Evidence map›Paper›PMID 35839240›Full record

ArticlePloS one2022

Left atrial remodeling in mitral regurgitation: A combined experimental-computational study.

Sjoerd Bouwmeester, Tim van Loon, Meike Ploeg, Thomas P Mast, Nienke J Verzaal, Lars B van Middendorp, Marc Strik, Frans A van Nieuwenhoven, Lukas R Dekker, Frits W Prinzen and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

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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

12 authors at 3 institutions in 2 countries.

Sjoerd BouwmeesterDepartment of Cardiology, Catharina Hospital Eindhoven, Eindhoven, The Netherlands.ORCID 0000-0002-8358-2231
Tim van LoonDepartment of Biomedical Engineering, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands.
Meike PloegDepartment of Physiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands.
Thomas P MastDepartment of Cardiology, Catharina Hospital Eindhoven, Eindhoven, The Netherlands.
Nienke J VerzaalDepartment of Physiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands.
Lars B van MiddendorpDepartment of Physiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands.
Marc StrikBordeaux University Hospital (CHU), Cardio-Thoracic Unit, Pessac, France.
Frans A van NieuwenhovenDepartment of Physiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands.
Lukas R DekkerDepartment of Cardiology, Catharina Hospital Eindhoven, Eindhoven, The Netherlands.
Frits W PrinzenDepartment of Physiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands.
Joost LumensDepartment of Biomedical Engineering, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands.
Patrick HouthuizenDepartment of Cardiology, Catharina Hospital Eindhoven, Eindhoven, The Netherlands.
Maastricht University · NLRadboud University Nijmegen · NLCentre Hospitalier Universitaire de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsProgressive changes to left atrial (LA) structure and function following mitral regurgitation (MR) remain incompletely understood. This study aimed to demonstrate potential underlying mechanisms using experimental canine models and computer simulations.

methodsA canine model of MR was created by cauterization of mitral chordae followed by radiofrequency ablation-induced left bundle-branch block (LBBB) after 4 weeks (MR-LBBB group). Animals with LBBB alone served as control. Echocardiography was performed at baseline, acutely after MR induction, and at 4 and 20 weeks, and correlated with histology and computer simulations.

resultsAcute MR augmented LA reservoir and contractile strain (40±4 to 53±6% and -11±5 to -22±9% respectively, p<0.05). LA fractional area change increased significantly (47±4 to 56±4%, p<0.05) while LA end-systolic area remained unchanged (7.2±1.1 versus 7.9±1.1 cm2 respectively, p = 0.08). LA strain 'pseudonormalized' after 4 weeks and decompensated at 20 weeks with both strains decreasing to 25±6% and -3±2% respectively (p<0.05) together with a progressive increase in LA end-systolic area (7.2±1.1 to 14.0±6.3 cm2, p<0.05). In the LBBB-group, LA remodeling was less pronounced. Histology showed a trend towards increased interstitial fibrosis in the LA of the MR-LBBB group. Computer simulations indicated that the progressive changes in LA structure and function are a combination of progressive eccentric remodeling and fibrosis.

conclusionMR augmented LA strain acutely to supranormal values without significant LA dilation. However, over time, LA strain gradually decreases (pseudornormal and decompensated) with LA dilation. Histology and computer simulations indicated a correlation to a varying degree of LA eccentric remodeling and fibrosis.

Indexed as

Atrial RemodelingMitral Valve InsufficiencyAnimalsBundle-Branch BlockDogsEchocardiographyFibrosisHeart Atria

Identifiers

PMID35839240
PMCPMC9286246
OpenAlexW4285492532

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.