Evidence map›Paper›PMID 33907929›Full record

ReviewHeart failure reviews2022

Is heart failure with preserved ejection fraction a 'dementia' of the heart?

Giacomo Tini, Antonio Cannatà, Marco Canepa, Pier Giorgio Masci, Matteo Pardini, Mauro Giacca, Gianfranco Sinagra, Niccolò Marchionni, Federica Del Monte, James E Udelson and 1 more

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

5 citing papers in PubMed, 13 citations in OpenAlex.

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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

11 authors at 7 institutions in 3 countries.

Giacomo TiniCardiovascular Disease Unit, IRCCS Ospedale Policlinico San Martino, University of Genova, Genova, Italy. giacomo.comotini@gmail.com.ORCID 0000-0001-8520-152X
Antonio CannatàCardiothoracic Department, Azienda Sanitaria Universitaria Integrata Di Trieste, University of Trieste, Trieste, Italy.
Marco CanepaCardiovascular Disease Unit, IRCCS Ospedale Policlinico San Martino, University of Genova, Genova, Italy.
Pier Giorgio MasciDepartment of Cardiovascular Imaging, School of Biomedical Engineering and Imaging Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Matteo PardiniDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genova, Genova, Italy.
Mauro GiaccaSchool of Cardiovascular Medicine & Sciences, King's College London British Heart Foundation Centre, London, UK.
Gianfranco SinagraCardiothoracic Department, Azienda Sanitaria Universitaria Integrata Di Trieste, University of Trieste, Trieste, Italy.
Niccolò MarchionniCardiothoracovascular Department, Careggi University Hospital, Florence, Italy.
Federica Del MonteDepartment of Medicine, Medical University of South Carolina, Charleston, SC, USA.
James E UdelsonDivision of Cardiology, Tufts Medical Center, Boston, MA, USA.
Iacopo OlivottoCardiomyopathy Unit, Careggi University Hospital, Florence, Italy.
Azienda Ospedaliero-Universitaria Careggi · ITKing's College London · GBOspedale Policlinico San Martino · ITUniversity of Trieste · ITMedical University of South Carolina · USOspedale San Giacomo Apostolo · ITTufts Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure with preserved ejection fraction (HFpEF) remains an elusive entity, due to its heterogeneous clinical profile and an arbitrarily defined nosology. Several pathophysiological mechanisms recognized as central for the development of HFpEF appear to be in common with the process of physiological aging of the heart. Both conditions are characterized by progressive impairment in cardiac function, accompanied by left ventricular hypertrophy, diastolic dysfunction, sarcomeric, and metabolic abnormalities. The neurological paradigm of dementia-intended as a progressive, multifactorial organ damage with decline of functional reserve, eventually leading to irreversible dysfunction-is well suited to represent HFpEF. In such perspective, certain phenotypes of HFpEF may be viewed as a maladaptive response to environmental modifiers, causing premature and pathological aging of the heart. We here propose that the 'HFpEF syndrome' may reflect the interplay of adverse structural remodelling and erosion of functional reserve, mirroring the processes leading to dementia in the brain. The resulting conceptual framework may help advance our understanding of HFpEF and unravel potential therapeutical targets.

Indexed as

DementiaHeart FailureHeartHumansStroke VolumeVentricular Function, LeftCalcium handlingCardiac agingDementiaHFpEFLeft ventricular hypertrophyMyocardial fibrosis

Identifiers

PMID33907929
OpenAlexW3157859804

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.