Evidence map›Paper›PMID 34737219›Full record

ReviewThe European respiratory journal2022

The physiological basis of pulmonary arterial hypertension.

Robert Naeije, Manuel J Richter, Lewis J Rubin

Open access · bronzeAbstract readReview
In one paragraph

Review in The European respiratory journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
19.1field-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

117 citing papers in PubMed, 189 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
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  8. Fisetin alleviates pulmonary arterial hypertension by inhibiting the TGF-β1/Smad 2/3 signaling pathway.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026
    Article
  9. Review
  10. Article
  11. Nocturnal Hypoxaemia in PAH Patients Living at High Altitude Relocated to Low Altitude.Respiration; international review of thoracic diseases · 2026
    Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Journal of preventive medicine and hygiene · 2026
    Article
  17. Review
  18. Review
  19. Article
  20. Review

57 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

3 authors at 2 institutions in 2 countries.

Robert NaeijeFree University of Brussels, Brussels, Belgium rnaeije@gmail.com.
Manuel J RichterDept of Internal Medicine, Justus Liebig-University, Universities of Giessen and Marburg Lung Center (UGMLC), Giessen, Germany.
Lewis J RubinUniversity of California, San Diego, La Jolla, CA, USA.
Universities of Giessen and Marburg Lung Center · DEUniversity of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a rare dyspnoea-fatigue syndrome caused by a progressive increase in pulmonary vascular resistance and eventual right ventricular (RV) failure. In spite of extensive pulmonary vascular remodelling, lung function in PAH is generally well preserved, with hyperventilation and increased physiological dead space, but minimal changes in lung mechanics and only mild to moderate hypoxaemia and hypocapnia. Hypoxaemia is mainly caused by a low mixed venous oxygen tension from a decreased cardiac output. Hypocapnia is mainly caused by an increased chemosensitivity. Exercise limitation in PAH is cardiovascular rather than ventilatory or muscular. The extent of pulmonary vascular disease in PAH is defined by multipoint pulmonary vascular pressure-flow relationships with a correction for haematocrit. Pulsatile pulmonary vascular pressure-flow relationships in PAH allow for the assessment of RV hydraulic load. This analysis is possible either in the frequency domain or in the time domain. The RV in PAH adapts to increased afterload by an increased contractility to preserve its coupling to the pulmonary circulation. When this homeometric mechanism is exhausted, the RV dilates to preserve flow output by an additional heterometric mechanism. Right heart failure is then diagnosed by imaging of increased right heart dimensions and clinical systemic congestion signs and symptoms. The coupling of the RV to the pulmonary circulation is assessed by the ratio of end-systolic to arterial elastances, but these measurements are difficult. Simplified estimates of RV-pulmonary artery coupling can be obtained by magnetic resonance or echocardiographic imaging of ejection fraction.

Indexed as

Heart FailureHypertension, PulmonaryPulmonary Arterial HypertensionVentricular Dysfunction, RightFamilial Primary Pulmonary HypertensionHumansHypocapniaHypoxiaPulmonary ArteryVentricular Function, Right

Identifiers

PMID34737219
PMCPMC9203839
OpenAlexW3208579920

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.