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F J Claydon

Publications and source records attributed to F J Claydon.

8 recordsLinked to original sources
PubMed1999

Patterns of and mechanisms for shock-induced polarization in the heart: a bidomain analysis.

This paper examines the combined action of cardiac fiber curvature and transmural fiber rotation in polarizing the myocardium under the conditions of a strong electrical shock. The study utilizes a three-dimensional finite element model and the continuous bidomain representation of cardiac tissue to model steady-state polarization resulting from a defibrillation-strength uniform applied field. Fiber architecture is incorporated in the model via the shape of the heart, an ellipsoid of variable ellipticity index, and via an analytical function, linear or nonlinear, describing the transmural fiber rotation. Analytical estimates and numerical results are provided for the location and shape of the "bulk" polarization (polarization away from the tissue boundaries) as a function of the fiber field, or more specifically, of the conductivity changes in axial and radial direction with respect to the applied electrical field lines. Polarization in the tissue "bulk" is shown to exist only under the condition of unequal anisotropy ratios in the extra- and intracellular spaces. Variations in heart geometry and, thus, fiber curvature, are found to lead to change in location of the zones of significant membrane polarization. The transmural fiber rotation function modulates the transmembrane potential profile in the radial direction. A higher gradient of the transmural transmembrane potential is observed in the presence of fiber rotation as compared to the no rotation case. The analysis presented here is a step forward in understanding the interaction between tissue structure and applied electric field in establishing the pattern of membrane polarization during the initial phase of the defibrillation shock.

Anisotropy↗
PubMed1999

Defibrillation efficacy of different electrode placements in a human thorax model.

The objective of this study was to measure the defibrillation threshold (DFT) associated with different electrode placements using a three-dimensional anatomically realistic finite element model of the human thorax. Coil electrodes (Endotak DSP, model 125, Guidant/CPI) were placed in the RV apex along the lateral wall (RV), withdrawn 10 mm away from the RV apex along the lateral wall (RVprox), in the RV apex along the anterior septum (RVseptal), and in the SVC. An active pulse generator (can) was placed in the subcutaneous prepectoral space. Five electrode configurations were studied: RV-->SVC, RVprox-->SVC, RVSEPTAL-->SVC, RV-->Can, and RV-->SVC + Can. DFTs are defined as the energy required to produce a potential gradient of at least 5 V/cm in 95% of the ventricular myocardium. DFTs for RV-->SVC, RVprox-->SVC, RVseptal-->SVC, RV-->Can, and RV-->SVC + Can were 10, 16, 7, 9, and 6 J, respectively. The DFTs measured at each configuration fell within one standard deviation of the mean DFTs reported in clinical studies using the Endotak leads. The relative changes in DFT among electrode configurations also compared favorably. This computer model allows measurements of DFT or other defibrillation parameters with several different electrode configurations saving time and cost of clinical studies.

Computer Simulation↗
PubMed1999

Membrane polarization induced in the myocardium by defibrillation fields: an idealized 3-D finite element bidomain/monodomain torso model.

This study develops a three-dimensional finite element torso model with bidomain myocardium to simulate the transmembrane potential (TMP) of the heart induced by defibrillation fields. The inhomogeneities of the torso are modeled as eccentric spherical volumes with both the curvature and the rotation features of cardiac fibers incorporated in the myocardial region. The numerical computation of the finite element bidomain myocardial model is validated by a semianalytic solution. The simulations show that rotation of fiber orientation through the depth of the myocardial wall changes the pattern of polarization and decreases the amount of cardiac tissue polarized compared to the idealized analytic model with no fiber rotation incorporated. The TMP induced by transthoracic and transvenous defibrillation fields are calculated and visualized. The TMP is quantified by a continuous measure of the percentage of myocardial mass above a potential gradient threshold. Using this measure, the root mean square differences in TMP distribution produced by reversing the electrode polarity for anterior-posterior and transvenous electrode configurations are 13.6 and 28.6%, respectively. These results support the claim that a bidomain model of the heart predicts a change of defibrillation threshold with reversed electrode polarity.

