Evidence map›Paper›PMID 36434327›Full record

ArticleThe international journal of cardiovascular imaging2022

Subclinical myocardial dysfunction is revealed by speckle tracking echocardiography in patients with Cornelia de Lange syndrome.

Laura Trujillano, Ariadna Ayerza-Casas, Beatriz Puisac, Gonzalo González García, Ángela Ascaso, Ana Latorre-Pellicer, María Arnedo, Cristina Lucia-Campos, Marta Gil-Salvador, Frank J Kaiser and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The international journal of cardiovascular imaging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Non-Classic Cornelia de Lange Syndrome Due toChildren (Basel, Switzerland) · 2025
    Review
  2. 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

13 authors at 4 institutions in 3 countries.

Laura TrujillanoUnit of Clinical Genetics and Functional Genomics, Department of Pharmacology-Physiology-Legal Medicine, School of Medicine, Universidad de Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Ariadna Ayerza-CasasUnit of Clinical Genetics and Functional Genomics, Department of Pharmacology-Physiology-Legal Medicine, School of Medicine, Universidad de Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Beatriz PuisacUnit of Clinical Genetics and Functional Genomics, Department of Pharmacology-Physiology-Legal Medicine, School of Medicine, Universidad de Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Gonzalo González GarcíaDepartment of Pediatrics, Hospital Clínico Universitario Lozano Blesa, Zaragoza, Spain.
Ángela AscasoUnit of Clinical Genetics and Functional Genomics, Department of Pharmacology-Physiology-Legal Medicine, School of Medicine, Universidad de Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Ana Latorre-PellicerUnit of Clinical Genetics and Functional Genomics, Department of Pharmacology-Physiology-Legal Medicine, School of Medicine, Universidad de Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
María ArnedoUnit of Clinical Genetics and Functional Genomics, Department of Pharmacology-Physiology-Legal Medicine, School of Medicine, Universidad de Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Cristina Lucia-CamposUnit of Clinical Genetics and Functional Genomics, Department of Pharmacology-Physiology-Legal Medicine, School of Medicine, Universidad de Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Marta Gil-SalvadorUnit of Clinical Genetics and Functional Genomics, Department of Pharmacology-Physiology-Legal Medicine, School of Medicine, Universidad de Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Frank J KaiserInstitute for Human Genetics, University Hospital Essen, University of Duisburg-Essen, 45147, Essen, Germany.
Feliciano J RamosUnit of Clinical Genetics and Functional Genomics, Department of Pharmacology-Physiology-Legal Medicine, School of Medicine, Universidad de Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain. framos@unizar.es.ORCID https://orcid.org/0000-0002-5732-2209
Juan PiéUnit of Clinical Genetics and Functional Genomics, Department of Pharmacology-Physiology-Legal Medicine, School of Medicine, Universidad de Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain. juanpie@unizar.es.ORCID https://orcid.org/0000-0003-3203-6254
Gloria Bueno-LozanoDepartment of Pediatrics, Hospital Clínico Universitario Lozano Blesa, Zaragoza, Spain. mgbuenol@unizar.es.ORCID https://orcid.org/0000-0002-0409-4791
Universidad de Zaragoza · ESHospital Clínico Universitario Lozano Blesa · ESHebron University · PSUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study assesses a possible cardiac dysfunction in individuals with Cornelia de Lange syndrome (CdLS) without diagnosed congenital heart disease (CHD) and its association with other factors. Twenty patients and 20 controls were included in the study divided into three age-dependent groups (A: < 10 yrs, B: 10-20 yrs, C: > 20 yrs), and were evaluated using conventional echocardiography, tissue doppler imaging (TDI), two-dimensional speckle tracking and genetic and biochemical analyses. The left ventricular global longitudinal strain (GLS) was altered (< 15.9%) in 55% of patients, being pathological in the older group (A: 19.7 ± 6.6; B: -17.2 ± 4.7; C: -13.6 ± 2.9). The speckle tracking technique revealed a downward trend in the values of strain, strain rate and velocity, especially in the oldest group. Likewise, the ejection fraction (LVEF) and shortening fraction (LVFS) values, although preserved, also showed a decreased with age (p < 0.05). The analytical markers of cardiovascular risk and cardiac function showed no alterations. The molecular analyses revealed 16 individuals carrying pathogenic variants in NIPBL, two with variants in SMC1A, one with a variant in RAD21 and one with a HDAC8 variant. This is the first systematic approach that demonstrates that individuals with CdLS may present early cardiomyopathy, which can be detected by speckle tracking technique even before the appearance of clinical symptoms and the alteration of other echocardiographic or analytical parameters. For all these reasons, cardiological followup is suggested even in the absence of CHD, especially from adolescence onwards.

Indexed as

CardiomyopathiesDe Lange SyndromeHeart Defects, CongenitalAdolescentCell Cycle ProteinsChildEchocardiographyHistone DeacetylasesHumansPredictive Value of TestsRepressor ProteinsStroke VolumeCell Cycle ProteinsHDAC8 protein, humanHistone DeacetylasesNIPBL protein, humanRepressor ProteinsCornelia deEchocardiographyLange syndromeMyocardial dysfunctionNIPBLSpeckle trackingStrain

Identifiers

PMID36434327
PMCPMC9700592
OpenAlexW4280621644

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.