Evidence map›Paper›PMID 35956182›Full record

ArticleJournal of clinical medicine2022

The Paradox of Pulmonary Vascular Resistance: Restoration of Pulmonary Capillary Recruitment as a

David Langleben, Stylianos E Orfanos, Benjamin D Fox, Nathan Messas, Michele Giovinazzo, John D Catravas

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. The Acute Effects of Prostacyclin on Right Ventricular Contractility and Pulmonary Artery Coupling.American journal of respiratory and critical care medicine · 2023
    Article
  7. 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

6 authors at 4 institutions in 4 countries.

David LanglebenCenter for Pulmonary Vascular Disease, Azrieli Heart Center and Lady Davis Research Institute, Jewish General Hospital, McGill University, Montreal, QC H3T 1E2, Canada.
Stylianos E Orfanos1st Department of Critical Care and Pulmonary Services, Pulmonary Hypertension Center, Evangelismos Hospital, National and Kapodistrian University of Athens Medical School, 10676 Athens, Greece.
Benjamin D FoxPulmonary Division, Yitzchak Shamir Hospital, Tel Aviv University, Tzrifin 69978, Israel.
Nathan MessasCenter for Pulmonary Vascular Disease, Azrieli Heart Center and Lady Davis Research Institute, Jewish General Hospital, McGill University, Montreal, QC H3T 1E2, Canada.
Michele GiovinazzoCenter for Pulmonary Vascular Disease, Azrieli Heart Center and Lady Davis Research Institute, Jewish General Hospital, McGill University, Montreal, QC H3T 1E2, Canada.
John D CatravasFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA 23529, USA.ORCID 0000-0002-5098-295X
Jewish General Hospital · CANational and Kapodistrian University of Athens · GROld Dominion University · USTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exercise-induced increases in pulmonary blood flow normally increase pulmonary arterial pressure only minimally, largely due to a reserve of pulmonary capillaries that are available for recruitment to carry the flow. In pulmonary arterial hypertension, due to precapillary arteriolar obstruction, such recruitment is greatly reduced. In exercising pulmonary arterial hypertension patients, pulmonary arterial pressure remains high and may even increase further. Current pulmonary arterial hypertension therapies, acting principally as vasodilators, decrease calculated pulmonary vascular resistance by increasing pulmonary blood flow but have a minimal effect in lowering pulmonary arterial pressure and do not restore significant capillary recruitment. Novel pulmonary arterial hypertension therapies that have mainly antiproliferative properties are being developed to try and diminish proliferative cellular obstruction in precapillary arterioles. If effective, those agents should restore capillary recruitment and, during exercise testing, pulmonary arterial pressure should remain low despite increasing pulmonary blood flow. The effectiveness of every novel therapy for pulmonary arterial hypertension should be evaluated not only at rest, but with measurement of exercise pulmonary hemodynamics during clinical trials.

Indexed as

exercisehemodynamicspulmonary arterial hypertensionpulmonary capillarypulmonary hypertension therapypulmonary microvasculaturepulmonary vascular resistance

Identifiers

PMID35956182
PMCPMC9369805
OpenAlexW4289866320

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.