Computer Simulation↗
PubMed1998

Extracting isovolumes from three-dimensional torso geometry using PROLOG.

Three-dimensional (3-D) finite element torso models are widely used to simulate defibrillation field quantities, such as potential, gradient, and current density. These quantities are computed at spatial nodes that comprise the torso model. These spatial nodes typically number between 10(5) and 10(6), which makes the comprehension of torso defibrillation simulation output difficult. Therefore, the objective of this study is to rapidly prototype software to extract a subset of the geometric model of the torso for visualization in which the nodal information associated with the geometry of the model meets a specified threshold value (e.g., minimum gradient). The data extraction software is implemented in PROLOG, which is used to correlate the coordinate, structural, and nodal data of the torso model. A PROLOG-based environment has been developed and is used to rapidly design and test new methods for sorting, collecting, and optimizing data extractions from defibrillation simulations in a human torso model for subsequent visualization.

Algorithms↗
PubMed1991

Effects of myocardial infarction on cardiac electrical field properties using a numerical expansion technique.

This study was undertaken to quantify basic cardiac electrical field properties using the Karhounen-Loeve (K-L) numerical expansion technique after experimental myocardial infarction. Transmural anterior myocardial infarction was produced in seven dogs by injection of liquid latex into the anterior descending artery; posterior myocardial infarction was produced in five dogs by injection of the circumflex artery. Body surface potentials from 84 electrodes were recorded during sinus rhythm prior to and 1 week after infarction. Electrical field properties during the QRS, ST, and QRST intervals were computed by the K-L method based upon areas calculated for each lead. The ratio of the sum of magnitude of the first three eigenvectors to the sum of all computed eigenvectors expressed as a percentage was used as a measure analogous to field dipolarity. Values before infarction were high during the QRS (97.1% +/- 2.0%, mean +/- 1SD), ST (96.0% +/- 5.1%), and QRST (97.7% +/- 2.7%) intervals, with no significant difference between the three periods. After infarction, the ratio during QRS decreased significantly, with lower values after posterior (61.9% +/- 11.7%) than after anterior (91.1% +/- 6.0%) infarction (p less than 0.001). Values during ST and QRST intervals were not significantly changed by infarction. Spatial patterns of the first eigenvector indicated that the derived QRS area electric field is directed away from the myocardial lesion for both anterior and posterior infarcts. Thus, experimental myocardial infarction produces significant changes in cardiac electrical field properties as measured by the K-L technique.

Animals↗
PubMed1986

The potential gradient field created by epicardial defibrillation electrodes in dogs.

Knowledge of the potential gradient field created by defibrillation electrodes is important for the understanding and improvement of defibrillation. To obtain this knowledge by direct measurements, potentials were recorded from 60 epicardial, eight septal, and 36 right ventricular transmural electrodes in six open-chest dogs while 1 to 2 V shocks were given through defibrillation electrodes on the right atrium and left ventricular apex (RA. V) and on the right and left ventricles (RV .LV). The potential gradient field across the ventricles was calculated for these low voltages. Ventricular fibrillation was electrically induced, and ventricular activation patterns were recorded after delivering high-voltage shocks just below the defibrillation threshold. With the low-voltage shocks, the potential gradient field was very uneven, with the highest gradient near the epicardial defibrillation electrodes and the weakest gradient distant from the defibrillation electrodes for both RA. V and RV .LV combinations. The mean ratio of the highest to the lowest measured gradient over the entire ventricular epicardium was 19.4 +/- 8.1 SD for the RA. V combination and 14.4 +/- 3.4 for the RV .LV combination. For both defibrillation electrode combinations, the earliest sites of activation after unsuccessful shocks just below the defibrillation threshold were located in areas where the potential gradient was weak for the low-voltage shocks. We conclude that there is a markedly uneven distribution of potential gradients for epicardial defibrillation electrodes with most of the voltage drop occurring near the electrodes, the potential gradient field is significant because it determines where shocks fail to halt fibrillation, and determination of the potential gradient field should lead to the development of improved electrode locations for defibrillation.

Animals↗