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A E Pollard

Publications and source records attributed to A E Pollard.

22 records · Page 2Linked to original sources
PubMed1991

Computer simulations of activation in an anatomically based model of the human ventricular conduction system.

Simulations of the electrical activity during excitation were performed in an anatomically based model of the human ventricular conduction system. Each of the 33,000 elements of this model represented a unit bundle of Purkinje or atrioventricular nodal tissue. The Ebihara-Johnson model for sodium defined the active membrane characteristics. Using a combination of new and existing modeling techniques, simulations of excitation were completed in approximately 5 min CPU time on an IBM 3090 at the Cornell National Supercomputer Facility. Activation times at sites in the model were compared to experimental measurements for the excitation of the ventricular myocardium on the endocardial surface. These "literature-based" times were estimated from a number of reported human heart mapping studies. Initially, the times fit poorly. The major factor for the discrepancy was the conduction velocities of the elements, which were a result of the physical and electrical parameters derived from a review of histologic and electrical properties studies. In addition, there was a latency between activation of the system in the left ventricle of the model and that in the right ventricle when compared to the experimental work. When the times were scaled to adjust for the conduction velocity and ventricular latency effects, the match between the simulation and literature-based times was much improved. Quantitative comparison between normalized times resulted in correlation coefficients CCF = 0.76 for the right ventricle and CCF = 0.64 for the left ventricle.

Atrial Function↗
PubMed1990

The construction of an anatomically based model of the human ventricular conduction system.

The ventricular conduction system is a complicated network of specialized muscle cells responsible for the transmission of electrical activity between the atria and the ventricles of the human heart. It has been the focus of numerous electrical and anatomical studies at both the microscopic and macroscopic levels. An understanding of its behavior at both levels is considered important, because it is primarily responsible for the spread of excitation in the ventricles. Previous computer models have been very simple ones that have been primarily adjuncts to models of the ventricles. This paper describes a strategy for the construction of conduction system models which is based on real microscopic and macroscopic features, although the model still is much simpler than reality. The model contains almost 35,000 individual cylindrical elements, each of whose physical dimensions approximate unit bundles of Purkinje and atrioventricular nodal cells. The model, whose physical appearance closely resembles that of the conduction system, was generated from limited anatomical data in less than 2 min CPU time on an IBM 3090 at the Cornell National Supercomputer Facility.

Atrioventricular Node↗
PubMedDate not supplied

A model study of intramural dispersion of action potential duration in the canine pulmonary conus.

Regional gradients of action potential duration (APD) due to electrophysiological differences between endocardial, midmyocardial, and epicardial myocytes may exist across the ventricular wall. In addition, activation sequence-induced gradients of APD may occur if intramural fiber rotation accelerates or decelerates the depolarization wave front. To investigate relative contributions of regional and activation sequence-induced gradients to intramural APD dispersion, we simulated action potential propagation in two-dimensional models with idealized geometries representing the canine pulmonary conus. Ionic currents for endocardial myocytes were described using the Luo-Rudy membrane equations. Modifications to I(Ks) approximated action potentials of epicardial and midmyocardial cells. Spatial coupling was modeled with a bidomain representation of tissue structure that included unequal anisotropic conductivity ratios. Activation sequence-induced gradients reached 69 ms cm(-1) during a nonuniform activation sequence where the change in orientation between endocardial and epicardial fibers accelerated the depolarization wave front. Regional gradients reached 133 ms cm(-1) at the boundary between endocardial and midmyocardial cells. When regional and activation sequence-induced gradients were oriented in opposite directions, overall APD dispersion decreased. When the gradients were oriented in the same direction, overall dispersion measured as high as 202 ms cm(-1). This gradient exceeded values previously estimated as sufficient to induce cardiac arrhythmia during premature stimulation and suggests that regional and activation sequence-induced gradients increase arrhythmia vulnerability in the presence of other arrhythmogenic conditions.

Action Potentials↗