)-bioavailability and consequently endothelial dysfunction leads to LV stiffness and diastolic dysfunction of the heart. Besides shear stress, high-density lipoprotein (HDL) stimulates endothelial cells to increased production of NO via phosphorylation of endothelial nitric oxide synthase (eNOS). For patients with heart failure with reduced ejection fraction, earlier studies demonstrated a positive impact of exercise training (ET) on HDL-mediated eNOS activation. The study aims to investigate the influence of ET on HDL-mediated phosphorylation of eNOS in HFpEF patients. METHODS AND

resultsThe present study is a substudy of the OptimEx-Clin trial. The patients were randomized to three groups: (i) HIIT (high-intensity interval training; (ii) MCT (moderate-intensity continuous training); and (iii) CG (control group). Supervised training at study centres was offered for the first 3 months. From months 4-12, training sessions were continued at home with the same exercise protocol as performed during the in-hospital phase. Blood was collected at baseline, after 3, and 12 months, and HDL was isolated by ultracentrifugation. Human aortic endothelial cells were incubated with isolated HDL, and HDL-induced eNOS phosphorylation at Ser

conclusionsThe present study documented that HIIT but not MCT exerts beneficial effects on HDL-mediated eNOS phosphorylation and HDL-associated Pon1 activity in HFpEF patients. These beneficial effects of HIIT were reduced as soon as the patients switched to home-based ET.

Indexed as

Heart FailureAryldialkylphosphataseEndothelial CellsHumansLipoproteins, HDLStroke VolumeThiobarbituric Acid Reactive SubstancesAryldialkylphosphataseLipoproteins, HDLPON1 protein, humanThiobarbituric Acid Reactive SubstanceseNOSExercise trainingHDLHeart failure with preserved ejection fraction

Identifiers

PMID35747946
PMCPMC9715788
OpenAlexW4283447544

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.