Evidence map›Paper›PMID 32397294›Full record

ArticleInternational journal of molecular sciences2020

Myeloproliferative Diseases as Possible Risk Factor for Development of Chronic Thromboembolic Pulmonary Hypertension-A Genetic Study.

Christina A Eichstaedt, Jeremias Verweyen, Michael Halank, Nicola Benjamin, Christine Fischer, Eckhard Mayer, Stefan Guth, Christoph B Wiedenroth, Benjamin Egenlauf, Satenik Harutyunova and 6 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. ImpairedERJ open research · 2026
    Article
  2. How Genomic and Structural Context Could Shape JAK-STAT Variant Pathogenicity.Twin research and human genetics : the official journal of the International Society for Twin Studies · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Clonal Hematopoiesis in Chronic Thromboembolic Pulmonary Hypertension.Journal of the American Heart Association · 2024
    Article
  7. Myeloproliferative Neoplasms and Cardiovascular Disease: A Review.Current treatment options in oncology · 2024
    Review
  8. Review
  9. Genetically Identifying the "Thromboembolic" in Chronic Thromboembolic Pulmonary Hypertension.American journal of respiratory and critical care medicine · 2024
    Article
  10. Defining the clinical validity of genes reported to cause pulmonary arterial hypertension.Genetics in medicine : official journal of the American College of Medical Genetics · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. Reduction ofGenes · 2022
    Article
  15. Article
  16. 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

16 authors at 5 institutions in 2 countries.

Christina A EichstaedtCentre for Pulmonary Hypertension, Thoraxklinik Heidelberg gGmbH, Heidelberg University Hospital, Röntgenstr. 1, 69126 Heidelberg, Germany.ORCID 0000-0001-7288-8297
Jeremias VerweyenCentre for Pulmonary Hypertension, Thoraxklinik Heidelberg gGmbH, Heidelberg University Hospital, Röntgenstr. 1, 69126 Heidelberg, Germany.
Michael HalankDepartment of Internal Medicine I, Carl Gustav Carus University Hospital, Technical University of Dresden, Fetscherstraße 74, 01307 Dresden, Germany.
Nicola BenjaminCentre for Pulmonary Hypertension, Thoraxklinik Heidelberg gGmbH, Heidelberg University Hospital, Röntgenstr. 1, 69126 Heidelberg, Germany.
Christine FischerLaboratory of Molecular Genetic Diagnostics, Institute of Human Genetics, Heidelberg University, Im Neuenheimer Feld 366, 69120 Heidelberg, Germany.
Eckhard MayerKerckhoff Heart and Thorax Center, Department of Thoracic Surgery, Benekestr. 2-8, 61231 Bad Nauheim, Germany.
Stefan GuthKerckhoff Heart and Thorax Center, Department of Thoracic Surgery, Benekestr. 2-8, 61231 Bad Nauheim, Germany.
Christoph B WiedenrothKerckhoff Heart and Thorax Center, Department of Thoracic Surgery, Benekestr. 2-8, 61231 Bad Nauheim, Germany.
Benjamin EgenlaufCentre for Pulmonary Hypertension, Thoraxklinik Heidelberg gGmbH, Heidelberg University Hospital, Röntgenstr. 1, 69126 Heidelberg, Germany.
Satenik HarutyunovaCentre for Pulmonary Hypertension, Thoraxklinik Heidelberg gGmbH, Heidelberg University Hospital, Röntgenstr. 1, 69126 Heidelberg, Germany.
Panagiota XanthouliCentre for Pulmonary Hypertension, Thoraxklinik Heidelberg gGmbH, Heidelberg University Hospital, Röntgenstr. 1, 69126 Heidelberg, Germany.
Alberto M MarraCentre for Pulmonary Hypertension, Thoraxklinik Heidelberg gGmbH, Heidelberg University Hospital, Röntgenstr. 1, 69126 Heidelberg, Germany.
Heinrike WilkensDepartment of Internal Medicine V-Pneumology, Allergology and Critical Care Medicine, University Hospital of Saarland, Kirrberger Str., 66424 Homburg, Saar, Germany.
Ralf EwertDepartment of Internal Medicine B-Cardiology, Intensive Care, Pulmonary Medicine and Infectious Diseases, University of Greifswald, Ferdinand-Sauerbruch-Str., 17475 Greifswald, Germany.
Katrin HinderhoferLaboratory of Molecular Genetic Diagnostics, Institute of Human Genetics, Heidelberg University, Im Neuenheimer Feld 366, 69120 Heidelberg, Germany.
Ekkehard GrünigCentre for Pulmonary Hypertension, Thoraxklinik Heidelberg gGmbH, Heidelberg University Hospital, Röntgenstr. 1, 69126 Heidelberg, Germany.
Heidelberg University · DEKerckhoff Klinik · DESaarland University · DEUniversitätsmedizin Greifswald · DEUniversity Hospital Carl Gustav Carus · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare disease which is often caused by recurrent emboli. These are also frequently found in patients with myeloproliferative diseases. While myeloproliferative diseases can be caused by gene defects, the genetic predisposition to CTEPH is largely unexplored. Therefore, the objective of this study was to analyse these genes and further genes involved in pulmonary hypertension in CTEPH patients. A systematic screening was conducted for pathogenic variants using a gene panel based on next generation sequencing. CTEPH was diagnosed according to current guidelines. In this study, out of 40 CTEPH patients 4 (10%) carried pathogenic variants. One patient had a nonsense variant (c.2071A>T p.Lys691*) in the

Indexed as

Genetic Predisposition to DiseaseAgedBone Morphogenetic Protein Receptors, Type IIChronic DiseaseCodon, NonsenseFemaleHigh-Throughput Nucleotide SequencingHumansHypertension, PulmonaryJanus Kinase 2MaleMiddle AgedMutation, MissenseMyeloproliferative DisordersPulmonary EmbolismRisk FactorsBMPR2 protein, humanBone Morphogenetic Protein Receptors, Type IICodon, NonsenseJAK2 protein, humanJanus Kinase 2chronic thromboembolic pulmonary hypertensiongenetic predispositionJanus kinase 2 (JAK2)pulmonary vascular resistance

Identifiers

PMID32397294
PMCPMC7246715
OpenAlexW3021134383

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.