Evidence map›Paper›PMID 40544172›Full record

ReviewNature reviews. Cardiology2025

Vascular (dys)function in the failing heart.

Luca Liberale, Dirk Jan Duncker, Derek John Hausenloy, Simon Kraler, Hans Erik Bøtker, Bruno Karl Podesser, Gerd Heusch, Petra Kleinbongard

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–field-weighted citation impact
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

41 citing papers in PubMed.

  1. Article
  2. Molecular Mechanisms Governing Vascular Function in Heart Failure.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  3. Article
  4. Article
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  6. Article
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  8. Observational
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  14. Observational
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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

8 authors.

Luca LiberaleDepartment of Internal Medicine, University of Genoa, Genoa, Italy. luca.liberale@unige.it.ORCID 0000-0003-1472-7975
Dirk Jan DunckerDivision of Experimental Cardiology, Department of Cardiology, Thoraxcenter, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands.ORCID 0000-0003-2836-2241
Derek John HausenloyCardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore.
Simon KralerCenter for Molecular Cardiology, University of Zurich, Schlieren, Switzerland.ORCID 0000-0002-8245-7287
Hans Erik BøtkerDepartment of Clinical Medicine, Sections of Cardiology and Clinical Epidemiology, Faculty of Health, Aarhus University, Aarhus, Denmark.
Bruno Karl PodesserLudwig Boltzmann Institute for Cardiovascular Research at the Center for Biomedical Research and Translational Surgery, Medical University of Vienna, Vienna, Austria.
Gerd HeuschCardioprotection Unit, Institute for Pathophysiology, West German Heart and Vascular Center, University of Essen Medical School, University of Duisburg-Essen, Essen, Germany.ORCID 0000-0001-7078-4160
Petra KleinbongardCardioprotection Unit, Institute for Pathophysiology, West German Heart and Vascular Center, University of Essen Medical School, University of Duisburg-Essen, Essen, Germany. petra.kleinbongard@uk-essen.de.ORCID 0000-0003-3576-3772

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure (HF) is not confined to contractile failure of cardiomyocytes or myocardial fibrosis. Coronary and systemic vascular dysfunction contributes to the initiation and progression of HF with or without reduced ejection fraction. Furthermore, HF compromises vascular function, creating and sustaining a vicious cycle with deranging effects on coronary blood flow, cardiac metabolism and cardiac function. In HF, systemic arterial dysfunction, characterized by increased arterial stiffness and resistance, raises cardiac afterload and impedes myocardial contractile function. Reduced coronary blood flow impairs myocardial oxygen delivery and consequently cardiomyocyte metabolism and function. Coronary microvascular dysfunction is heterogeneous in its pathogenesis and manifestations, complicating the diagnosis and management across different HF phenotypes. Understanding the alterations in function in different segments of the vasculature, from the aorta to the capillary level, offers mechanistic insights into disease drivers and therapeutic interventions. Interventional approaches can improve vascular haemodynamics, whereas established and emerging pharmacotherapies target the neurohumoral axis and reduce extravascular compression, inflammation, and oxidative stress, thereby improving vascular function and HF-related outcomes. In this Review, we provide a mechanistic framework of vascular dysfunction in the pathogenesis of HF with or without reduced ejection fraction, pointing towards integrated therapies that consider the vascular implications of contemporary HF management across HF phenotypes.

Indexed as

Coronary VesselsHeart FailureAnimalsCoronary CirculationHemodynamicsHumansStroke VolumeVascular Stiffness

Identifiers

What OpenQuestion holds

Textmetadata
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.