Evidence map›Paper›PMID 35582996›Full record

ArticlePhysiological reports2022

Right ventricular myocardial energetic model for evaluating right heart function in pulmonary arterial hypertension.

Jacqueline V Scott, Tanuf U Tembulkar, Meng-Lin Lee, Bradley T Faliks, Kelly L Koch, Anton Vonk-Noordegraaf, Keith E Cook

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. A Mitochondrial Basis for Heart Failure Progression.Cardiovascular drugs and therapy · 2024
    Review
  3. Article
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.

Jacqueline V ScottDepartment of Biomedical Engineering, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA.
Tanuf U TembulkarDepartment of Biomedical Engineering, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA.
Meng-Lin LeeDivision of Cardiovascular Surgery, Department of Surgery, Cathay General Hospital, Taipei, Taiwan.
Bradley T FaliksDepartment of Surgery, University of Michigan, Ann Arbor, Michigan, USA.
Kelly L KochDepartment of Surgery, University of Michigan, Ann Arbor, Michigan, USA.
Anton Vonk-NoordegraafDepartment of Pulmonary Medicine, Amsterdam University Medical Centers, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
Keith E CookDepartment of Biomedical Engineering, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA.ORCID 0000-0002-5604-3718
Carnegie Mellon University · USUniversity of Michigan · USAmsterdam University Medical Centers · NLCathay General Hospital · TW

Funding

Compliant Thoracic Artificial LungsR01HL089043 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COOK, KEITH E · 2009 to 2017
$4.2M
NHLBI NIH HHS R01 HL089043
6 · The paper itself

Abstract

backgroundPulmonary arterial hypertension (PAH) increases right ventricular (RV) workload and decreases myocardial oxygen reserve, eventually leading to poor cardiac output. This study created and assessed a novel model of RV work output based on RV hemodynamics and oxygen supply, allowing new insight into causal mechanisms of RV dysfunction.

methodsThe RV function model was built upon an earlier, left ventricular model and further adjusted for more accurate clinical use. The model assumes that RV total power output (1) is the sum of isovolumic and stroke power and (2) is linearly related to its right coronary artery oxygen supply. Thus, when right coronary artery flow is limited or isovolumic power is elevated, less energy is available for producing cardiac output. The original and adjusted models were validated via data from patients with idiopathic PAH (n = 14) and large animals (n = 6) that underwent acute pulmonary banding with or without hypoxia.

resultsBoth models demonstrated strong, significant correlations between RV oxygen consumption rate and RV total power output for PAH patients (original model, R

conclusionRight ventricular total power output can be accurately estimated directly from pulmonary hemodynamics and right coronary perfusion during PAH. This model highlights the increased vulnerability of PAH patients with compromised right coronary flow coupled with high afterload.

Indexed as

Hypertension, PulmonaryPulmonary Arterial HypertensionStrokeVentricular Dysfunction, RightAnimalsHemodynamicsHumansOxygenSheepVentricular Function, RightOxygenpulmonary arterial hypertensionright heart failureright ventricular energetics

Identifiers

PMID35582996
PMCPMC9115705
OpenAlexW4280501802

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.