Evidence map›Paper›PMID 28356405›Full record

ReviewEuropean respiratory review : an official journal of the European Respiratory Society2017

The pathophysiology of chronic thromboembolic pulmonary hypertension.

Gérald Simonneau, Adam Torbicki, Peter Dorfmüller, Nick Kim

Open access · diamondAbstract readReview
In one paragraph

Review in European respiratory review : an official journal of the European Respiratory Society, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 230 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
230citing papers in PubMed, 3 pooled it
24.5field-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

230 citing papers in PubMed, 3 syntheses or guidelines pooled it, 434 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Haemoptysis in chronic pulmonary vascular disease: a narrative review.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Clinical Updates in Pulmonary Hypertension.Reviews in cardiovascular medicine · 2026
    Review
  16. Review
  17. Animal models of chronic thromboembolic pulmonary hypertension.Animal models and experimental medicine · 2026
    Review
  18. Review
  19. Review
  20. Article

170 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 2 countries.

Gérald SimonneauAssistance Publique-Hôpitaux de Paris, Service de Pneumologie, Hôpital Bicêtre, Le Kremlin-Bicêtre, Hôpital Marie Lannelongue, Paris Sud University, Paris, France gerald.simonneau@gmail.com.
Adam TorbickiDept of Pulmonary Circulation and Thromboembolic Diseases, Centre of Postgraduate Medical Education, Europejskie Centrum Zdrowia Otwock, Otwock, Poland.
Peter DorfmüllerDept of Pathology, Paris Sud University, Hôpital Marie Lannelongue, Le Plessis-Robinson, France.
Nick KimDivision of Pulmonary and Critical Care Medicine, University of California San Diego, La Jolla, CA, USA.
Bicêtre Hospital · FRUniversité Paris-Sud · FRUniversity of California System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare, progressive pulmonary vascular disease that is usually a consequence of prior acute pulmonary embolism. CTEPH usually begins with persistent obstruction of large and/or middle-sized pulmonary arteries by organised thrombi. Failure of thrombi to resolve may be related to abnormal fibrinolysis or underlying haematological or autoimmune disorders. It is now known that small-vessel abnormalities also contribute to haemodynamic compromise, functional impairment and disease progression in CTEPH. Small-vessel disease can occur in obstructed areas, possibly triggered by unresolved thrombotic material, and downstream from occlusions, possibly because of excessive collateral blood supply from high-pressure bronchial and systemic arteries. The molecular processes underlying small-vessel disease are not completely understood and further research is needed in this area. The degree of small-vessel disease has a substantial impact on the severity of CTEPH and postsurgical outcomes. Interventional and medical treatment of CTEPH should aim to restore normal flow distribution within the pulmonary vasculature, unload the right ventricle and prevent or treat small-vessel disease. It requires early, reliable identification of patients with CTEPH and use of optimal treatment modalities in expert centres.

Indexed as

HemodynamicsPulmonary CirculationAdultAnimalsFemaleHumansHypertension, PulmonaryMaleMiddle AgedPatient SelectionPredictive Value of TestsPrognosisPulmonary ArteryPulmonary EmbolismRisk AssessmentRisk Factors

Identifiers

PMID28356405
PMCPMC9488693
OpenAlexW2597740492

What OpenQuestion 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 OpenQuestion graph.