Functional properties of the myocardium are mediated by the tissue structure. Consequently, proper physiological studies and modeling necessitate a precise knowledge of the fiber orientation. Magnetic resonance (MR) diffusion tensor imaging techniques have been used as a nondestructive means to characterize tissue fiber structure; however, the descriptions so far have been mostly qualitative. This study presents a direct, quantitative comparison of high-resolution MR fiber mapping and histology measurements in a block of excised canine myocardium. Results show an excellent correspondence of the measured fiber angles not only on a point-by-point basis (average difference of −2.30 ± 0.98°, n = 239) but also in the transmural rotation of the helix angles (average correlation coefficient of 0.942 ± 0.008 with average false-positive probability of 0.004 ± 0.001, n = 24). These data strongly support the hypothesis that the eigenvector of the largest MR diffusion tensor eigenvalue coincides with the orientation of the local myocardial fibers and underscore the potential of MR imaging as a noninvasive, three-dimensional modality to characterize tissue fiber architecture.

The simulations demonstrate the sensitivity of spread of activation and potential time courses and distributions to the underlying electrical properties in both thick and thin slabs. The bidomain model is shown to be a useful representation of cardiac tissue for interpreting experimental data of activation.

This article investigates the quantitative predictive capabilities of region-specific models by comparing experimental electrograms obtained from in vivo mapping of the ventricular free wall with those obtained through simulation of a region specific three-dimensional bidomain model that incorporates measured fiber orientations. Epicardial electrograms were recorded from canine left ventricles during and after unipolar pacing using a 528-channel electrode plaque. Fiber directions throughout the tissue were estimated from diffusion-weighted MRI and from pace mapping. Electrograms were computed in the bidomain model with experimentally derived properties during paced activations at the same spatiotemporal resolution as those recorded experimentally. Epicardial potentials from model and experiment were directly compared, and sensitivities of these comparisons to reference electrode location and to the choice of material properties were analyzed. The comparisons performed here demonstrate, that (1) the stimulus artifact can be used to estimate the in vivo myocardial fiber architecture, (2) the correlation between simulated and experimental electrograms decreases with increasing pacing depth, and (3) the quantitative comparisons between bidomain model and experimental data are sensitive to both the description of the fiber architecture, and the location of the unipolar reference electrode, but relatively insensitive to moderate changes in the bidomain conductivities.

Ventricular myocardium comprises at least three electrophysiologically distinct cell types: epicardial, endocardial and M cells. Epicardial and M cells, but not endocardial cells, display action potentials with a notched or spike-and-dome morphology: the result of a prominent, transient, outward current-mediated phase 1. M cells are distinguished from endocardial and epicardial cells by the ability of their action potential to disproportionately prolong in response to a slowing down of rate and/or in response to agents with class III actions. This intrinsic electrical heterogeneity contributes to the inscription of the electrocardiogram (ECG) as well as to the development of a variety of cardiac arrhythmias. Heterogeneous response of the three cell types to pharmacological agents and/or pathophysiological states results in amplification of intrinsic electrical heterogeneities, thus providing a substrate as well as a trigger for the development of re-entrant arrhythmias, including Torsade de Pointes, commonly associated with the long-QT syndrome (LQTS), and the polymorphic ventricular tachycardia/ventricular fibrillation (VT/VF) encountered in the Brugada syndrome. Despite an abundance of experimental data describing the heterogeneity of cellular electrophysiology that exists across the ventricular wall, relatively few computer models have been developed to investigate the physiological and pathophysiological consequences of such electrical heterogeneity. As computer power increases and numerical algorithms improve, three-dimensional computer models of ventricular conduction that combine physiological membrane kinetics with realistic descriptions of myocardial structure and geometry will become more feasible. With sufficient detail and accuracy, these models should illuminate the complex mechanisms underlying the initiation and maintenance of Torsade de Pointes and other arrhythmias.

A bidomain model of cardiac tissue was used to examine the effect of transmural fiber rotation during bipolar stimulation in three-dimensional (3-D) myocardium. A 3-D tissue block with unequal anisotropy and two types of fiber rotation (none and moderate) was stimulated along and across fibers via bipolar electrodes on the epicardial surface, and the resulting steady-state interstitial (phi e) and transmembrane (Vm) potentials were computed. Results demonstrate that the presence of rotated fibers does not change the amount of tissue polarized by the point surface stimuli, but does cause changes in the orientation of phi e and Vm in the depth of the tissue, away from the epicardium. Further analysis revealed a relationship between the Laplacian of phi e, regions of virtual electrodes, and fiber orientation that was dependent upon adequacy of spatial sampling and the interstitial anisotropy. These findings help to understand the role of fiber architecture during extracellular stimulation of cardiac muscle.