Evidence map›Paper›PMID 25638299›Full record

ArticleThe Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation2015

Impaired right ventricular-pulmonary vascular function in myeloproliferative neoplasms.

Emir C Roach, Margaret M Park, W H Wilson Tang, James D Thomas, Kewal Asosingh, Matt Kalaycio, Serpil C Erzurum, Samar Farha

Open access · greenAbstract read
In one paragraph

Article in The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Myeloproliferative Neoplasms and Cardiovascular Disease: A Review.Current treatment options in oncology · 2024
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Myeloid-Derived Suppressor Cells and Pulmonary Hypertension.International journal of molecular sciences · 2018
    Review
  9. Myeloid Targets for Pulmonary Arterial Hypertension: Time for Another Look.American journal of respiratory and critical care medicine · 2016
    Article
  10. Pulmonary hypertension in patients with chronic myeloproliferative disorders.European respiratory review : an official journal of the European Respiratory Society · 2015
    Review
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

8 authors at 2 institutions in 2 countries.

Emir C RoachDepartment of Pathobiology, Lerner Research Institute.
Margaret M ParkHeart & Vascular Institute.
W H Wilson TangHeart & Vascular Institute.
James D ThomasHeart & Vascular Institute.
Kewal AsosinghDepartment of Pathobiology, Lerner Research Institute.
Matt KalaycioTaussig Cancer Institute.
Serpil C ErzurumDepartment of Pathobiology, Lerner Research Institute; Respiratory Institute, Cleveland Clinic, Cleveland, Ohio.
Samar FarhaDepartment of Pathobiology, Lerner Research Institute; Respiratory Institute, Cleveland Clinic, Cleveland, Ohio. Electronic address: farhas@ccf.org.
Cancer Institute (WIA) · INCleveland Clinic Lerner College of Medicine · US

Funding

Pulmonary Hypertension Breakthrough InitiativeR24HL123767 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ALDRED, MICHEALA A, ERZURUM, SERPIL C. · 2014 to 2017
$10.1M
NITRIC OXIDE PRODUCTION AND REACTIONS IN THE LUNGR01HL060917 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI Serpil C. Erzurum · 1999 to 2026
$6.3M
Airway redox biochemistry as a deteriminant of asthma phenotype during adolescen*U10HL109250 · NHLBI · UNIVERSITY OF VIRGINIA · PI ERZURUM, SERPIL C., GASTON, BENJAMIN · 2011 to 2016
$4.2M
Nitric Oxide in Pulmonary HypertensionR37HL060917 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI ERZURUM, SERPIL C. · 2009 to 2018
$3.9M
Nitrative stress in heart failureR01HL103931 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI TANG, WAI HONG WILSON · 2010 to 2014
$3.8M
Pulmonary Vascular-Right Ventricular Axis Research ProgramR01HL115008 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI ERZURUM, SERPIL C., PRASAD, SATHYAMANGLA V · 2012 to 2016
$3.1M
NHLBI NIH HHS HL-103931NHLBI NIH HHS HL-115008NHLBI NIH HHS HL-60917NHLBI NIH HHS R01 HL060917NHLBI NIH HHS R01 HL103931NHLBI NIH HHS R01 HL115008NHLBI NIH HHS R24 HL123767NHLBI NIH HHS R37 HL060917NHLBI NIH HHS U10 HL109250
6 · The paper itself

Abstract

backgroundIncreased bone marrow hemangioblast numbers, alterations in erythroid/myeloid lineages, increased reticulin, and greater circulating bone marrow progenitor cells are present in patients with pulmonary arterial hypertension (PAH). The data suggest that myeloid progenitors contribute to the pathogenesis of PAH, but there are little data on the prevalence of pulmonary vascular disease among the different forms of myeloid diseases. We hypothesized that there would be a higher prevalence of pulmonary vascular disease in myeloproliferative neoplasms that have high circulating progenitor cells, such as myelofibrosis and chronic myelogenous leukemia (CML), compared with those with low circulating progenitors, such as in aplastic anemia.

methodsPatients with myelofibrosis, CML, and aplastic anemia who underwent echocardiographic evaluation of cardiac function in preparation for bone marrow transplantation at the Cleveland Clinic between 1997 and 2012 were identified and their electronic medical records were queried for demographic data, blood cell counts, and pulmonary function tests. All echocardiograms were uniformly analyzed in a blinded fashion by an advanced sonographer and cardiologist for measures of right and left ventricular function and estimation of pulmonary vascular disease.

resultsGender and race distribution among disease groups was similar. Patients with myelofibrosis (n = 19) and aplastic anemia (n = 30) had increased right ventricle (RV) wall thickness compared with CML (n = 82) patients (aplastic anemia, 0.7 ± 0.1; CML, 0.5 ± 0.1; and myelofibrosis, 0.7 ± 0.1; p = 0.02). Patients with myelofibrosis had higher levels of estimated RV systolic pressure compared with the other groups (aplastic anemia, 29.9 ± 1.5; CML, 26.2 ± 1.1; and myelofibrosis, 36.7 ± 3.7 mm Hg; p < 0.01).

conclusionsThe findings suggest an important role for myeloid progenitors in the maintenance of pulmonary-vascular health, in which abnormal myeloproliferative progenitors are associated with RV pathology.

Indexed as

Pulmonary CirculationAdultBone Marrow TransplantationFemaleHumansHypertension, PulmonaryMaleMiddle AgedMyeloproliferative DisordersPrognosisRetrospective StudiesVascular ResistanceVentricular Dysfunction, RightVentricular Function, Rightchronic myelogenous leukemiamyeloid progenitorspulmonary arterial hypertensionpulmonary vascular disease

Identifiers

PMID25638299
PMCPMC4377111
OpenAlexW2167480911

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.