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    Modeling ventricular repolarization: effects of transmural and apex-to-base heterogeneities in action potential durations

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    Advanced multiscale models in computational electrocardiology offer a detailed representation of the heart bioelectrical activity, ranging from the microscopic description of ion channels of the cellular membrane to the macroscopic properties of anisotropic front propagation in the whole heart. Our model consists of a Monodomain or Bidomain tissue representation that includes orthotropic anisotropy, transmural fiber rotation and homogeneous or heterogeneous intrinsic membrane properties, described by Luo-Rudy type models. We consider membrane heterogeneities due either to the presence of midwall cells (M-cells) with different action potential durations (APDs) or to the presence of subendocardial ischemic regions. We present the results of large-scale simulations of an entire heartbeat with epicardial or endocardial pacing of three-dimensional ventricular blocks. We will also discuss some numerical features of our simulations, including parallel scalability, multilevel preconditioning and space-time adaptivity

    Epicardial and intramural excitation during ventricular pacing: effect of myocardial structure.

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    Published studies show that ventricular pacing in canine hearts produces three distinct patterns of epicardial excitation: elliptical isochrones near an epicardial pacing site, with asymmetric bulges; areas with high propagation velocity, up to 2 or 3 m/s and numerous breakthrough sites; and lower velocity areas (<1 m/s), where excitation moves across the epicardial projection of the septum. With increasing pacing depth, the magnitude of epicardial potential maxima becomes asymmetric. The electrophysiological mechanisms that generate the distinct patterns have not been fully elucidated. In this study, we investigated those mechanisms experimentally. Under pentobarbital anesthesia, epicardial and intramural excitation isochrone and potential maps have been recorded from 22 exposed or isolated dog hearts, by means of epicardial electrode arrays and transmural plunge electrodes. In five experiments, a ventricular cavity was perfused with diluted Lugol solution. The epicardial bulges result from electrotonic attraction from the helically shaped subepicardial portions of the wave front. The high-velocity patterns and the associated multiple breakthroughs are due to involvement of the Purkinje network. The low velocity at the septum crossing is due to the missing Purkinje involvement in that area. The asymmetric magnitude of the epicardial potential maxima and the shift of the breakthrough sites provoked by deep stimulation are a consequence of the epi-endocardial obliqueness of the intramural fibers. These results improve our understanding of intramural and epicardial propagation during premature ventricular contractions and paced beats. This can be useful for interpreting epicardial maps recorded at surgery or inversely computed from body surface ECGs
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