Evidence map›Paper›PMID 32294958›Full record

ReviewJournal of clinical medicine2020

Transitioning from Preclinical to Clinical Heart Failure with Preserved Ejection Fraction: A Mechanistic Approach.

Antoni Bayes-Genis, Felipe Bisbal, Julio Núñez, Enrique Santas, Josep Lupón, Patrick Rossignol, Walter Paulus

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Immunology of heart failure with preserved ejection fraction.Expert review of clinical immunology · 2025
    Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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

7 authors at 4 institutions in 3 countries.

Antoni Bayes-GenisHeart Institute, Hospital Universitari Germans Trias i Pujol, 08916 Badalona, Spain.
Felipe BisbalHeart Institute, Hospital Universitari Germans Trias i Pujol, 08916 Badalona, Spain.
Julio NúñezCIBERCV, Instituto de Salud Carlos III, Madrid, Spain.
Enrique SantasCIBERCV, Instituto de Salud Carlos III, Madrid, Spain.
Josep LupónHeart Institute, Hospital Universitari Germans Trias i Pujol, 08916 Badalona, Spain.
Patrick RossignolCentre d'Investigation Clinique Plurithématique 1433 -INSERM- CHRU de Nancy, Inserm U1116 & FCRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists), Université de Lorraine, Vandoeuvre-les-Nancy, France.
Walter PaulusAmsterdam Cardiovascular Sciences, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Instituto de Salud Carlos III · ESUniversitat de València · ESAmsterdam University Medical Centers · NLInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To better understand heart failure with preserved ejection fraction (HFpEF), we need to better characterize the transition from asymptomatic pre-HFpEF to symptomatic HFpEF. The current emphasis on left ventricular diastolic dysfunction must be redirected to microvascular inflammation and endothelial dysfunction that leads to cardiomyocyte remodeling and enhanced interstitial collagen deposition. A pre-HFpEF patient lacks signs or symptoms of heart failure (HF), has preserved left ventricular ejection fraction (LVEF) with incipient structural changes similar to HFpEF, and possesses elevated biomarkers of cardiac dysfunction. The transition from pre-HFpEF to symptomatic HFpEF also involves left atrial failure, pulmonary hypertension and right ventricular dysfunction, and renal failure. This review focuses on the non-left ventricular mechanisms in this transition, involving the atria, right heart cavities, kidneys, and ultimately the currently accepted driver-systemic inflammation. Impaired atrial function may decrease ventricular hemodynamics and significantly increase left atrial and pulmonary pressure, leading to HF symptoms, irrespective of left ventricle (LV) systolic function. Pulmonary hypertension and low right-ventricular function are associated with the incidence of HF. Interstitial fibrosis in the heart, large arteries, and kidneys is key to the pathophysiology of the cardiorenal syndrome continuum. By understanding each of these processes, we may be able to halt disease progression and eventually extend the time a patient remains in the asymptomatic pre-HFpEF stage.

Indexed as

atrial failureheart failure with preserved ejection fractioninflammationpulmonary arteryrenal functionright ventricle

Identifiers

PMID32294958
PMCPMC7230997
OpenAlexW3016263743

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.