A simulation study evaluating the performance of high-density electrode arrays on myocardial tissue.

Multielectrode arrays used to detect cellular activation have become so dense (electrodes per square millimeter) as to jeopardize the basic assumptions of activation mapping; namely, that electrodes are points adequately separated as to not interfere with the tissue or each other. This paper directly tests these assumptions for high-density electrode arrays. Using a finite element model with modified Fitzhugh-Nagumo kinetics, we represent electrodes as isopotential surfaces of varying widths and spacing ratio (SR) (center-to-center spacing divided by electrode width). We examine the signal strength and ability of a single electrode to detect activation due to a passing wavefront. We find that high-density arrays do not cause significant wavefront curvature or alter activation timing in the underlying tissue. Relationships between signal strength, cross talk, and array design are explained by the interaction of the propagating wavefront and induced sources on the isopotential electrodes. Sensitivity analysis shows that these results may be generalized to a wide range of physiologically relevant designs and applications. We conclude that electrode array designs in which electrode spacing greatly exceeds electrode diameter are overly conservative and that arrays with a SR of less than 2.0 may perform successfully in electrophysiological studies.

Impact of transvenous lead position on active-can ICD defibrillation: a computer simulation study.

Optimizing lead placement in transvenous defibrillation remains central to the clinical aspects of the defibrillation procedure. Studies involving superior vena cava (SVC) return electrodes have found that left ventricular (LV) leads or septal positioning of the right ventricular (RV) lead minimizes the voltage defibrillation threshold (VDFT) in endocardial lead-->SVC defibrillation systems. However, similar studies have not been conducted for active-can configurations. The goal of this study was to determine the optimal lead position to minimize the VDFT for systems incorporating an active can. This study used a high resolution finite element model of a human torso that includes the fiber architecture of the ventricular myocardium to find the role of lead positioning in a transvenous LEAD-->can defibrillation electrode system. It was found that, among single lead systems, posterior positioning of leads in the right ventricle lowers VDFTs appreciably. Furthermore, a septal location of leads resulted in lower VDFTs than free-wall positioning. Increasing the number of leads, and thus the effective lead surface area in the right ventricle also resulted in lower VDFTs. However, the lead configuration that resulted in the lowest VDFTs is a combination of mid-cavity right ventricle lead and a mid-cavity left ventricle lead. The addition of a left ventricular lead resulted in a reduction in the size of the low gradient regions and a change of its location from the left ventricular free wall to the septal wall.

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.