Evidence map›Paper›PMID 31866998›Full record

ArticleFrontiers in immunology2019

Modeling Cardiac Dysfunction Following Traumatic Hemorrhage Injury: Impact on Myocardial Integrity.

Johanna Wall, Sriveena Naganathar, Banjerd Praditsuktavorn, Oscar F Bugg, Simon McArthur, Christoph Thiemermann, Jordi L Tremoleda, Karim Brohi

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 40 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Johanna WallCentre for Trauma Sciences, Neuroscience, Surgery and Trauma, Blizard Institute, Queen Mary University of London, London, United Kingdom.
Sriveena NaganatharCentre for Trauma Sciences, Neuroscience, Surgery and Trauma, Blizard Institute, Queen Mary University of London, London, United Kingdom.
Banjerd PraditsuktavornCentre for Trauma Sciences, Neuroscience, Surgery and Trauma, Blizard Institute, Queen Mary University of London, London, United Kingdom.
Oscar F BuggCentre for Trauma Sciences, Neuroscience, Surgery and Trauma, Blizard Institute, Queen Mary University of London, London, United Kingdom.
Simon McArthurCentre for Oral Immunobiology & Regenerative Medicine, Institute of Dentistry, Queen Mary University of London, London, United Kingdom.
Christoph ThiemermannCentre for Trauma Sciences, Neuroscience, Surgery and Trauma, Blizard Institute, Queen Mary University of London, London, United Kingdom.
Jordi L TremoledaCentre for Trauma Sciences, Neuroscience, Surgery and Trauma, Blizard Institute, Queen Mary University of London, London, United Kingdom.
Karim BrohiCentre for Trauma Sciences, Neuroscience, Surgery and Trauma, Blizard Institute, Queen Mary University of London, London, United Kingdom.
Queen Mary University of London · GBWilliam Harvey Research Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac dysfunction (CD) importantly contributes to mortality in trauma patients, who survive their initial injuries following successful hemostatic resuscitation. This poor outcome has been correlated with elevated biomarkers of myocardial injury, but the pathophysiology triggering this CD remains unknown. We investigated the pathophysiology of acute CD after trauma using a mouse model of trauma hemorrhage shock (THS)-induced CD with echocardiographic guidance of fluid resuscitation, to assess the THS impact on myocardial integrity and function. Mice were subjected to trauma (soft tissue and bone fracture) and different degrees of hemorrhage severity (pressure controlled ~MABP < 35 mmHg or <65 mmHg) for 1 h, to characterize the acute impact on cardiac function. In a second study, mice were subjected to trauma and hemorrhage (MABP < 35 mmHg) for 1 h, then underwent two echocardiographic-guided resuscitations to baseline stroke volume at 60 and 120 min, and were monitored up to 180 min to study the longer impact of THS following resuscitation. Naïve and sham animals were used as controls. At 60 min post-THS injury, animals showed a lower cardiac output (CO) and stroke volume (SV) and an early rise of heart fatty acid-binding protein (H-FABP = 167 ± 38 ng/ml; 90% increase from shams, 3.54 ± 3.06 ng/ml), when subjected to severe hemorrhage and injury. Despite resuscitation, these animals maintained lower CO (6 ml/min vs. 23 ml/min), lower SV (10 μl vs. 46 μl; both ~75% decreased), and higher H-FABP (levels (340 ± 115 ng/ml vs. 10.3 ± 0.2 ng/ml; all THS vs. shams,

Indexed as

Models, CardiovascularAnimalsBiomarkersDisease Models, AnimalHeartHemodynamicsHemorrhageHumansMaleMiceMyocardiumShock, HemorrhagicVentricular DysfunctionWounds and InjuriesBiomarkerscardiac dysfunctionhaemorrhagic injurymurine modelsmyocardial damagetrauma

Identifiers

PMID31866998
PMCPMC6908477
OpenAlexW2992312734

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.