Evidence map›Paper›PMID 26481221›Full record

ArticlePediatric cardiology2016

Comparison of Immune Profiles in Fetal Hearts with Idiopathic Dilated Cardiomyopathy, Maternal Autoimmune-Associated Dilated Cardiomyopathy and the Normal Fetus.

Lynne E Nield, Ingo von Both, Najla Popel, Kate Strachan, Cedric Manlhiot, Patrick Shannon, Brian W McCrindle, Adelle Atkinson, Steven E S Miner, Edgar T Jaeggi and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Pediatric cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Trial
  2. Article
  3. 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

11 authors at 3 institutions in 1 country.

Lynne E NieldDivision of Cardiology, Labatt Family Heart Centre, The Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8, Canada. lynne.nield@sickkids.ca.
Ingo von BothDepartment of Pathobiology and Laboratory Medicine, University of Toronto, Toronto, ON, Canada.
Najla PopelUniversity of Toronto, Toronto, ON, Canada.
Kate StrachanDepartment of Pathology, Mount Sinai Hospital, Toronto, ON, Canada.
Cedric ManlhiotDivision of Cardiology, Labatt Family Heart Centre, The Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8, Canada.
Patrick ShannonDepartment of Pathology, Mount Sinai Hospital, Toronto, ON, Canada.
Brian W McCrindleDivision of Cardiology, Labatt Family Heart Centre, The Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8, Canada.
Adelle AtkinsonDivision of Immunology and Allergy, The Hospital for Sick Children, Toronto, ON, Canada.
Steven E S MinerUniversity of Toronto, Toronto, ON, Canada.
Edgar T JaeggiDivision of Cardiology, Labatt Family Heart Centre, The Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8, Canada.
Glenn P TaylorDepartment of Pathology, Mount Sinai Hospital, Toronto, ON, Canada.
Hospital for Sick Children · CAUniversity of Toronto · CAMount Sinai Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The etiology of idiopathic dilated cardiomyopathy (iDCM) remains unknown. Immune therapies have improved outcome in fetuses with DCM born to mothers with autoimmune disease (aDCM). The purpose of this retrospective study was to compare the myocardial B and T cell profiles in fetuses and neonates with idiopathic DCM (iDCM) versus autoimmune-mediated DCM (aDCM) and to describe the normal cell maturation within the human fetal myocardium. Of 60 fetal autopsy cases identified from institutional databases, 10 had aDCM (18-38 weeks), 12 iDCM (19-37 weeks) and 38 had normal hearts (11-40 weeks). Paraffin-embedded myocardium sections were stained for all lymphocyte (CD45), B cells (CD20, CD79a), T cells (CD3, CD4, CD7, CD8) and monocyte (CD68) surface markers. Two independent, blinded cell counts were performed. Normal hearts expressed all B and T cell markers in a bimodal fashion, with peaks at 22 and 37 weeks of gestation. The aDCM cohort was most distinct from normal hearts, with less overall T cell markers [EST -9.1 (2.6) cells/mm(2), p = 0.001], CD4 [EST -2.0 (0.6), p = 0.001], CD3 [EST -3.9 (1.0), p < 0.001], CD7 [EST -3.0 (1.1), p = 0.01] overall B cell markers [EST -4.9 (1.8), p = 0.01] and CD79a counts [EST -2.3 (0.9), p = 0.01]. The iDCM group had less overall B cell markers [EST -4.0 (1.8), p = 0.03] and CD79a [EST -1.7 (0.9), p = 0.05], but no difference in T cell markers. Autoimmune-mediated DCM fetuses have less B and T cell markers, whereas iDCM fetuses have less B cell markers compared with normal fetal hearts. The fetal immune system may play a role in the normal development of the heart and evolution of dilated cardiomyopathy.

Indexed as

AutopsyBiomarkersB-LymphocytesCardiomyopathy, DilatedCase-Control StudiesDatabases, FactualFemaleFetal HeartHumansInfant, NewbornLinear ModelsMaleMyocardiumOntarioRetrospective StudiesT-LymphocytesBiomarkersCardiomyopathyEndocardial fibroelastosisFetusImmune systemMyocardium

Identifiers

PMID26481221
OpenAlexW1805696824

What OpenQuestion holds

Textmetadata
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.