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Mark L Trew

Publications and source records attributed to Mark L Trew.

5 recordsLinked to original sources

Cardiac electrophysiology and tissue structure: bridging the scale gap with a joint measurement and modelling paradigm.

Significant tissue structures exist in cardiac ventricular tissue that are of supracellular dimension. It is hypothesized that these tissue structures contribute to the discontinuous spread of electrical activation, may contribute to arrhymogenesis and also provide a substrate for effective cardioversion. However, the influences of these mesoscale tissue structures in intact ventricular tissue are difficult to understand solely on the basis of experimental measurement. Current measurement technology is able to record at both the macroscale tissue level and the microscale cellular or subcellular level, but to date it has not been possible to obtain large volume, direct measurements at the mesoscales. To bridge this scale gap in experimental measurements, we use tissue-specific structure and mathematical modelling. Our models have enabled us to consider key hypotheses regarding discontinuous activation. We also consider the future developments of our intact tissue experimental programme.

Action Potentials↗

Solving the cardiac bidomain equations for discontinuous conductivities.

Fast simulations of cardiac electrical phenomena demand fast matrix solvers for both the elliptic and parabolic parts of the bidomain equations. It is well known that fast matrix solvers for the elliptic part must address multiple physical scales in order to show robust behavior. Recent research on finding the proper solution method for the bidomain equations has addressed this issue whereby multigrid preconditioned conjugate gradients has been used as a solver. In this paper, a more robust multigrid method, called Black Box Multigrid, is presented as an alternative to conventional geometric multigrid, and the effect of discontinuities on solver performance for the elliptic and parabolic part is investigated. Test problems with discontinuities arising from inserted plunge electrodes and naturally occurring myocardial discontinuities are considered. For these problems, we explore the advantages to using a more advanced multigrid method like Black Box Multigrid over conventional geometric multigrid. Results will indicate that for certain discontinuous bidomain problems Black Box Multigrid provides 60% faster simulations than using conventional geometric multigrid. Also, for the problems examined, it will be shown that a direct usage of conventional multigrid leads to faster simulations than an indirect usage of conventional multigrid as a preconditioner unless there are sharp discontinuities.

Action Potentials↗

Do intramural virtual electrodes facilitate successful defibrillation? Model-based analysis of experimental evidence.

INTRODUCTION: Recent computer model and experimental studies have suggested that microscopic intramural collagenous planes may facilitate successful defibrillation through the generation of shock-induced virtual electrodes deep within the ventricular wall. Evidence supporting the existence of intramural virtual electrodes has been drawn from several recent studies, which map shock-induced membrane potential (Vm) over the cut transmural surface of dissected segments of porcine left ventricle (LV). The artificially created transmural boundary in these experiments is impermeable to intracellular current. It is not known how this constraint limits the interpretation of these experiments in terms of the shock response of the intact ventricle. METHODS AND RESULTS: This study uses a realistic 3D computer model of LV myocardium to aid experimental interpretation. The model incorporates a microstructural description of intramural cleavage plane discontinuities measured by confocal microscopy of rat LV. Electrical shocks are applied across the model tissue, with and without introduced transmural boundaries. Shocks of varying strength (4-40 V/cm) are also applied to the model and the response analyzed. Results show that shock-induced Vm changes (deltaVm) on a transmural tissue boundary are significantly different to deltaVm of the intact ventricle, and the extent of difference depends on boundary orientation. However, the presence and qualitative behavior of intramural virtual electrodes is preserved irrespective of boundary placement. The model also confirms experimental observations that most rapid transmural activation occurs for shocks of strength 5-10 V/cm. Two distinct mechanisms suppress virtual electrode propagation, and hence slow tissue activation, outside of this optimal shock strength range. CONCLUSIONS: This study supports the hypothesis that distributed microscopic intramural virtual electrodes contribute to rapid activation of the ventricular wall during defibrillation.

Animals↗

Modeling cardiac electrical activity at the cell and tissue levels.

Significant tissue structures exist in cardiac ventricular tissue, which are of supracellular dimension. It is hypothesized that these tissue structures contribute to the discontinuous spread of electrical activation, may contribute to arrhythmogenesis, and also provide a substrate for effective cardioversion. However, the influences of these mesoscale tissue structures in intact ventricular tissue are difficult to understand solely on the basis of experimental measurement. Current measurement technology is able to record at both the macroscale tissue level and the microscale cellular or subcellular level, but to date it has not been possible to obtain large volume, direct measurements at the mesoscales. To bridge this scale gap in experimental measurements, we use tissue-specific structure and mathematical modeling. Our models, which can incorporate ion channel models at the cell level into the reaction-diffusion equations at the tissue level, have enabled us to consider key hypotheses regarding discontinuous activation.

Heart↗

A generalized finite difference method for modeling cardiac electrical activation on arbitrary, irregular computational meshes.

A generalized finite difference (GFD) method is presented that can be used to solve the bi-domain equations modeling cardiac electrical activity. Classical finite difference methods have been applied by many researchers to the bi-domain equations. However, these methods suffer from the limitation of requiring computational meshes that are structured and orthogonal. Finite element or finite volume methods enable the bi-domain equations to be solved on unstructured meshes, although implementations of such methods do not always cater for meshes with varying element topology. The GFD method solves the bi-domain equations on arbitrary and irregular computational meshes without any need to specify element basis functions. The method is useful as it can be easily applied to activation problems using existing meshes that have originally been created for use by finite element or finite difference methods. In addition, the GFD method employs an innovative approach to enforcing nodal and non-nodal boundary conditions. The GFD method performs effectively for a range of two and three-dimensional test problems and when computing bi-domain electrical activation moving through a fully anisotropic three-dimensional model of canine ventricles.

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