4.5 Article

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

Journal

BIOMECHANICS AND MODELING IN MECHANOBIOLOGY
Volume 15, Issue 6, Pages 1535-1555

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s10237-016-0782-5

Keywords

Wave intensity analysis; Cardiac perfusion; Poromechanics; Computational modelling

Funding

  1. Engineering and Physical Sciences Research Council [EP/G0075727/2, EP/H046410/1]
  2. Centre of Excellence in Medical Engineering - Wellcome Trust
  3. EPSRC [WT 088641/Z/09/Z]
  4. Department of Health, via the National Institute for Health Research (NIHR) comprehensive Biomedical Research Centre award to Guy's and Thomas' NHS Foundation Trust in partnership with King's College London
  5. Kings College Hospital NHS Foundation Trust
  6. Engineering and Physical Sciences Research Council [EP/H046410/1, EP/J013250/1] Funding Source: researchfish
  7. EPSRC [EP/H046410/1, EP/J013250/1] Funding Source: UKRI

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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.

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