Evidence map›Paper›PMID 32897746›Full record

ReviewCirculation2020

Altered Hemodynamics and End-Organ Damage in Heart Failure: Impact on the Lung and Kidney.

Frederik H Verbrugge, Marco Guazzi, Jeffrey M Testani, Barry A Borlaug

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Circulation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed, 2 pooled it
15.6field-weighted citation impact, top 1% 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

111 citing papers in PubMed, 2 syntheses or guidelines pooled it, 206 citations in OpenAlex.

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51 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 3 countries.

Frederik H VerbruggeDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN (F.H.V., B.A.B.).
Marco GuazziCardiology University Department, Heart Failure Unit, University of Milano, IRCCS Policlinico San Donato, Milan, Italy (M.G.).
Jeffrey M TestaniSection of Cardiovascular Medicine, Yale University, New Haven, CT (J.M.T.).
Barry A BorlaugDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN (F.H.V., B.A.B.).
Mayo Clinic · USIRCCS Policlinico San Donato · ITYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
HL-Inorganic Nitrite to Enhance Benefits from Exercise Training in Heart Failure with preserved Ejection FractionR01HL128526 · NHLBI · MAYO CLINIC ROCHESTER · PI BORLAUG, BARRY A. · 2016 to 2019
$2.4M
Redefining Pulmonary Hypertension through Pulmonary Vascular Disease Phenomics: Clinical Centers (CC) (U01).U01HL125205 · NHLBI · MAYO CLINIC ROCHESTER · PI FRANTZ, ROBERT PAUL · 2014 to 2018
$1.5M
NCATS NIH HHS UL1 TR001863NHLBI NIH HHS R01 HL128526NHLBI NIH HHS U01 HL125205
6 · The paper itself

Abstract

Heart failure is characterized by pathologic hemodynamic derangements, including elevated cardiac filling pressures ("backward" failure), which may or may not coexist with reduced cardiac output ("forward" failure). Even when normal during unstressed conditions such as rest, hemodynamics classically become abnormal during stressors such as exercise in patients with heart failure. This has important upstream and downstream effects on multiple organ systems, particularly with respect to the lungs and kidneys. Hemodynamic abnormalities in heart failure are affected by processes that extend well beyond the cardiac myocyte, including important roles for pericardial constraint, ventricular interaction, and altered venous capacity. Hemodynamic perturbations have widespread effects across multiple heart failure phenotypes, ranging from reduced to preserved ejection fraction, acute to chronic disease, and cardiogenic shock to preserved perfusion states. In the lung, hemodynamic derangements lead to the development of abnormalities in ventilatory control and efficiency, pulmonary congestion, capillary stress failure, and eventually pulmonary vascular disease. In the kidney, hemodynamic perturbations lead to sodium and water retention and worsening renal function. Improved understanding of the mechanisms by which altered hemodynamics in heart failure affect the lungs and kidneys is needed in order to design novel strategies to improve clinical outcomes.

Indexed as

Cardiac OutputHeart FailureKidneyKidney DiseasesLungLung DiseasesHumansMyocytes, Cardiacheart failurehemodynamicskidneylung

Identifiers

PMID32897746
PMCPMC7482031
OpenAlexW3084342635

What OpenQuestion holds

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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.