In one paragraphObservational study in Cardiovascular diabetology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04064450 (MyoVasc - An Epidemiological Cohort Study to Investigate the Development and Progression of Heart Failure and the Interaction With Vascular Disease), which is not on this map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from itWhat 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 registryThe 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.
MyoVasc - An Epidemiological Cohort Study to Investigate the Development and Progression of Heart Failure and the Interaction With Vascular Disease
TypeobservationalSponsorJohannes Gutenberg University MainzRan2013 to 2028Enrolled3,289ConditionsHeart Failure
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
14 authors.
Noémie BélangerPreventive Cardiology and Preventive Medicine, Department of Cardiology and Clinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131, Mainz, Germany.ORCID http://orcid.org/0009-0001-9267-8788 Silav ZeidPreventive Cardiology and Preventive Medicine, Department of Cardiology and Clinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131, Mainz, Germany.
David VelmedenPreventive Cardiology and Preventive Medicine, Department of Cardiology and Clinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131, Mainz, Germany.ORCID http://orcid.org/0009-0006-3714-312X Andreas SchulzPreventive Cardiology and Preventive Medicine, Department of Cardiology and Clinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131, Mainz, Germany.ORCID http://orcid.org/0000-0003-1394-680X Thomas KoeckPreventive Cardiology and Preventive Medicine, Department of Cardiology and Clinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131, Mainz, Germany.ORCID http://orcid.org/0000-0002-2644-8917 Felix RauschPreventive Cardiology and Preventive Medicine, Department of Cardiology and Clinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131, Mainz, Germany.ORCID http://orcid.org/0000-0002-7328-1056 Benedikt FooßPreventive Cardiology and Preventive Medicine, Department of Cardiology and Clinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131, Mainz, Germany.
Fawad Kazemi-AsrarPreventive Cardiology and Preventive Medicine, Department of Cardiology and Clinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131, Mainz, Germany.ORCID http://orcid.org/0009-0006-8245-8243 Jürgen H ProchaskaPreventive Cardiology and Preventive Medicine, Department of Cardiology and Clinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131, Mainz, Germany.ORCID http://orcid.org/0000-0001-5078-9992 Perikles SimonSports Medicine and Disease Prevention, Department of Sports Medicine, Prevention and Rehabilitation, Johannes Gutenberg-University Mainz, Mainz, Germany.ORCID http://orcid.org/0000-0002-7996-4034 Philipp S WildPreventive Cardiology and Preventive Medicine, Department of Cardiology and Clinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstr. 1, 55131, Mainz, Germany. philipp.wild@unimedizin-mainz.de.ORCID http://orcid.org/0000-0003-4413-9752 Funding
No grant is acknowledged in the PubMed record.
6 · The paper itselfAbstract
backgroundCardiac autonomic dysfunction plays a pivotal role in the heart failure syndrome. Metabolic dysregulation affects both autonomic function and heart failure, but these relationships remain incompletely understood. This study aimed at investigating the role of glucose and insulin metabolism for parasympathetic reactivation.
methodsData from the MyoVasc study (NCT04064450), a prospective heart failure cohort study, were analyzed. Participants underwent a highly standardized 5-hour examination, including venous blood sampling. To assess the impact of glucose and insulin metabolism (HbA
resultsThe analysis sample included 1,588 individuals (median age 64.0 years [IQR 55.0;72.0]; 33% women) in a fasting state. Symptomatic heart failure was present in 43.7% of the subjects. Median HRR
conclusionsThis study demonstrates the relevance of insulin status for vagal activity of cardiac autonomic function, particularly in heart failure. The pathophysiological implications underlying the relationship between insulin status and parasympathetic activity merit further mechanistic exploration.
Indexed as
Blood GlucoseHeartHeart FailureHeart RateInsulinParasympathetic Nervous SystemVagus NerveAgedBiomarkersC-PeptideCross-Sectional StudiesFemaleGlycated HemoglobinHumansInsulin ResistanceLongitudinal StudiesBiomarkersBlood GlucoseC-PeptideGlycated Hemoglobinhemoglobin A1c protein, humanInsulinCardiac autonomic dysfunctionC-peptideHeart failureHeart rate recoveryHyperglycemiaInsulin resistanceParasympathetic reactivation
Identifiers
PMID41508011
PMCPMC12849475
What OpenQuestion holds
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LicenceCC BY
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