Evidence map›Paper›PMID 33770307›Full record

ArticleBiomechanics and modeling in mechanobiology2021

Fluid-structure interaction in a fully coupled three-dimensional mitral-atrium-pulmonary model.

Liuyang Feng, Hao Gao, Nan Qi, Mark Danton, Nicholas A Hill, Xiaoyu Luo

Open access · hybridAbstract read
In one paragraph

Article in Biomechanics and modeling in mechanobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

5 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. 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

6 authors at 3 institutions in 2 countries.

Liuyang FengSchool of Mathematics and Statistics, University of Glasgow, Glasgow, G12 8SQ, UK. Liuyang.Feng@glasgow.ac.uk.ORCID http://orcid.org/0000-0003-3099-6710
Hao GaoSchool of Mathematics and Statistics, University of Glasgow, Glasgow, G12 8SQ, UK.
Nan QiInstitute of Marine Science and Technology, Shandong University, Shangdong, 266237, People's Republic of China.
Mark DantonDepartment of Cardiac Surgery, Royal Hospital for Children, Glasgow, UK.
Nicholas A HillSchool of Mathematics and Statistics, University of Glasgow, Glasgow, G12 8SQ, UK.
Xiaoyu LuoSchool of Mathematics and Statistics, University of Glasgow, Glasgow, G12 8SQ, UK.
University of Glasgow · GBRoyal Hospital for Children · GBShandong University · CN

Funding

Engineering and Physical Sciences Research Council EP/N014642Engineering and Physical Sciences Research Council EP/S020950Engineering and Physical Sciences Research Council EP/S030875/1
6 · The paper itself

Abstract

This paper aims to investigate detailed mechanical interactions between the pulmonary haemodynamics and left heart function in pathophysiological situations (e.g. atrial fibrillation and acute mitral regurgitation). This is achieved by developing a complex computational framework for a coupled pulmonary circulation, left atrium and mitral valve model. The left atrium and mitral valve are modelled with physiologically realistic three-dimensional geometries, fibre-reinforced hyperelastic materials and fluid-structure interaction, and the pulmonary vessels are modelled as one-dimensional network ended with structured trees, with specified vessel geometries and wall material properties. This new coupled model reveals some interesting results which could be of diagnostic values. For example, the wave propagation through the pulmonary vasculature can lead to different arrival times for the second systolic flow wave (S2 wave) among the pulmonary veins, forming vortex rings inside the left atrium. In the case of acute mitral regurgitation, the left atrium experiences an increased energy dissipation and pressure elevation. The pulmonary veins can experience increased wave intensities, reversal flow during systole and increased early-diastolic flow wave (D wave), which in turn causes an additional flow wave across the mitral valve (L wave), as well as a reversal flow at the left atrial appendage orifice. In the case of atrial fibrillation, we show that the loss of active contraction is associated with a slower flow inside the left atrial appendage and disappearances of the late-diastole atrial reversal wave (AR wave) and the first systolic wave (S1 wave) in pulmonary veins. The haemodynamic changes along the pulmonary vessel trees on different scales from microscopic vessels to the main pulmonary artery can all be captured in this model. The work promises a potential in quantifying disease progression and medical treatments of various pulmonary diseases such as the pulmonary hypertension due to a left heart dysfunction.

Indexed as

Heart AtriaAtrial FibrillationBlood Flow VelocityComputer SimulationDiastoleElasticityHumansLungMitral ValveMitral Valve InsufficiencyModels, AnatomicModels, CardiovascularModels, TheoreticalPulmonary CirculationPulmonary VeinsSystoleFluid–structure interactionLeft atriumMitral regurgitationMitral valvePulmonary circulationPulmonary hypertension

Identifiers

PMID33770307
PMCPMC8298265
OpenAlexW3136560263

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.