Collision-based spiral acceleration in cardiac media: roles of wavefront curvature and excitable gap.

We have previously shown in experimental cardiac cell monolayers that rapid point pacing can convert basic functional reentry (single spiral) into a stable multiwave spiral that activates the tissue at an accelerated rate. Here, our goal is to further elucidate the biophysical mechanisms of this rate acceleration without the potential confounding effects of microscopic tissue heterogeneities inherent to experimental preparations. We use computer simulations to show that, similar to experimental observations, single spirals can be converted by point stimuli into stable multiwave spirals.

The role restitution in pacing induced spiral wave acceleration.

Attempts to terminate monomorphic tachycardia by rapid pacing occasionally lead to acceleration of the tachycardia rate followed by fibrillation. Previous experimental studies have shown that rapid pacing can convert a single-wave functional reentry into a stable multi-wave reentry with accelerated rate, but only when the single spiral rate is significantly lower than the rate the tissue can sustain. In addition the acceleration was facilitated by broad and deep conduction velocity restitution.

An integrative model of mouse cardiac electrophysiology from cell to torso.

Aims: Although the transgenic mouse has become an important new tool in the study of human diseases and the design of new therapies, a complete picture of cardiac electrophysiology in the mouse, from genome to body surface, is lacking. A computational model of the mouse heart is presented, which is used to study the impact of ion-channel and structural manipulations on the distributions of extracellular potentials on the heart and body surface.

Methods: A model of the mouse heart anatomy, fibre organization and torso geometry was constructed from DTMRI images.

Analytical model of extracellular potentials in a tissue slab with a finite bath.

Extracellular potentials are often used to assess the activation and repolarization of transmembrane action potentials in cardiac tissue under a variety of experimental conditions. An analytical model of the extracellular potentials arising from a planar wavefront propagating in a three-dimensional slab of cardiac tissue with a variably thick adjacent volume conductor or bath is presented. Starting with the transmembrane potential, the model yields the extracellular potentials at various points in the bath and inside tissue.

Genesis of the monophasic action potential: role of interstitial resistance and boundary gradients.

The extracellular potential at the site of a mechanical deformation has been shown to resemble the underlying transmembrane action potential, providing a minimally invasive way to access membrane dynamics. The biophysical factors underlying the genesis of this signal, however, are still poorly understood. With the use of data from a recent experimental study in a murine heart, a three-dimensional anisotropic bidomain model of the mouse ventricular free wall was developed to study the currents and potentials resulting from the application of a point mechanical load on cardiac tissue.