Evidence map›Paper›PMID 27587711›Full record

ArticlePhysiological reports2016

A critical appraisal of transpulmonary and diastolic pressure gradients.

M Louis Handoko, Frances S De Man, Frank P T Oosterveer, Harm-Jan Bogaard, Anton Vonk-Noordegraaf, Nico Westerhof

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Hemodynamic indices in pulmonary hypertension: a narrative review.Cardiovascular diagnosis and therapy · 2022
    Review
  6. Article
  7. Observational
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
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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

6 authors at 1 institution in 1 country.

M Louis HandokoDepartment of Cardiology, VU University Medical Center/Institute for Cardiovascular Research, Amsterdam, The Netherlands ml.handoko@vumc.nl.
Frances S De ManDepartment of Pulmonary Diseases, VU University Medical Center/Institute for Cardiovascular Research, Amsterdam, The Netherlands Department of Physiology, VU University Medical Center/Institute for Cardiovascular Research, Amsterdam, The Netherlands.
Frank P T OosterveerDepartment of Pulmonary Diseases, VU University Medical Center/Institute for Cardiovascular Research, Amsterdam, The Netherlands.
Harm-Jan BogaardDepartment of Pulmonary Diseases, VU University Medical Center/Institute for Cardiovascular Research, Amsterdam, The Netherlands.
Anton Vonk-NoordegraafDepartment of Pulmonary Diseases, VU University Medical Center/Institute for Cardiovascular Research, Amsterdam, The Netherlands.
Nico WesterhofDepartment of Pulmonary Diseases, VU University Medical Center/Institute for Cardiovascular Research, Amsterdam, The Netherlands Department of Physiology, VU University Medical Center/Institute for Cardiovascular Research, Amsterdam, The Netherlands.
Amsterdam UMC Location VUmc · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary hypertension (PH) resulting from left heart failure is an increasingly recognized clinical entity. To distinguish isolated postcapillary PH from combined post- and precapillary PH, the use of a diastolic pressure gradient (DPG = diastolic Pulmonary Artery Pressure - Pulmonary Arterial Wedge Pressure, dPAP - PAWP) has been advocated over the transpulmonary pressure gradient (TPG = mean Pulmonary Artery Pressure - PAWP, mPAP - PAWP) since DPG was suggested to be independent of cardiac output (CO) and only slightly related to PAWP, while TPG depends on both. We quantitatively derived and compared the DPG and TPG Using right heart catheterization data (n = 1054), we determined systolic pulmonary artery pressure (sPAP), dPAP and mPAP, PAWP, and CO From this data, we derived TPG and DPG and tested their dependence on PAWP and CO We found that dPAP and sPAP are proportional with mPAP over a wide range of PAWP (1-31 mmHg), with dPAP = 0.62mPAP and sPAP = 1.61mPAP As a consequence, TPG and DPG are equally dependent on PAWP: TPG = mPAP - PAWP, and DPG = 0.62mPAP - PAWP Furthermore, we showed that both TPG and DPG depend on CO The absolute increase in DPG with CO is 62% of the TPG increase with CO, but the relative dependence is the same. Both TPG and DPG depend on PAWP and CO Thus, in principle, there are no major advantages for using DPG to distinguish postcapillary pulmonary hypertension from combined post- and precapillary pulmonary hypertension.

Indexed as

AdolescentAdultAgedBlood PressureCardiac CatheterizationCardiac OutputDiastoleFemaleHeart FailureHumansHypertension, PulmonaryMaleMiddle AgedPulmonary ArteryPulmonary Wedge PressureRetrospective StudiesCardiac outputheart failurephysiologypulmonary hypertensionpulmonary wedge pressure

Identifiers

PMID27587711
PMCPMC5027345
OpenAlexW2511516266

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.