Evidence map›Paper›PMID 27008197›Full record

ArticleBiomechanics and modeling in mechanobiology2016

In silico coronary wave intensity analysis: application of an integrated one-dimensional and poromechanical model of cardiac perfusion.

Jack Lee, David Nordsletten, Andrew Cookson, Simone Rivolo, Nicolas Smith

Abstract read
In one paragraph

Article in Biomechanics and modeling in mechanobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. A poroelastic immersed finite element framework for modelling cardiac perfusion and fluid-structure interaction.International journal for numerical methods in biomedical engineering · 2021
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Impact of coronary bifurcation morphology on wave propagation.American journal of physiology. Heart and circulatory physiology · 2016
    Article
  13. 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

5 authors.

Jack LeeDepartment of Biomedical Engineering, King's College London, 3rd Floor, Lambeth Wing, St Thomas' Hospital, London, UK. jack.lee@kcl.ac.uk.
David NordslettenDepartment of Biomedical Engineering, King's College London, 3rd Floor, Lambeth Wing, St Thomas' Hospital, London, UK.
Andrew CooksonDepartment of Biomedical Engineering, King's College London, 3rd Floor, Lambeth Wing, St Thomas' Hospital, London, UK.
Simone RivoloDepartment of Biomedical Engineering, King's College London, 3rd Floor, Lambeth Wing, St Thomas' Hospital, London, UK.
Nicolas SmithDepartment of Biomedical Engineering, King's College London, 3rd Floor, Lambeth Wing, St Thomas' Hospital, London, UK.

Funding

Department of Health [UK]Wellcome Trust 088641/Z/09/Z
6 · The paper itself

Abstract

Coronary wave intensity analysis (cWIA) is a diagnostic technique based on invasive measurement of coronary pressure and velocity waveforms. The theory of WIA allows the forward- and backward-propagating coronary waves to be separated and attributed to their origin and timing, thus serving as a sensitive and specific cardiac functional indicator. In recent years, an increasing number of clinical studies have begun to establish associations between changes in specific waves and various diseases of myocardium and perfusion. These studies are, however, currently confined to a trial-and-error approach and are subject to technological limitations which may confound accurate interpretations. In this work, we have developed a biophysically based cardiac perfusion model which incorporates full ventricular-aortic-coronary coupling. This was achieved by integrating our previous work on one-dimensional modelling of vascular flow and poroelastic perfusion within an active myocardial mechanics framework. Extensive parameterisation was performed, yielding a close agreement with physiological levels of global coronary and myocardial function as well as experimentally observed cumulative wave intensity magnitudes. Results indicate a strong dependence of the backward suction wave on QRS duration and vascular resistance, the forward pushing wave on the rate of myocyte tension development, and the late forward pushing wave on the aortic valve dynamics. These findings are not only consistent with experimental observations, but offer a greater specificity to the wave-originating mechanisms, thus demonstrating the value of the integrated model as a tool for clinical investigation.

Indexed as

Models, CardiovascularPerfusionBiomechanical PhenomenaBlood Flow VelocityComputer SimulationCoronary CirculationCoronary VesselsCardiac perfusionComputational modellingPoromechanicsWave intensity analysis

Identifiers

PMID27008197
PMCPMC5106513

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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.